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Avascular Necrosis for Orthopaedic Exams
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Avascular Necrosis for Orthopaedic Exams
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Segment:0 .
Welome guy, welcome to this Wednesday's FRCS teaching. The session tonight is delivered by Hermanta Das, he's a specialty doctor from the UK works in Boston. He's very experienced and clinically and also with that, particularly with the exam. Um, and he was he picked this topic, which is very commonly asked. It was called necrosis and also we tell us about his experience with the exam and how to answer questions and how to target your responses.
And also with us is Kashif. And we have David, also, David, at the end of this presentation will also tell us about very excellent course, clinical course that he runs. So over to you now. Hi, guys, come see everyone. Hope most of the guys are here. As first mentioned that it's a very commonly asked topic, and I can tell you from a shot as it gets born that secondary to ischemia, we all talk about the femoral head, but we have got the other parts as you could see that the humeral head is something to be commonly asked in my own experience.
We're all aware of the tolerance as host phenomenon. The lunate is there as it gets, but. The still medial epicondyle the song is another topic altogether. Just be aware that they can come from any corner that they want to.
A bit of epidemiology 50 male dominated 50% can be bilateral, relatively young age group problem. It is a challenge to pick up early. That's why we've got all the problems and grossly it happens due to disruption of blood supply or compartment syndrome of the anatomic area. But it's also important to emphasize that it is still poorly understood and I'll come to details of that.
This is what they call the laundry list, and we have all read this the different causes of avian or osteonecrosis, whichever way you want to say it. The key bits are in bowls, which is the idiopathic is 40% Steroids account for 37% and high alcohol 20% So you can do the maths. That's the vast majority of patients that we're going to see.
However, exams or exams, I the first time I got that humeral, a subtle one. I was told that this patient is being treated for a brain tumor. And I had to comment on why is this patient getting a humeral head event? And I had no idea you can make it up, whichever way you want to.
But essentially, if you look down the list, it's the haematological malignancies, the lymphoma leukemia that can cause even. But grossly, they can give you different types of presentations, and they like to do that. So we'll talk about this later in the viewer's. These are some facts about the natural history.
75% of symptomatic patients will end up with collapse in three years. Important figures. 64% of the pre collapsed patients are symptomatic. MRD positive only patients, if you take the cohort. 75% will be symptomatic at six years, so. Now or later, it will be a problem, it will be symptomatic.
And if you're young. And if you have got lumps and degenerative disease, you will end up having another blast. These are just facts. So come to pathology. This is just an overview slide. The examiners are very keen to ask you about why is this happening? And I face this question both times.
They told me, well, first to make the diagnosis, then they give you the patient's history and then they ask you, why is this happening? Whatever you say, the reason the etiology of this pathology, they'll ask you, why is this happening? So there comes the nitty-gritty of it. So for all candidates, you have to prepare a paragraph in your mind, what are you going to say when that question comes?
All right. There's a lot in there, but you have to as with most things, you have to prepare something in your mind to say when the question comes. There's a lot, so you have to prepare your own paragraph. So the pathology involves local changes and not inflow or outflow. There could be a hemorrhage or could be edema in the marrow. And the key thing is the vicious cycle.
It always becomes a vicious cycle. There is increased in ferocious pressure that causes vascular compromise, leading to further edema, and it goes on and they skinnier causes necrosis. It is literally one thing leading to other and. The UV initially get an attempt to regrowth. There is some vascular infiltration, which gives rise to the sclerotic area, but the part that is necrotic continues to collapse.
That's what you see. This is a picture from a book that shows the vicious cycle nicely. So you and there are some etiologies that actually directly cause these. If I go back to my etiology slide, I've tried to. First, we have tried to group them into and the pathology where you've got a few under arterial insufficiency, some under artigo or some capillary.
So those are grossly some bigger headings under which it come. So what are you getting? Somehow you're getting an arterial occlusion that's leading to marrow edema, that's compressing the sinus sides and hence you've got venous stiffness. So what? Can everyone hear properly?
I hear you very well. Himanta thank you. Nice, nice space for us to keep, you know, following you and we can see you everything, all good or good. We just been quiet listening to you, but we don't want to interrupt you. That's all. You there are several theories about why it happened. What's the etiology of putting a few it just for people to have a little read later on because this is not really a good forum to develop concepts, but this is more information, and I'm putting a lot of emphasis on pathology and etiology purely because they ask it.
