CME Trauma & Sports Medicine

Current Concepts on the Treatment of Talar Osteochondral Lesions

Steve A Brigido, DPM

Steve Brigido, DPM begins with an overview of injuries commonly found in the talar dome, including a discussion of presenting symptoms, mechanism of injury, classification systems and finally available treatment options. Dr Brigido specifically focuses his discussion on the Hepple classification system for MRI findings that correlates well with selection of treatment. At the end of the presentation, He provides a summary of the advanced techniques, indications for use, and detailed description of the procedure.

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Goals and Objectives
  1. List the presenting symptoms for patients with osteochondral lesions of the talus.
  2. Describe the classification systems (Berndt-Hardy and Hepple) for osteochondral lesions of the talus.
  3. Recognize the appropriate treatment options for patients with various levels of injury to the talar dome.
  4. Identify the mechanism of injury for common locations of lesions in the talar dome.
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    PRESENT eLearning Systems, LLC is approved by the Council on Podiatric Medical Education as a provider of continuing education in podiatric medicine.

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    Release Date: 03/16/2018 Expiration Date: 12/31/2018

  • Author
  • Steve A Brigido, DPM

    Director, Fellowship for Foot and Ankle Reconstruction Coordinated Health
    Bethlehem, PA

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    Steve A Brigido has disclosed to be a consultant/advisor for Stryker, Bacterin International and Wright Medical. And also has disclosed receiving consulting fees from BMTI and Nextremity Solutions.

  • Lecture Transcript
  • Male Speaker: I’m going to call upon Dr. Brigido to deal with talar dome lesions.

    Dr. Brigido: Alright. Good morning. Thank you guys for -- thanks for having me. I know its early Sunday morning. So, we’ll try to keep it somewhat fluid here. So as Dr. Sean has mentioned, we are going to talk this morning a little bit about how we go about and treat, you know, our osteochondral lesions of the talus in particular. Now these -- a lot of these principles can certainly be applied to the first metatarsophalangeal joint in any of the cartilaginous surfaces of the foot and ankle as well, but for the most part we’re going to keep the discussion focal to the ankle joint. So osteochondritis dissecans or your typical cartilage lesion was first described by König back in the late 1800’s and they found that there were some loose body formation associated with the articular surface of the knee and that area had subchondral bone fracture. This research and evaluation of cartilage damage was then followed up by Capuz [phonetic] back in early 1920s when he was looking at the talus. That’s when the first talar dome shoulder lesion was described. And as you know, we’ve certainly -- you know, as a practicing foot and ankle surgeon you’ll see, you know, that the clinical challenges that these cartilage lesions present to us on a daily basis are very unique, in the sense that most of the patients that come into the office will describe this nagging kind of tooth -- you know, this toothpick type pain that will, you know, penetrate into the gutters, often radiate to the opposite side of the ankle that the lesion is associated from. And it is, it is something that these patients don’t often know that they have. They’ll often describe an injury that occurred many, many years ago. They’ll sometimes describe an ankle sprain that occurred six to nine months ago. And because of that they come in and when you get an image, sometimes your plain film x-rays don’t show the lesion. You have to get an advanced image to understand it and to see the location of it. But basically what -- it lends itself to the challenges because these mature chondrocyte, these cartilage cells that we have in our joint are unable to potentiate once they’ve been damaged. And I'm going to show you some charts that basically show the benefits of having a Juvenile chondrocyte or an immature chondral cell and its ability to potentiate versus that of somebody who is 15 years old or older, it really slows down significantly. And because of that when patients have an ankle sprain and the data has shown that about 5% of all of our ankle sprains across the country will end up with an Osteochondral Lesions of the Talus. So, when you think about the number of sprains that are seen in the ER each day which is about 30,000 and 5% of that number is going to end up with some sort of Osteochondral Lesions of the Talus, it’s a pretty significant number and many of these patients are going out undiagnosed with chronic ankle pain. And they are not going to understand the -- what’s causing the issue until they see you in your office. When you see these patients in the office and you get your advanced imaging such as an MRI perhaps a CT, your plain film x-rays and you are good clinical physical exam, you are going to have to look at the lesion. You are going to have to understand how to classify it, because your classification is going be a main -- one of the main ways you kind of support what you are going to do to treat this. And we are all familiar with a Berndt and Harty classification and basically what -- what we see in the Berndt and Harty classification is what’s basically starts as an indentation to a fracture -- to a flat fracture without displacement and then a fracture with significant displacement. And this can be applied to either the medial or lateral shoulder of the Talus. So, these are -- this classification and more importantly what I will get into is, as we get through this talk is the amount of subchondral bone damage is also going to dictate what we do. When we are talking to our fellows about how they are going to treat these chondral lesions that sometimes can be very complex, the question often arises is, well, when do we do micro fracture versus when do we do something else. And you’re basic orthopedic literature will tell you that micro fracture should be the first line of defense for almost all lesions. And I can tell you that in our clinical setting that’s probably the case for most instances, because sometimes you’ll look at a scan and you see a patient that has a significant stage 4 lesion that’s got a very cystic nonviable or perhaps a vascular or dysvascular subchondral bone plate. And you just look at it and you know that a micro fracture probably isn’t going to do the job. And that’s when we have to start looking at other options. The path of physiology of these chondral lesions is that such where you can almost look at the lesion itself on the image that shows it and because of the shape of that lesion you can understand how the patient had that occur in the first place. When we have anterolateral lesions, this is an inversion dorsiflexion type instance where we have shallow way for this type of lesion due to the sheer force of the Tibia and a talus bumping into each other. The medial lesions are more often post traumatic and they’re typical comes from inversion plantar flexion injury.


