• LecturehallAvascular Necrosis
  • Lecture Transcript
  • Male Speaker: Okay. So we're going to get started here with my mini marathon. I think, I've got, like, four talks coming up. I feel bad for all for you. But try to keep us on track. When Harold asked me last week to kind of step in, this is one of the topics that he asked if I had. And luckily, I had something that was relatively similar. AVN is really a difficult subject in general. And it doesn't matter where it occurs, whether it's in the hip, whether it's in the talus, in the first met head. These are tough things to treat. So this is what this talk is really about. But we're going to focus really on the talus.

    So really AVN, what is it? If you take a look at from a definition standpoint and it is kind of a hot topic with us especially for those of you who were here last night for my total ankle replacement talk. This becomes a really touchy subject when we talk about ankle replacement and other types of procedures, especially even ankle fusion, because if we know or we have it documented that the bone is no good and then we go and try to replace an ankle, we go and try to fuse it, this is where we run into issues. So there are ways to prevent it. And there are also ways to repair it. And some of these things work, some of them don't work so well so we'll kind of hit that.

    So what's the definition? Well, AVN when you look at this in your clinic setting or in your office setting, these are typically going to be related to ankle sprains in patients especially smokers that are going to present with these types of issues. And what you're going to see with these patients is sort of they're well past the era when the sprain should still be bothering them. But they're still having chronic pain. So what are you looking at with these patients? Well, in most cases, what you probably missed, and I can tell you I don't always get an MRI on all my patients that come in with ankle sprains. But if they're smokers, I tend to, and this is one of the reasons why.

    So when you take a look at the questions that I asked of myself and, you know, when we stop really examining our patients and we start getting a little bit too reliant on technology. And that's really the long and the short of it. We kind of pigeonholed ourselves into whatever some teleradiologist from, you know, Duluth is reading at 3:00 in the morning while drinking his coffee. We're going to go with that even though our suspicions or our clinical evidence tells us probably something differently. And what you will see with these patients is, again, just a lot of pain that's continuing on. But if you examine them really pressing on these areas, you will find out or you'll be able to identify that there is still something that is going on with this patient that's sort of above and beyond your typical ankle sprain. So here's the obvious patients and it's sort of, like, the obvious patients for fracture issues, surgery in general. These are your obvious people that you're going to have trouble with.

    So we're going to get through this pretty quickly. But things like this, high energy traumas where you got open fractures. Understand that when you have open fractures whether they be of the foot or the ankle or the lower extremity in general, there's a lot of vessel laceration that takes place. And especially arterial lacerations. So those feeder vessels to the bone are actually getting blown out at the time of injury at that index event. And so then we're going and we're putting all these fixation in and we're opening these patients up, and then we wonder and we're kind of kicking ourselves in the head later on when they don't heal and we don't understand why they didn't. Well, if you understand what the blood supplies and the fact that a lot of these trauma patients and even in sprains where you're getting a tremendous amount of torsion. And maybe there's no open fracture but the sprain is ripping those vessels especially to the talus then you end up with this talar body AVN that sort of shows up. And it's a very indolent process that takes place. Very slowly but it just continues to progress as time goes on.

    Other things that other patients, I mean, include if they’re immunocompromised such as HIV patients, substance abuse. These are things that patients don't readily reveal to you. These are things you sort of, like, pry and open a clam trying to get information out of them. Are you a smoker? Do you drink a lot? And then there's always, Well, how much, you know, do you smoke? And maybe their perception of a lot of smoking is different than your perception which is any smoking. A lot of drinking versus, you know, are you having a six-pack a night or are you having a beer a night? Things like that. So all these things are going to clearly -- and in the end, they're going to affect the way things heal. And they are certainly going be laying the groundwork or sort of the index force for developing AVN.

    And we all know about cigarette smoking and its effects on wounds and also on bone healing. But the not so obvious patients are the inflammatory patients, elderly people -- you know, RA patients have been on steroids for a long period of time. And these patients, you have to be very, very suspicious of too. They come in with just a regular ankle sprain. They continue on [0:05:00] with pain. Months later, it really does fall to you to get that MRI and at least get a look at it. And again, today's elderly patients are not like the elderly patients back in the ‘70s and ‘80s that I remember. And they're a lot more active. I mean, you know, take Dr. Sean House for example -- I'm sorry, I get one dig into conference that I want to work with him so that was my one dig. He's not in the room so I got it in now.