They do ask it and they like to hear something from you that you have got a concept, that you have got some ideas or some knowledge about it, and you can talk about the pathology for a minute. I think if you can talk about the pathology for a minute, you pass that situation seriously. And that's the bit that the opinion. So the first, Uh, theory is in atrocious hypertension, where?
People have consistently found raised in ferocious pressures in Indian patients, so they found that the blood flow through the intravenous compartment is inversely proportional to the bone marrow pressure, so that makes sense. And of course, increases in the pressure produces a decrease in the blood flow. So that will lead to ischemia and subsequent osteonecrosis or even so in ferocious hypertension.
Being the primary culprit is one theory. And hence, everything else follows the next theory is abnormal, extra cautious blood flow. Mind you, extra cautious could be introduced as well, but this is extra cautious. So if you've got consistent loss of Trump's cortical blood flow. And this is just related to the femoral right, that's why it's so rectangular arteries and alteration in the squarish revascularization process that's demonstrated in avian patients and alteration of the revascularization process considered to be a contributory feature of long, reversible avian.
So you can see that. And these are all observations, you can imagine that people have done experiments and they've seen things which have happened and hence the theories have come. So the avian that is not getting reversed from this particular process happening? Yeah the next theory is fat embolism, and this is, I think, something important to remember because a few of the etiologies would tally with these so fatty osteoarthritis necrosis thought to progress to degeneration of necrotic osteoarthritis and adipocytes subcultural fat overload leads to vascular stasis, causing local hyper debility, endothelial damage, subsequent intravascular coagulation, histologically intereses thrombosis and peripheral hemorrhage can be seen now.
These are difficult to remember. These are difficult to remember. I totally appreciate it. The reason I have done so many slides on these again, I'm just repeating myself that it's to emphasize the point that this is important to know the pathology. You read it at your own time. You try to explain it in your mind, in whichever you want.
But the final result is that you have to come out with an answer. Yeah, Yeah. Can I say something? Yeah, sure. Because I found this particular area of aviation very confusing and difficult to remember, and I do. It's a bit complex. It is complicated.
I totally understand, but important to point out to the examiner. The first line of the answer is that there are multiple pathogenesis theories. They are not fully understood. You say that as a first line? Yeah and then you say all these causes that are saying talking about, you know, atrocious, extra cautious fat and so on, but make it clear to the examiner there are multiple pathogenesis theories and it's not fully understood.
So you're not committing yourself to one single cause because no one knows really. So I think the interest is hypertension and fat cell embolism are the two bits that probably is possible to remember on the vyver table, and you can probably get your answer centered on those two things. And I think it's perfectly reasonable to say that I do not know exactly how this etiology is leading to this pathology, but the common pathology that is noticed in the final pathway is this.
I think even if you say that, that will be good enough. Yeah yeah, it could be asked this one as boring as it is, but it could be ask and has been asked so many times. This is one pathology question that they liked asking about. But again, you don't need to go into great details about each etiology. If you remember that theory interest, extra cautious theories, and I think that will get you, that will pass you, you could add a few other things like Stromboli theory and things, but that will get you through this question.
I think here the fat cell abnormalities theory is directly related to the high dose corticosteroid exposure. So if you're given a patient who has got a history of steroid overuse or high dose steroid, you can definitely mention this as a direct correlation. OK and for the candidates to distinguish for the candidates between pathogenesis theories and etiological risk factors.
So yeah, and it's very easy for us to get confused. So please. And that's what the examiner is one of the things they are looking for. You are defining a line between these two cause etiological causing factors, which you go through in your surgical CV or the pathogenesis theories. So there are two different issues here. Yeah, generally when they present you the case in a way, they will very likely after you are diagnosed it on the x-ray, of course they will give you a history of the patient generally.
So this is your patient. And from there you get the etiology. So once you have mentioned you've got your etiology, then they'll ask you to link it to the pathology. How is it? So that is the question. Right, so how do we diagnose them in? Historically, it was diagnosed with biopsy, but now we have got imaging good imaging and then we come to classifications, which starts with Finkelstein, then which is more X-ray based.