    They are deep in cup shape, these are the once that we see most often in our practice. I would tell you that the literature says that these are 85% of all Osteochondral Lesions of the talus. I would tell you that it’s probably in our clinical setting even greater. It’s probably more than 90% to 95% range. Here is an example again that anterolateral lesion of the ankle and this is a kid that went to Penn State that was going to fail an exam, pass the exam, was running around for the stair -- was running grabbed on to a telephone pole and trying to swing across it and ended up with this injury. You can see that the wafer shaped area of the lesion -- it does not have a lot of depth to it. But it is full thickness through the subchondral plate. You can see we’ve got it elevated, but not displaced, significantly its displaced cartilage lesion. This is a class example of that dorsiflexion type inversion injury where the dorsal lateral talus bumps into the distal tibia and it causes that shear which causes that lesion. This is a classic medial Osteochondral Lesion. This is where we’ve got an inversion plantar flexion injury, you can see that the talus here will bump into -- the tibia here will bump into that a talus there. And you can even see here you’ve got some sort of kissing lesion. We’ve got a significant amount of subchondral depth and there is damage there. And this is an example of a situation where I would actually question. And again I’m not saying that it is -- that it wouldn’t work, but I would question whether or not micro fracture would actually be considered to be standard of care in this particular instance. Especially in the new literature, this has been a constant debate for about the last 20 years. And we will have – there will be clinics that have looked at significant randomize control studies where micro fracture has been shown to be beneficial and then you will have randomized controlled studies that show micro fracture is an absolute waste of time. The constant debate of this at the Academy of Orthopedic Surgery every year for the knee is tremendous. If you let the surgeons discuss it, it would go on for literally 8 hours and at the end of the session you would have no more information or knowledge than you would have when you started at 8 hours prior because the debate is that significant. So, one of the ways that I think is the best way to classify how we are going to treat these lesions is to utilize the Hepple’s MRI staging back from 1999. And his MRI staging really looked at not only the amount of significant subchondral bone loss, but the viability of that bone loss measured by signal intensity and how much cystic formation was associated with that particular lesion. And you know at stage one lesion was an – articular surface damage with only cartilage injury. Stage 2 is cartilage injury was subchondral bone fracture and it’s separated in 2 compartments fracture with edema and no edema. Then we’ve got stage 3 which is a detach fracture, but not displaced that’s when you see a rim sign or a little outline of the lesion on your MR that shows that the lesion popped out and then popped back into place. Number 4 is when it’s displaced and then number 5 is when we have a subchondral cyst. So what I like to do and this is a schematic showing that you can see the subchondral cystic formations which are probably the most challenging of the Osteochondral lesions that we see in a routine basis. As well as the display subchondral bone fragment with the articular surface attached to it, these are also very challenging. What we are going to do is, we’re going to kind of go through the different Hepple classifications and I’m going to talk to you a little about how we approach these, because this a great way for us to help our fellows understand the best way to attack these lesion which many of them can be extremely challenging. Well, certainly a Hepple one lesion which again is just articular surface damage only, basically it’s a commonly depressed cartilage injury of the talus typically on the medial shoulder, its partial thickness at times, sometimes it can be full thickness without subchondral bone loss avoid. And many of these patients will respond to conservative treatment. They will respond immobilization. They’ll respond to physical therapy and in some instances we’re even utilizing an off label approach which is hyaluronic acid treatments. But when these patients do fail conservative treatment, the surgical option for the most part is, it’s a relatively simple and straightforward arthroscopy. These patients tend to do very well. We typically will tell them after an arthroscopy that you’ll feel 80% better within a month and then the last 20% will typically take about 6 months to occur, because again you’ve got to allow that type 2 or the fiber cartilage to fill into the area. And that does not happen quickly. That fiber cartilage formation can take up to 6 to 12 months and sometimes even longer depending on the size of the lesion. Hepple 2 for both A and B lesions are again fracture with or without edema. So, you can see here that we’ve got a fracture of the medial shoulder the talus, there is very of edema in this area. These can be significant depending on the type of the edema or how dysvascular that these lesions are. It can range from anything from a conservative treatment all the way to something as complex as a mosaicplasty or an oats.


