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Michael Troiano has disclosed that he is a consultant for Stryker and Smith and Nephew.
TAPE STARTS – [00:00]
Dr. Troiano: So final thing is osteochondral defects or osteochondral lesions. So osteochondral lesions are pretty significant severe injury. They are hard to treat because a lot of them don't get better. The medial ones kind of do but you know if it's large enough -- this is basically when you think of a cross-section of the talus, it's such a small bone and so much weight of that body goes right through that talus and when you have an osteochondral defect, boy is that train going down the track. Age obviously will impair the patient. If they are younger, weight obviously will impair the patient and there is not really a great treatment right now. There has been studies Genzyme and other studies that are coming up with cartilage replacements, hopefully in the next 10 to 15 years but right now we really just don't have a good one. So we are going to go through the best of the worst, I guess, treatments. OCD lesions, local injury, the articular surface and subchondral bone can oftentimes lead to avascular necrosis. Obviously, if you get avascular necrosis of the talus, the only way you really going to fix that is via subtalar fusion. If you fix the subtalar joint and fuse that, you might get some blood flow into the talus to stop the AVM but what you are going to do obviously is affect angle joint motion. So now you are looking at an ankle joint replacement or what have you. So it just becomes one problem confounding upon another. The diagnosis of OCD is improving with advanced imaging. I think a lot of the problem we see is by the time we identify an OCD, oftentimes it's too late. Trauma is most common cause. 98% lateral lesions, 70 of the medial lesions are caused by trauma. So very trauma specific. There can be ischemic changes and bone infarcts.
There is congenital predisposition developmental abnormalities based on blood flow but realistically trauma is a number one cause and be that it may it's usually the ankle sprain. The incident of osteochondral defects is 1% of all talar fractures. However, the average length of time from the onset of the injury to symptoms or diagnosis, concrete diagnosis is up to three years. So what do you do? Do you let the patient kind of know if they start to get pain going up and downstairs, maybe they have an osteochondral defects to get back in to see it right away. Get MRI or acute ankle sprains to see if they are developing an OCD. I don't know. I don't know what the right answer is. OCD lesions are present 6.5% of 133 sprained ankles by the most recent study. Average age is 25 is your active people. There is no specific pathognomonic signs or clinical presentation for OCD. Some people say clicking and popping of the joint but obviously that can happen without an OCD. Some people say you combine the method of injury, inversion injury. Some people say that it's the history. Some people say up and downstairs. If the patient is having pain going downstairs especially then that's pathognomonic but there is no exact test for an OCD, which is I think why it's so far in the back of our head oftentimes until it's too late when we get the MRI and we say holy smokes, they got this big 1-cm osteochondral defect. Again, the pathognomonic signs late in the pathology are locking the joint stiffness, instability, chronic sprain and joint effusions. But by then, it's oftentimes too late. So the classic classification system is the Berndt and Harty classification system from 1959. Again, there is a Wang [phonetic] addition, which is a stage 5 and Steve Raikin addition, which is stage 6. I don't really include those because they are not extremely well accepted at this point even though they are probably greater than 10 to 15 years old.
I don't know if they are going to become accepted, so we will just stick with Berndt and Harty. Stage 1, which you will see in the picture on the right - excuse me top left here is just a smooshing of the cartilage. Stage 2 is lifting of the cartilage with most of the cartilage intact. Stage 3 is the cartilage actually being broken away but laying in position. Stage 4 is the cartilage flipped upside down. So stage 4 is obviously the most difficult to treat. Stage 1, you have the best chance of conservative therapy working with cast mobilization physical therapy, what have you. Location, lateral 43% of lesions, middle third of the talar dome medially 56% of lesions, posterior third of the medial talar dome. Lateral lesions occur mostly with dorsiflexion inversion injuries. The anterior middle talar dome impacts the lateral malleolus and then you get the OCD that way. Lateral ligament rupture causing shearing effect and you get the shallow wafer-shaped like lesion. Medial lesions are caused primarily by plantar flexion and inversion. Medial border impacts the medial malleolus and posterior lip of the tibia and of course you get these deep cup shaped lesion oftentimes with deltoid ligament rupture. So again, lateral lesions are less common. They are more shallow, more often associated with trauma but oftentimes more symptomatic with poor healing potential, more frequently displaced. Why more healing potential? Not really sure. I think the accepted reason is number one usually more high velocity trauma and number two better blood supply on the posterior tibial artery medial aspect of the ankle joint than laterally where your biggest contributing artery is the perforating peroneal, which oftentimes doesn't exist, going to this area. So I think that’s the reason for the poor healing potential.