So this is we got. And we all know if we get I'll just run through these quickly and then with the MRI, Steinberg and. This is the Arco go through that this is just something to show you. So this is what it comes down. Whatever you read it, from, whichever classification you like to court, you're free to quote that I have been asked about classification of alien, so don't assume that they can't ask you classification.
This is all it comes down to the crease side, whether you have see it on an X-ray and MRI or whatever, but this is what it comes down to. And if you go through the classifications, any of those, you'll see that the crease sign is the key differentiator before or after. So I don't think it matters which classification you caught in the exam. As long as the classification you can quote, I think anything you can use any classification.
So don't try too hard to remember these. I think if you just got figured that is fine, as long as you mentioned the importance of the present sign, I think that's good enough. Bone scan is another investigation. Just in case somebody throws it in or you are sucked into something that initially it is called before vascularization, but after it was canonisation, it becomes hot.
All right, so how do we manage the patient? So the key bit is the collapse stage. So either you've got a pre collapse patient or a post-collapse patient from the point of view of managing the patient. That's why we're seeing the present sign is the big demarcated and of course, the management differs accordingly. Symptom control, of course, is the main.
And if it is in the pre collapse stage, you do everything, try to prevent the collapse as early as you can. The patient with in a pretty club stage, would you stop something that you can see as the directly the agent that is directly causing it, which is either the steroid or the alcohol offloading the joint is the key thing.
Initially, again, the pharmacological agents are dependent on the etiology to some extent. I haven't gone in depth. I doubt whether you would be required to talk about this. But it's good to know what kind of drugs are used. So there is a role for drugs and particularly bisphosphonates. You can read up about that if you want to separately, but I doubt you would need this too much to know.
Yeah, but the main surgical procedure is called decompression. So it was started by figure as diagnostic and treatment and had good results if you compare with conservative management. But once collapse is established, it's not that effective. Yeah, and we have got variable success in literature.
15% to 30% failure rate in stage one sounds a lot, isn't it? And I don't think again, you need to know why or how, but. These are difficult operations, these are not straightforward surgeries. I'm sure there is a part to play with that. What about vascularized fibular graft? You have. It is controversial. Wherever things are controversial, I think it's quite good to mention it in the beginning of your answer.
It is not absolute or set in stone. It is controversial. All right. So the idea is to promote new bone formation. Hence, you're trying to prevent collapse. Preventing collapse is the key word. That's my aim of treatment. I want to prevent collapse. Yeah so.
There are variable reports. Some 80 percent, some say, delaying a hip replacement by seven years. But again, it's a difficult operation. You've got a donor site morbidity to deal with. Yeah a this picture just is this is the exterior shown in the Bible. Yeah I wouldn't be surprised if this does show this radiograph and ask you, what do you think is going on there?
All right. I don't know. And that's perhaps it depends on your symptoms and age. Of course, you can try cold decompression, you can. I think these are tricky questions when you're presented with a 22-year-old with an established collapse. What do you do? Are you going to try?
You're not going to try a cold decompression. I don't think anybody will blame you to try. However, understanding that it has got poorer results. These are tricky questions. So when the patient is older and if the patient has got arthritis sitting in, it's an easy choice you depending on the joints you resurface, you do a hemi or a total hip replacement or whatever.
And the other option in younger patients is Austria. So you have to think about all the treatment options. One after the other, OK, younger versus old. Pharmacologic agents, your called decompression vascularized fibular graft one or the other. Yeah, Austria. And then you come to arthroplasty.
So the summary is early diagnosis is difficult because it's difficult to pick up on standard x-rays, you need MRI scans. Sometimes when the patient is symptomatic, it's already a bit late. If you've got a patient in pre collapse, these are the options you stop the causative factors considered bisphosphonates or decompression vascular grafting.
I think osteotomy is something that comes after that. And when you've got a patient, it's already got a collapse. Again, you do symptom relief the best. You can consider decompression grafting, but you're looking at reconstruction sooner or later. So that's my last slide. if I go back to my original.
Thing is, they can give you this picture and immediately you think about a pre collapse patient, how you formulate your answer. Whereas this one is the post-collapse patient, so immediately you're thinking about reconstructive options that just examples. Exactly if you're in the exam, took principles.
Yeah, you know, salvage or salvage procedure procedures, and that's kind of things. So my advice to candidates from my experience is. If you talk about sound principles for the first minute of your five minutes, you pass the I mean, you pass that question.