    ACI transplant has juvenile cartilage transplant and something that I’m going to talk to you little about which is our allograph reconstruction and Dr. Sean [Indecipherable] [10:09] went into that a little bit – a little bit later. So, we are going to kind of skip over Hepple 2 A and B in a second. Hepple 3 is a detached, but not displaced fracture. You can see here, this is that gentleman with that anterolateral lesion from that shear injury of dancing around a telephone pole. Depending on the ability of the vascular supply and depending on how old that fragment can be, if it’s a fresh injury like we were able to get this young gentleman relatively quickly, you can go back in and you can actually utilize in a chondral dart, absorbable fixation, headless fixation. We can do a fibular osteotomy or a malunion osteotomy and then we can actually anchor this back down. And you can get this fragment fixated, so that when you can compress the subchondral bone fragment, you can get it fixated properly and the bone -- the vascularity of the bone will survive and these patients typically do very well. We like to utilize either absorbable fixation and/or headless fixation, so, that you can vary below the level of the -- of the collagenous surface and what will happen is above the screw you’ll get a nice layer of fiber cartilage and the patient does great. Now, fiber cartilage in the ankle because the surface of the ankle is so small typically doesn’t affect a patient too much. Now, if you have a surface of the knee which is significant and you’ve got a 2 or 3 centimeter area of fiber cartilage which is typically more unstable than type one cartilage, it can create a painful situation. But when you have a small area like this where you're utilizing a 2.0 diameter screw or 2.5 diameter screw in the head of that, you're only going to have a circumference of 2.5 millimeters of fiber cartilage formation. Typically that is not going to create instability enough that this going to cause the patient harm or discomfort. So, because of that, you can utilize a screw like this which is like a typical Herbert bone screw and do great with it. And not worry about any of the complications associated with the larger joints like the knee or the shoulder. The Hepple 4 classification is the displaced fragment, this is a situation where I really start to question whether or not a micro fracture with the repair is even worth doing and most of times patients that come to your office are going have this for quite some time significantly greater than 6 months, many times you’ll have patients that have had this for a few years. So, the question again becomes -- is an oats are not a possibility in doing – want to do a mosaicplasty for those for you are not familiar with a mosaicplasty, it’s basically an Oats, but it’s a multiple plug Oats in the same region or do we want to do holograph subchondral bone grafting with juvenile chondrocytes. So again I start to question significantly with Hepple 4 whether or not a micro fracture is even worth our time. And do we want to go to our patient population and say yes we are going to do the procedure which is relatively straight forward. We can do it arthroscopically, but there is a 50-50 chance it’s not going to work or do you want to do something more aggressive and give them a better option. We’ve gotten to the point now in our clinical setting where we’ve -- again it depends on the patient, but we’ve decided that we’re going to stay away from the micro fracture in most of those instances. And I’m going to talk to you about the Hepple 2 and Hepple 4 options in just a second, but we are going to skip over to Hepple 5. This is the subchondral cyst formation. This is a lady. She's a 45 year old postal worker who came into the office with the significant subchondral cyst. You can see she was walking 4 to 5 miles a day. She had some increased signal intensity, she had some edema on the MRI. And the way we approach these is typically with an open core decompression. The open core decompression can be done in 2 ways, it can be done through a sinus tarsi approach where if you need for a significant lesion like this which is very large, we can go and do an malleolar osteotomy such as we did on her. When we bring our osteotomy down, we’ll make a small cortical window on the medial wall of the talus, and then we’ll go into our core decompression. We’ll do some micro curettage, we’ll actually debride that cystic lesion out. We’ll evacuate it. And then we are going to utilize a biologic of our choice to fill that lesion. And typically what we will utilize is something like a calcium phosphate sulfate drill or something that will give you some tensile strength that will harden. It gives you the ability to fixate. And what we’ll do is also give you some stretch structural integrity. We’ll then replace our cortical window, replace our malleolar back into position, fixate our osteotomy and then keep these patient non weight bearing as we would for any sort for bone lesion or fracture. You can also utilize this through a sinus tarsi approach, where we utilize an arthroscopic core decompression. In this instance what we’re utilizing is basically like an ACL guide, which is going to triangulate our lesions. So, we’ll find our lesion on – in this instance the lateral talar dome and then we’ll go in through the medial sinus tarsi approach. We are going to isolate our lesion and then we are actually going to drill and ream into our lesion on the -- in this instance it was on the lateral wall of the talus as well is in head -- penetrating in to the central portion. We are going to do curettage through our open core decompression.