Medial lesions are more frequent. They are deeper but still have better healing potential oftentimes less symptomatic as well. Can oftentimes result in avascular necrosis in the region being is because the medial side of the talus is just darn thin in height. So the thickness is much greater laterally than medially. The students like to remember [indecipherable] [00:06:25] dorsiflexory inversion injury in correspondence to an anterior lateral talar dome, plantar flexor inversion injury, medial plantar dome lesion. You can see the sites of the osteochondral defect, oftentimes anterolateral or posteromedial. Anterior lateral, I think is probably easier to treat but again posteromedial, you don't usually have to treat. X-ray, of limited use. Small low-grade lesions may not be visualized. There can be a change in bone density of the talar dome margin but could just be the position where x-rays will, best visualized in a mortis view if you are going take one. Obviously, you should take on baseline. Stress views, talar tilt greater than 18% lesions are noted in 77% of cases. Here you can see an x-ray where you can see that smooshing of the cartilage medially with the type 1 Berndt-Harty classification of osteochondral defect. CT, sagittal cuts allow you to locate the lesion and will certainly identify the extent of subchondral necrosis should it exist. There is a good contrast between bone and soft tissue and you can use 2-mm cuts to get the best assessment of the lesion. So CT is of value but again more for bone pathology than soft tissue or cartilaginous pathology. MRI is by far the king here. It gives you nice precise evaluation information relative to stability of the lesion, allows evaluation of articular cartilage. You can identify partially attached stage 2 lesions much easier than you can on CT.
Stage 3 demonstrates a ring of fluid around the lesion. Here you can see MRI both with the cartilage and the bone. You can see the cartilage is actually intact in this person with the bone with some subchondral sclerosis there. Here you can see the cartilage is kind of not for this world posteromedially. Carr [phonetic] identified MRI is useful detection diagnostic tool in clinical orthopedics. His study identified that is especially useful in demonstrating acute-on-chronic tendon and ligamentous injuries as well. So obviously, these people are going to have some other soft tissue damage occurring with the osteochondral lesion. It's very, very infrequently and isolated event. Subtle fractures including osteochondral non-displaced and stress fractures are going to occur to the talus and tibia. So MRI is indicated with them as well. They are well shown in MRI but may be difficult to detect these on radiographs. Bone scan can also be used to detect these fractures; however, the MRI helps to determine the extent of the fracture. The MRI can also be useful in detecting complication, trauma or other traumas, ischemic necrosis and bone and soft tissue infarctions. So here again we see some MRI pictures. Here picture on the right, we can see the cartilage is tattered with type 3 lesion. Schweitzer identified basically same outcome to occur but reported MR is a greater asset and the tool diagnosing AVM and occult fracture in tendon pathology. So those two studies are pretty large studies, level two evidence and really support the use of MRI. There are other imaging modalities like bone scan. Obviously, a high sensitivity but low specificity, can obviously produce false negatives.
[indecipherable] [00:10:0]1 identified that the technetium-99 bone scan and SPECT/CT can be used in conjunction localizing characterizing impingement syndromes of soft tissue pathology. They also may complement the MRI and ultrasonography. That's nuclear med 2013 but realistically no overt -- these are three tests as compared to one test. So the cost is much more and the outcome is about the same. Arthrography used to be used. You inject 5 mm of air into the ankle joint with dye and can visualize the cartilage. Here is the nice picture of that. Here you can see this kind of saucer type posteromedial lesion right under the cartilage of the osteochondral defect. So it kind of looks like a wafer or half-eaten saucer here. Stage 1, 2 conservative treatment and mobilization nonweightbearing, again the thing is that by the time you are seeing stage 1 and 2, they probably progress for quite some time and become chronic and are unlikely to heal. Stage 3, there are many perspectives. You can resect the fragment, do subchondral drilling, fixate large fragments if they exist. Obviously, we have some absorbable fixation, which is nice now, but still can be a rough area and oftentimes doesn't absorb because there is now whole lot of blood flow to the cartilage. There is mixed results in literature as to outcomes and performance. Lateral stage is 3, is more likely to need surgery, stage 4 surgical intervention is needed oftentimes to remove the loose bodies, drill, curettage, reduction, fixation and OATS procedure, and of course oftentimes with stage 4 are larger sized lesions, needed surgical takedown of either malleoli lateral or the medial, which can lead to nonunion or damage to the actual cartilage itself from a different area. So here we see stage 1 for any osteochondral defect, which is debridement of the defunct or deficient cartilage.
Some people will leave this alone and hope that fibrous cartilage will develop. Some people believe that in a young enough person, there is live cartilage that kind of fill in that space and gloss it over but when I see something like this, I say boy, that surface area of the talus has now -- you know this is big hunk lesion one-third of the surface area. It's 220-pound male who is going to walk through this area and just smoosh that cartilage so that they are just hasting degeneration of this ankle joint. So here is your subchondral drilling or your microfracture. You can use a K-wire. You can use -- this is of obviously an arthroscopic pick. You want to get down to bleeding bone. After you do your picking or your drilling, you should certainly drop the tourniquet and visualize whether or not these portals are bleeding. If they are not, you have to go down farther. De Novo is a procedure that kind of was exciting procedure when it came out. It's actually juvenile donor. So children who have passed away and their cartilage is sectioned into small little minced cartilage pieces with the thinking that if anybody can grow cartilage at that age, it's a young person. So it's actually live cells and what you do here is comes in this pack in the upper left hand corner. Very expensive, it's about $3500 to $5000 for the packet and you drill your -- you are third stage, so first line of treatment is actually debridement with the scope and then microfracture. The second and third line treatment is De Novo, so you go back, you redo that again at the time of procedure and then using some glue, you prepare your base, you use the fibrin glue, lay these little pieces in, smoosh them down and tamp them into position and drop a couple of more cc of glue there. The idea is they stay glued in the place. The impaction of the way that the ankle joint will then smoosh them together and then they start to grow.