If you are hesitating or not showing enough confidence to talk about the basic principles, that's where you start being in the risky zone, you wouldn't be failed if you cannot talk about whether you can do a core decompression of another bone. But you can very easily say that I know about the three options for the event of a femoral head, and I do not have any experience of this, but I believe that similar principles may be applied.
I don't think there is any harm in saying things like that. What is beyond doubt is beyond our scope. Yeah, they do begin to give you more marks, but those are not past field questions. Yeah and the other question, I think there was one question sent to me about this young patient with a collapse. And I think I would like to say if you present it, for example, with the 30 years old who had collapsed overall hate.
Um, obviously pre collapse, you try to preserve it if it's collapsed. And what I would suggest the answer should be is that once it's collapsed, we tell them clearly collapse require replacement surgery. However, as the patient is very young, I would like to refer him to young adult hip surgeon for opinion. Because they won't.
I thank you, thank you so much. I think gas was a great presentation. Very important topic. And I think you started this with a lot of useful information. I mean. You concisely briefed us on many geological factors and some background, and I like what you said, a few things. It was very, very important in counseling the patients, and that's what the examiners also would test us all the candidates about.
They want to know you can counsel a patient when a patient comes to you with a collapse. What are you going to tell this patient? They will tell you, what are you going to tell this patient in front of you in clinic? They ask you, do I need a hip replacement? What do you tell them? Tell them. I'll ask you what will happen if I leave it, and I think we've got the answers here.
Today, 75% of the collapse of symptomatic patients will collapse in three years. So we know if we have even symptomatic patients, they're going to collapse in three years. They will require a hip replacement. We know what to tell the patients, and that's extremely important. That's a higher level there. And again, the classification, you know, you could start going into effect and modified Venkat Steinberg and things like that.
I will never remember those. The most important thing is the Crescent sign bridge collapse or first collapse. The Christian side, obviously, it's a subcontract collapse, so you might still see the shell of the bone, but they were subcontract collapse and that's classified as a collapsed stage because the bone can collapse in any moment. So I would emphasize that point, Chris, and sign again pathological theorists versus etiological risk factors to focus on.
And I think that's really this presentation covers all you need to know about HIV and particularly of the hip out of the principles apply to other joints and bones. Any other comments from our mentors, David, we have David here. Yep well, I was just going to say with the young patient, the meat of the points will come and we'll be talking about your discussion with regards to its collapse.
I think it's all mentioned that what do you do in the young patient? The key thing is that the shared decision, I think ATF did say it there. You're part of your consultation with the patient is saying to them, yes, you're young. We have these options and then you leave that decision process between the surgeon and the patient.
So I think that's where you're going to get your point there because there's no right answer in that situation because it's so difficult. And as Martha said, it's something that you're going to talk about at conferences more than in the exam situation. And is this fair enough to say this will be a controversial thing, but just say you're having a Frank and open discussion with the patient?
I think that's very important, also very important decision making, and Thanks for David and Otto for sharing this. I think we know it. Sometimes you have to say it, you have to save the exam and get one more point. Particularly, it's a very common topic and mostly tested in almost every exam.
So all the candidates should know, even inside out. I mean, it should be. You should expect anything in the exam. I would recommend that all of us should study even from A to Z. Everyone should be ready for anything any weird and wonder can come regarding your view. That's true. It's a favorable in theory and the. Unfavorable question.
That's right. That's why I have 1 minute question in the hot seat session, only one minute that would give the score 8 if the candidate answers, well, it's not a conference to discuss. You give an answer. Being a safe PTH surgeon, as Faraz was saying, you have the discussion with the patient explained to the patient.
The natural history always recognize that this is a difficult problem. It is very important to mention to the patient, to the examiner that this is a difficult problem. It's a difficult decision. There is no obvious, clear way to manage this, but there are options and this is best managed by a specialist dealing with this. This is if you say these things that passes you, the exam and cemented and cemented is way beyond passing.
It is important that if you spend more time reading evidence on cemented versus cemented on avian, and if you haven't done the first minute well enough, it's of no use. If you, you need to speak the first minute really well to pass the exam, not the last minute. Exactly, exactly. And that's the whole way. Why are we giving this whole teaching exam technique?