    And then we are going to apply a sheaf that actually back filing and place the putty of our choice or again – in this situation we utilize a phosphate sulfate combination. And what that will do is allow us to do it through a very small approach through the sinus tarsi. We can do a minimal incision approach. We can utilize our arthroscopy to guide us and again patients do great. So for those stage 2, 3 and 4 lesions what options are out there? Well, certainly, what we’ve decided and I’m going to skip through some of this is that we’ve found that cartilage, juvenile cartilage, a particular cartilage -- it can be very helpful. But we find the most important thing that we can do is create a nice healthy subchondral bone base. If we can do that, the subchondral bone what we found and what some researchers at hospital for special surgery has found is that the subchondral bone base is the most important predicting factor to creating good outcome. So, you can utilize things like juvenile chondrocytes. You can utilize things like ACI or MACI or any of those, but until you get a good healthy bone base underneath that cartilage you are going be – you are going to have problems with your success. This is just a quick chart showing that the juvenile chondrocytes -- again before age 15 they have the ability to potentiate very rapidly and very healthily. But once you get to become 15 years of age if you have a injury like this you are going to have a problem healing it, because your chondrocytes do not heal at the pace that we like them to, if at all. Again, for the sake of time, I’m going to kind of go all the way over to the procedure here. This is just an example of a knee that one of our partners did that -- a very large lesion. So, again here's a great example of a case study. We’ve got this Hepple -- in this case the Hepple 4 lesion, where got a significant medial shoulder collapse. Our subchondral bone quality is significantly dispatched and unhealthy, this patient would not be a great candidate for a micro fracture debridement. So, what we decided to do is again our medium malleolar osteotomy. And you can see once we open our osteotomy you can see the very large subchondral lesion that you can basically pull out with the forceps. And when you take a prob or even a forceps or a [Indecipherable] [17:16] you are pushing a subchondral bone, that subchondral bone is soft and dead. And what we are going to do then is we are going to take one of these reamers that are supplied by Bacterin international and we’re going to find the reamer that best matches the diameter of our subchondral bone void. And once we do that, we are going to either than place -- we’re going to place a guide wire into the lesion and you can utilize your tangulated reamer or you can do a free hand. We typically will do it free hand just because that guide wire for the ankle because we are working in small area, it does get in the way sometimes. But what we are going to do then is our core decompression of a subchondral plate, we are going to ream out that area down to the healthy subchondral bone and at that point we’re then going to take this holographs subchondral plate. And the subchondral plate again is also supplied by Bacterin international, but what it has is kind of where a subchondral plate as well as category of cancerous bone coming from talus. And these plugs match the diameter of your reamer. So, if you pick a 10 millimeter in diameter reamer you got to pick a 10 millimeter in diameter plug and you're going to then place that plug with the subchondral plate dorsal. And you are going to press fit it and tamp it down to the level of the subchondral bone so it’s consistent. At that point what we are kind of do, you can see our bone plug is now placed in their subchondral bone. We’ve now replaced our entire subchondral plate. So that we’ve got a good base for those chondrocytes to potentiate on and if we want to have fiber cartilage formation we can allow that to occur as well. We’re then going to take a piece of aluminum foil. We are going to make a mould of our 10 millimeter plug in our 10 millimeter void and we are going to take our juvenile particulate cartilage and we are going to secure that with some fiber and glue. And it’s going to create this jelly -- kind of is this like jelly plug or this gummy bear plug of juvenile chondrocytes, which are held together with some fiber and glue. And this little fiber and glue gummy bear is going to match the diameter of our subchondral bone plate specifically. And we are going to then take this and we are going to place this on top of our subchondral bone plug. And now we’ve reconstructed that entire area. We’ve got the juvenile cartilage that’s going to be able to potentiate and mature very quickly. We’ve got a nice healthy subchondral plate that’s going to allow for the regeneration of that articular surface. And we’ve got an ability for us to completely reconstruct that entire void without any complication. We are going to replace our malleolar osteotomy. We are going to keep them non weight bearing for about 6-8 weeks. We’re then going to start them in physical therapy in a boot, and we are going to get them going in a full sneaker in about the 3 month mark. We tell them it’s going to take 6-9 months before they feel completely better, because again it does take time for those cartilage cells to potentiate. This is a post operative image of what are our malleolar osteotomy looks like, this is the area that we reconstructed. For the sake of time, I’m going to stop now and then I’ll come back up to continue the discussion with the ankle sprains later. Thank you, guys.