    But if you think about it, we're going longer and do more than any of the generations that have preceded this generation. And in fact, I think it was on the cover of Time where they were saying, you know, they had a picture of a baby and they said there is a potential for this baby being 120 years old. And when you think about it in those terms, you go, Wow. Because I remember, you know, back then, old, to me in my mind, you know, someone, a centenarian hit a 100, that was amazing. I mean, they would be in the evening news. Now, the whole evening news would be taken up by people turning 100. So we're definitely living longer. But with that comes the other medical comorbidities and also that we're doing a lot more into our older age that would predispose us to injuries as well. Things like this, low-grade opens where you just have little openings. Again, vessel laceration are compromised. Clearly, gout, RA patients, things like this, this are going to complicate things because these patients are on medications that may restrict the bone from healing. Or they're just not going to allow it. BMI as well, you know, is it going to be a weight issue. You know, all these different things come into effect when you're taking about AVN.

    So just quickly, we're going to, like I said, just try to catch ourselves up here. And I do have a lot I have to go through in the next couple talks. But just so you understand, that the circumflex arterial supply to the talar body is very tenuous. It can be either disturbed surgically very easily. It can be disturbed by accident. Simplistic ankle sprains, even just simple grade 1, grade 2 rollovers can cause these types of patters. And what starts out as being what we call an OCD or an osteochondral defect as you see here, you can then progress onto an AVN. And why that happens, is the joint fluid actually uses a cartilage. And think about cartilage basically like a coffee filter. That's all it is. If fluid has the ability to pass through the membrane or cartilage and get underneath, it sort of like flows down from a geography standpoint and starts to wash away that bone underneath. And where does it stop? And that's the question. And it will continue on. And that's really the source of the pain. It's not really the lesion itself or the bone [indecipherable] [0:07:44]. It's actually the bone swelling that's taking place. And bone inflammation in these regions.

    So if you think about the talus in general and the shape of it, it's perfect. It does exactly what it's supposed to do. It's very isometric. It is resisting force. It's allowing a little bit of internal. A little bit of external. So when we start to get out of those parameters, we also increase from a biomechanics or path mechanics standpoint our ability to get AVN.

    So diagnosis, this is just my little quick diatribe on being way too reliant on technology and not thinking with our heads and not examining our patients and not asking the pertinent questions. If you take a look at, you know, CORR [phonetic] and what CORR [phonetic] stated back in 1990 in clinical orthopedics, it's clearly a very useful diagnostic tool. But if you take a look at that bottom bullet point, it is really good for diagnosing ischemic necrosis which is what it was called back then or avascular necrosis. So you can see your typical presentations and Schweitzer [phonetic] also looked at it for the hindfoot and ankle. And you see what they stressed, again, AVN. So I would say that I know we are very reliant on testing. But in terms of AVN, MRI is still really the gold standard test. I mean you can map it out a little better with CT scan. But for the most part, you're going to get your best information from an MRI just because of the sensitivity.

    And again, are we looking at a larger OCD here or are we looking at AVN? Is that full body AVN on the talus? Or is it just one big osteochondral lesion. And really, you don't know because the two things are so close in the way they present that it’s very difficult to delineate them. And again, you know, just taking a look at some of the different presentations on CT versus -- and this was a nice study that Moroder did, taking a look at bankart lesions, and what they found was actually in that particular scenario, that CT was shown less in accuracy than MRI. However, I would say to you that if you suspect an AVN, MRI is still the way to go with this. So something like this. Is this really, truly beginning of AVN or is it just an isolated [0:10:00] OCD?

    And again, you can also use things like single photon emission, CAT scan or SPECT scans. They’ve gained a lot of popularity especially with the joint replacement crowd which I'm part of in terms of determining when a patient has had pain after replacing them. Why are they still having pain? And we get this nice SPECT CTs or SPECT scans and it actually shows us where this implant is possibly impacting, if it's moving, if there's something else going on that we can identify clinically or with standard radiographs. CT scans in joint replacements are very difficult. It's a big block of metal. And it sends a lot of artifactual scatter. So we really don't see what's going on with the bone underneath a lot of these things. And that's a very helpful test.

    So how does AVN start? Well, I would say to you that most AVN starts unless it's in the presence of one of those patients that I talked about earlier with obvious. It can start just as your basic OCD and you can see that anterolateral lesion. And how that's different from the medial lesions, and the medial lesions having much higher potential for AVN. You say, Well, why is that? Well, the reason is, if you're bagging that whole medial -- dorsal medial, superior medial, shoulder of the talus, clearly there's probably been some injury that's also bagged the blood supply to that region. So the potential for disruption, so you got an articular and a bone disruption, now, with an anterior or blood supply disruption. And it's on the same ZIP code. So the chances of this progresses to an AVN are clearly there.

    And again, this is how these things will start. There's a subchondral lesion classification. They all have potential of becoming more than what they start out as. But I would say to you that in most cases, it's usually the medial lesions which are the culprits.