What you should talk about and what you should try to avoid and how to approach each section? And that's extremely crucial. So we have.
Segment:0 .
Welome guy, welcome to this Wednesday's FRCS teaching. The session tonight is delivered by Hermanta Das, he's a specialty doctor from the UK works in Boston. He's very experienced and clinically and also with that, particularly with the exam. Um, and he was he picked this topic, which is very commonly asked. It was called necrosis and also we tell us about his experience with the exam and how to answer questions and how to target your responses.
And also with us is Kashif. And we have David, also, David, at the end of this presentation will also tell us about very excellent course, clinical course that he runs. So over to you now. Hi, guys, come see everyone. Hope most of the guys are here. As first mentioned that it's a very commonly asked topic, and I can tell you from a shot as it gets born that secondary to ischemia, we all talk about the femoral head, but we have got the other parts as you could see that the humeral head is something to be commonly asked in my own experience.
We're all aware of the tolerance as host phenomenon. The lunate is there as it gets, but. The still medial epicondyle the song is another topic altogether. Just be aware that they can come from any corner that they want to.
A bit of epidemiology 50 male dominated 50% can be bilateral, relatively young age group problem. It is a challenge to pick up early. That's why we've got all the problems and grossly it happens due to disruption of blood supply or compartment syndrome of the anatomic area. But it's also important to emphasize that it is still poorly understood and I'll come to details of that.
This is what they call the laundry list, and we have all read this the different causes of avian or osteonecrosis, whichever way you want to say it. The key bits are in bowls, which is the idiopathic is 40% Steroids account for 37% and high alcohol 20% So you can do the maths. That's the vast majority of patients that we're going to see.
However, exams or exams, I the first time I got that humeral, a subtle one. I was told that this patient is being treated for a brain tumor. And I had to comment on why is this patient getting a humeral head event? And I had no idea you can make it up, whichever way you want to.
But essentially, if you look down the list, it's the haematological malignancies, the lymphoma leukemia that can cause even. But grossly, they can give you different types of presentations, and they like to do that. So we'll talk about this later in the viewer's. These are some facts about the natural history.
75% of symptomatic patients will end up with collapse in three years. Important figures. 64% of the pre collapsed patients are symptomatic. MRD positive only patients, if you take the cohort. 75% will be symptomatic at six years, so. Now or later, it will be a problem, it will be symptomatic.
And if you're young. And if you have got lumps and degenerative disease, you will end up having another blast. These are just facts. So come to pathology. This is just an overview slide. The examiners are very keen to ask you about why is this happening? And I face this question both times.
They told me, well, first to make the diagnosis, then they give you the patient's history and then they ask you, why is this happening? Whatever you say, the reason the etiology of this pathology, they'll ask you, why is this happening? So there comes the nitty-gritty of it. So for all candidates, you have to prepare a paragraph in your mind, what are you going to say when that question comes?
All right. There's a lot in there, but you have to as with most things, you have to prepare something in your mind to say when the question comes. There's a lot, so you have to prepare your own paragraph. So the pathology involves local changes and not inflow or outflow. There could be a hemorrhage or could be edema in the marrow. And the key thing is the vicious cycle.
It always becomes a vicious cycle. There is increased in ferocious pressure that causes vascular compromise, leading to further edema, and it goes on and they skinnier causes necrosis. It is literally one thing leading to other and. The UV initially get an attempt to regrowth. There is some vascular infiltration, which gives rise to the sclerotic area, but the part that is necrotic continues to collapse.
That's what you see. This is a picture from a book that shows the vicious cycle nicely. So you and there are some etiologies that actually directly cause these. If I go back to my etiology slide, I've tried to. First, we have tried to group them into and the pathology where you've got a few under arterial insufficiency, some under artigo or some capillary.
So those are grossly some bigger headings under which it come. So what are you getting? Somehow you're getting an arterial occlusion that's leading to marrow edema, that's compressing the sinus sides and hence you've got venous stiffness. So what? Can everyone hear properly?
I hear you very well. Himanta thank you. Nice, nice space for us to keep, you know, following you and we can see you everything, all good or good. We just been quiet listening to you, but we don't want to interrupt you. That's all. You there are several theories about why it happened. What's the etiology of putting a few it just for people to have a little read later on because this is not really a good forum to develop concepts, but this is more information, and I'm putting a lot of emphasis on pathology and etiology purely because they ask it.
They do ask it and they like to hear something from you that you have got a concept, that you have got some ideas or some knowledge about it, and you can talk about the pathology for a minute. I think if you can talk about the pathology for a minute, you pass that situation seriously. And that's the bit that the opinion. So the first, Uh, theory is in atrocious hypertension, where?
People have consistently found raised in ferocious pressures in Indian patients, so they found that the blood flow through the intravenous compartment is inversely proportional to the bone marrow pressure, so that makes sense. And of course, increases in the pressure produces a decrease in the blood flow. So that will lead to ischemia and subsequent osteonecrosis or even so in ferocious hypertension.
Being the primary culprit is one theory. And hence, everything else follows the next theory is abnormal, extra cautious blood flow. Mind you, extra cautious could be introduced as well, but this is extra cautious. So if you've got consistent loss of Trump's cortical blood flow. And this is just related to the femoral right, that's why it's so rectangular arteries and alteration in the squarish revascularization process that's demonstrated in avian patients and alteration of the revascularization process considered to be a contributory feature of long, reversible avian.
So you can see that. And these are all observations, you can imagine that people have done experiments and they've seen things which have happened and hence the theories have come. So the avian that is not getting reversed from this particular process happening? Yeah the next theory is fat embolism, and this is, I think, something important to remember because a few of the etiologies would tally with these so fatty osteoarthritis necrosis thought to progress to degeneration of necrotic osteoarthritis and adipocytes subcultural fat overload leads to vascular stasis, causing local hyper debility, endothelial damage, subsequent intravascular coagulation, histologically intereses thrombosis and peripheral hemorrhage can be seen now.
These are difficult to remember. These are difficult to remember. I totally appreciate it. The reason I have done so many slides on these again, I'm just repeating myself that it's to emphasize the point that this is important to know the pathology. You read it at your own time. You try to explain it in your mind, in whichever you want.
But the final result is that you have to come out with an answer. Yeah, Yeah. Can I say something? Yeah, sure. Because I found this particular area of aviation very confusing and difficult to remember, and I do. It's a bit complex. It is complicated.
I totally understand, but important to point out to the examiner. The first line of the answer is that there are multiple pathogenesis theories. They are not fully understood. You say that as a first line? Yeah and then you say all these causes that are saying talking about, you know, atrocious, extra cautious fat and so on, but make it clear to the examiner there are multiple pathogenesis theories and it's not fully understood.
So you're not committing yourself to one single cause because no one knows really. So I think the interest is hypertension and fat cell embolism are the two bits that probably is possible to remember on the vyver table, and you can probably get your answer centered on those two things. And I think it's perfectly reasonable to say that I do not know exactly how this etiology is leading to this pathology, but the common pathology that is noticed in the final pathway is this.
I think even if you say that, that will be good enough. Yeah yeah, it could be asked this one as boring as it is, but it could be ask and has been asked so many times. This is one pathology question that they liked asking about. But again, you don't need to go into great details about each etiology. If you remember that theory interest, extra cautious theories, and I think that will get you, that will pass you, you could add a few other things like Stromboli theory and things, but that will get you through this question.
I think here the fat cell abnormalities theory is directly related to the high dose corticosteroid exposure. So if you're given a patient who has got a history of steroid overuse or high dose steroid, you can definitely mention this as a direct correlation. OK and for the candidates to distinguish for the candidates between pathogenesis theories and etiological risk factors.
So yeah, and it's very easy for us to get confused. So please. And that's what the examiner is one of the things they are looking for. You are defining a line between these two cause etiological causing factors, which you go through in your surgical CV or the pathogenesis theories. So there are two different issues here. Yeah, generally when they present you the case in a way, they will very likely after you are diagnosed it on the x-ray, of course they will give you a history of the patient generally.
So this is your patient. And from there you get the etiology. So once you have mentioned you've got your etiology, then they'll ask you to link it to the pathology. How is it? So that is the question. Right, so how do we diagnose them in? Historically, it was diagnosed with biopsy, but now we have got imaging good imaging and then we come to classifications, which starts with Finkelstein, then which is more X-ray based.
So this is we got. And we all know if we get I'll just run through these quickly and then with the MRI, Steinberg and. This is the Arco go through that this is just something to show you. So this is what it comes down. Whatever you read it, from, whichever classification you like to court, you're free to quote that I have been asked about classification of alien, so don't assume that they can't ask you classification.