    So what do we do with these patients? Well, I mean, clearly, we need to get rid of that bad bone. There's no substitute for getting in there and you don't want the steam get in the way of a good physical exam in these instances because these things are not going to improve. And if you can stop them and get in there and replace them with some allergenic bone material or some bone marrow aspirate, these patients have a very good chance of getting better. And we've extrapolated this from a knee literature which showed that patients that were on par on schedule for total knee replacement and had these cystic developments with OCD actually avoided getting knee replacement by simply going in underneath that tibial plateau and blowing that bone back up. In other words, lifting up the roof of the tent again. And by doing that and expanding and lifting that joint line up, things were able to function better because it was not actually the articular damage that had been done. It was actually the cystic damage and the chronic pain was associated again with that leakage of the fluid into the bone beneath it. And there's just some more examples of that.

    I mean clearly, in these cases, where you even got an intact cartilage roof like you see in that picture, these are cases that do very, very well with just retrograde drilling and getting in there. But you can see, this looks like a relatively innocuous x-ray. And so I superimposed the MRI of the same patient on top of it. And a lot of times, we just sort of -- you know, I think, you just need some physical therapy. But if a patient is really continuing to come in with a lot of pain, and you really can't put your finger on it, you saw them, they just had an ankle sprain. If it's an athlete as well, you need to work these things up and make sure there isn’t some sort of microfracture going on or things like that. Or that they've got a developing AVN in the talar body. And we'll get into that a little bit in the next talk on lateral ankle stabilization.

    So here's a typical case of AVN. Typical, one, because this one actually involves the subtalar joint. So we don't have -- we got an intact roof on the top but we've got nothing beneath. So we're basically dripping or we basically got an upflow of fluid from the subtalar joint into this lesion which is creating a much larger defect. So what do you do with a patient like this? You're already questioning the blood supply. The patient’s got psoriatic arthritis. So they're on steroids for a long period of time. Now, what are you going to do and how are you going to address this? So how I opted to do this is to do the case with the patient in a prone position. Since what I was looking to do was actually bring some blood supply from the calcaneus into the talus. Mark a spot on the anterior tibia. Draw some bone marrow aspirate which you see there. Those are all [indecipherable] [0:14:25] all done with the tourniquet down. And by holding the foot up in that position, I basically allow the bone marrow aspirate to drip down to the tibia where I'm working.

    Once that has been completed, I actually mark up the spot and I know where I'm going from a lesion perspective. So if I can aim right for that spot, drive in a guide wire and I can hit it -- which I did in this case -- then I used a flexible reaming drill -- not a standard drill but a flexible one -- just sort of create a bone channel into that. The flexible drill also has the grade benefit of actually evacuating a lot of dead nasty bone at the same time [0:15:00]. So once this is done, then you can actually take a suction device and suck out all that fluid that's build up in there. And that's actually a [indecipherable] [0:15:09] chip that you're seeing there in the x-ray. And once this is done, I can actually take an arthroscope and jump in there and actually look and see do I have bleeding in there. If I created enough microfructure, enough bleeding that I feel that this can adequately fuse. And once I feel that I've got, I can inject some bone marrow aspirate as you see there. And you see my syringe there on x-ray and the needle going in. And that's going right into the spot. I fill that in with some allergenic material which has a harding property that I can actually place a screw through. And I'm going to just blow that right into the talus and just kind of walk my way or paint my way out of the room and come backwards. At that point, just place a single screw and that's the end of that case. That patient has done very well. And I think, he's at this point, about four years out. I just saw him for his other foot for another issue probably about a month ago. So I should have grabbed some follow-up x-rays on him. But that's what you can do with AVN and how you treat it.

    And how to look for -- I have to caution any of you, if you have patients that continue on with this ankle sprains -- like I said, we're going to get into it a little bit more in this next topic -- you need to really look very hard at them and see where this pain is located. And do not hesitate to pull the trigger on getting an MRI. Now, here's just an example of where we can get kind of wronged by MRI. So this is medial and lateral pain. And you look at the MRI and you say, It doesn't look too good. And then you look at the CT scan. Same patient. So this is a perfect example of just over-reading a bone island. And that's what came out on the MR. Alright. So there it is when you see it in the sagittal slice. And the treatment for her, absolutely nothing. This resolved uneventfully. Once I was able to deal with her sprain -- and in fact, the one thing I didn't mention was there's a large cyst in her heel bone that wasn't brought up and which we picked on CT scan.

    So be reliant on the testing. Don't be afraid to hesitate -- or don't hesitate in ordering these things. You clearly have to in these instances. If you have the gun held to your head and you want to come up with an answer with some of these patients, you're going to have to get a little bit further testing and understand once it's done how to read it and what to do with the information that you're getting. Thank you. That's it for the first talk.