This is all it comes down to the crease side, whether you have see it on an X-ray and MRI or whatever, but this is what it comes down to. And if you go through the classifications, any of those, you'll see that the crease sign is the key differentiator before or after. So I don't think it matters which classification you caught in the exam. As long as the classification you can quote, I think anything you can use any classification.
So don't try too hard to remember these. I think if you just got figured that is fine, as long as you mentioned the importance of the present sign, I think that's good enough. Bone scan is another investigation. Just in case somebody throws it in or you are sucked into something that initially it is called before vascularization, but after it was canonisation, it becomes hot.
All right, so how do we manage the patient? So the key bit is the collapse stage. So either you've got a pre collapse patient or a post-collapse patient from the point of view of managing the patient. That's why we're seeing the present sign is the big demarcated and of course, the management differs accordingly. Symptom control, of course, is the main.
And if it is in the pre collapse stage, you do everything, try to prevent the collapse as early as you can. The patient with in a pretty club stage, would you stop something that you can see as the directly the agent that is directly causing it, which is either the steroid or the alcohol offloading the joint is the key thing.
Initially, again, the pharmacological agents are dependent on the etiology to some extent. I haven't gone in depth. I doubt whether you would be required to talk about this. But it's good to know what kind of drugs are used. So there is a role for drugs and particularly bisphosphonates. You can read up about that if you want to separately, but I doubt you would need this too much to know.
Yeah, but the main surgical procedure is called decompression. So it was started by figure as diagnostic and treatment and had good results if you compare with conservative management. But once collapse is established, it's not that effective. Yeah, and we have got variable success in literature.
15% to 30% failure rate in stage one sounds a lot, isn't it? And I don't think again, you need to know why or how, but. These are difficult operations, these are not straightforward surgeries. I'm sure there is a part to play with that. What about vascularized fibular graft? You have. It is controversial. Wherever things are controversial, I think it's quite good to mention it in the beginning of your answer.
It is not absolute or set in stone. It is controversial. All right. So the idea is to promote new bone formation. Hence, you're trying to prevent collapse. Preventing collapse is the key word. That's my aim of treatment. I want to prevent collapse. Yeah so.
There are variable reports. Some 80 percent, some say, delaying a hip replacement by seven years. But again, it's a difficult operation. You've got a donor site morbidity to deal with. Yeah a this picture just is this is the exterior shown in the Bible. Yeah I wouldn't be surprised if this does show this radiograph and ask you, what do you think is going on there?
All right. I don't know. And that's perhaps it depends on your symptoms and age. Of course, you can try cold decompression, you can. I think these are tricky questions when you're presented with a 22-year-old with an established collapse. What do you do? Are you going to try?
You're not going to try a cold decompression. I don't think anybody will blame you to try. However, understanding that it has got poorer results. These are tricky questions. So when the patient is older and if the patient has got arthritis sitting in, it's an easy choice you depending on the joints you resurface, you do a hemi or a total hip replacement or whatever.
And the other option in younger patients is Austria. So you have to think about all the treatment options. One after the other, OK, younger versus old. Pharmacologic agents, your called decompression vascularized fibular graft one or the other. Yeah, Austria. And then you come to arthroplasty.
So the summary is early diagnosis is difficult because it's difficult to pick up on standard x-rays, you need MRI scans. Sometimes when the patient is symptomatic, it's already a bit late. If you've got a patient in pre collapse, these are the options you stop the causative factors considered bisphosphonates or decompression vascular grafting.
I think osteotomy is something that comes after that. And when you've got a patient, it's already got a collapse. Again, you do symptom relief the best. You can consider decompression grafting, but you're looking at reconstruction sooner or later. So that's my last slide. if I go back to my original.
Thing is, they can give you this picture and immediately you think about a pre collapse patient, how you formulate your answer. Whereas this one is the post-collapse patient, so immediately you're thinking about reconstructive options that just examples. Exactly if you're in the exam, took principles.
Yeah, you know, salvage or salvage procedure procedures, and that's kind of things. So my advice to candidates from my experience is. If you talk about sound principles for the first minute of your five minutes, you pass the I mean, you pass that question.
If you are hesitating or not showing enough confidence to talk about the basic principles, that's where you start being in the risky zone, you wouldn't be failed if you cannot talk about whether you can do a core decompression of another bone. But you can very easily say that I know about the three options for the event of a femoral head, and I do not have any experience of this, but I believe that similar principles may be applied.
I don't think there is any harm in saying things like that. What is beyond doubt is beyond our scope. Yeah, they do begin to give you more marks, but those are not past field questions. Yeah and the other question, I think there was one question sent to me about this young patient with a collapse. And I think I would like to say if you present it, for example, with the 30 years old who had collapsed overall hate.
Um, obviously pre collapse, you try to preserve it if it's collapsed. And what I would suggest the answer should be is that once it's collapsed, we tell them clearly collapse require replacement surgery. However, as the patient is very young, I would like to refer him to young adult hip surgeon for opinion. Because they won't.
I thank you, thank you so much. I think gas was a great presentation. Very important topic. And I think you started this with a lot of useful information. I mean. You concisely briefed us on many geological factors and some background, and I like what you said, a few things. It was very, very important in counseling the patients, and that's what the examiners also would test us all the candidates about.
They want to know you can counsel a patient when a patient comes to you with a collapse. What are you going to tell this patient? They will tell you, what are you going to tell this patient in front of you in clinic? They ask you, do I need a hip replacement? What do you tell them? Tell them. I'll ask you what will happen if I leave it, and I think we've got the answers here.
Today, 75% of the collapse of symptomatic patients will collapse in three years. So we know if we have even symptomatic patients, they're going to collapse in three years. They will require a hip replacement. We know what to tell the patients, and that's extremely important. That's a higher level there. And again, the classification, you know, you could start going into effect and modified Venkat Steinberg and things like that.
I will never remember those. The most important thing is the Crescent sign bridge collapse or first collapse. The Christian side, obviously, it's a subcontract collapse, so you might still see the shell of the bone, but they were subcontract collapse and that's classified as a collapsed stage because the bone can collapse in any moment. So I would emphasize that point, Chris, and sign again pathological theorists versus etiological risk factors to focus on.
And I think that's really this presentation covers all you need to know about HIV and particularly of the hip out of the principles apply to other joints and bones. Any other comments from our mentors, David, we have David here. Yep well, I was just going to say with the young patient, the meat of the points will come and we'll be talking about your discussion with regards to its collapse.
I think it's all mentioned that what do you do in the young patient? The key thing is that the shared decision, I think ATF did say it there. You're part of your consultation with the patient is saying to them, yes, you're young. We have these options and then you leave that decision process between the surgeon and the patient.
So I think that's where you're going to get your point there because there's no right answer in that situation because it's so difficult. And as Martha said, it's something that you're going to talk about at conferences more than in the exam situation. And is this fair enough to say this will be a controversial thing, but just say you're having a Frank and open discussion with the patient?
I think that's very important, also very important decision making, and Thanks for David and Otto for sharing this. I think we know it. Sometimes you have to say it, you have to save the exam and get one more point. Particularly, it's a very common topic and mostly tested in almost every exam.
So all the candidates should know, even inside out. I mean, it should be. You should expect anything in the exam. I would recommend that all of us should study even from A to Z. Everyone should be ready for anything any weird and wonder can come regarding your view. That's true. It's a favorable in theory and the. Unfavorable question.
That's right. That's why I have 1 minute question in the hot seat session, only one minute that would give the score 8 if the candidate answers, well, it's not a conference to discuss. You give an answer. Being a safe PTH surgeon, as Faraz was saying, you have the discussion with the patient explained to the patient.
The natural history always recognize that this is a difficult problem. It is very important to mention to the patient, to the examiner that this is a difficult problem. It's a difficult decision. There is no obvious, clear way to manage this, but there are options and this is best managed by a specialist dealing with this. This is if you say these things that passes you, the exam and cemented and cemented is way beyond passing.
It is important that if you spend more time reading evidence on cemented versus cemented on avian, and if you haven't done the first minute well enough, it's of no use. If you, you need to speak the first minute really well to pass the exam, not the last minute. Exactly, exactly. And that's the whole way. Why are we giving this whole teaching exam technique?
What you should talk about and what you should try to avoid and how to approach each section? And that's extremely crucial. So we have.
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