I have had kind of mixed and matched results with it. I had probably done about 40 of them and I would say 10 of them are doing really, really well. The other half -- excuse me, 20 of the other 40 probably haven't been doing so well, but I guess on the VAS score, they are admitting to a little better pain scale and then some of them have no benefit whatsoever and actually have worsen. This is the OATS procedure. This is procedure whereby we can take a plug either from the non-articular portion of the knee or non-articular portion of the plantar aspect of the talus taken appropriately sized graft and plug it into position. Again, having had the best of outcomes but some of them do well. It's definitely worth it. As you can see in picture C, it's very, very hard to realign that either medial or lateral malleolar cut down and of course when you do the cut down, you are also violating cartilage. So you are taking one problem and trading it for two in that cartilage may not heal with the OATS number one and number two, you are now creating another defect in the articular cartilage of the tibia or the fibula where there wasn't one. The picture on the right is the mosaicplasty. Okay, these are smaller pieces of cartilage implanted. Basically, they cover more surface area for more distinct injury or larger injury. Of course, fixation of these pieces can be done either with stainless steel, screws or absorbable screws. There are different advocates for both, but I think stainless steel is probably the most accepted, although Arthrex does have these little text that you can use, that workout well. Surgical indications, absolute failure of conservative treatment, fragmented cartilage cap in stage 4 and 5 lesions, 5 again is Wang's addition. It's a very large osteochondral defect by nature of the addition. Subchondral lesions, the goal is to protect and maintain intact cartilage, retrograde drilling.
So even if the cartilage is intact, if it doesn't have a base or foundational smoosh right down into the talus, so back filling is a technique that we will get into a minute. You want to back fill beneath the cartilage, otherwise the cartilage is going to collapse down and you are going to have a real problem. So this is retrograde drilling of the osteochondral lesion of the talus. It was first reported in 1981. You drill and then it creates a vascular access channels and then you back fill bone graft. This is where you are going to use your ortho biologic like your Pro-Stim or some injectable putty or what have you. So here we see our lesion. This is actually a shoulder instrument. It allows you to -- with the picture the long targeting guide on the right, put it right where the osteochondral defect is and from a satellite location, drill from the different part of the talus to get to the osteochondral defect. You can confirm this under fluoroscopy that you are not going into the ankle joint and you can confirm it under arthroscopy. So you know right where you are. It's a combination open and close technique. You can also do this freehand or you can use this 45-degree angle targeter. So there is an intraoperative picture of the ball actually on the osteochondral defect and you can see how the drill is going to go right through lateral side of the talus and drill right to the osteochondral defect. After you do this, you are going to drill through, make a nice portal for yourself. Obviously, you want to avoid any adjacent cartilage and then once you drill right over this cannula, you are going to inject your orthobiologic and hunker in the position basically. It will harden, then you drop the tourniquet, not until it hardens obviously and you are good to go.
This is just more pictures. OsteoSponge, this is another way to back fill these lesions as well. OsteoSponge has osteo-conductive and inductive property used for larger osteochondral defects. Actually, there is just an article written about it. Dr. Schoenhaus and myself put together. We have had decent results with this. Here you are going to do your medial malleolar or lateral malleolar cut down with your saw, obviously, private joint apart. Here we see our osteochondral defect on the shoulder of the talus. We are going go down and prepare the area with the plug. The OsteoSponge actually comes with a kit. To do so, this is going to be a little bit larger than size of the defect. We are going to drill down to subchondral bone and then insert our OsteoSponge right down the graft. This is picked to the size of the defect, which you have obviously drilled over. You are going to plug it into position. Here you can see it tamped down the OsteoSponge right in the position mixed with some PRP. At this level, our bone marrow aspirate, there is some active cells there. And then once contour is laid into place, you are going to fix the fibula. Point of interest, if you are doing this procedure, you probably throw your K-wires or your screws first so that they line up perfectly when you fixate the medial mal and lateral mal again. Here you can see back into position with very minimal diminution of the articular surface of talus in the tibia. Lew Schon and Adams put out a nice algorithm. So if we can spend a minute here, osteochondral lesion of the talus is OLT, DB is debridement, MS is marrow stimulation or otherwise known as subchondral drilling.
OATS is the Oats procedure, the osteochondral autograft transfer and then PG CAT is juvenile particular cartilage, so like De Novo. So what Adams and Schon kind of found was if the lesion is less than 1.5 cm, primary treatment should consist only of debridement, microfracture and OATS. If it gets bigger than 1.5 cm or any revision treatment, so in other words if you have done stage 1 and failed even if it's less than 1.5 cm, then you are going to go onto the right here. If the shoulder lesion, you are looking at osteochondral transplant procedure, this is the autograft transplant procedure. It's much like OsteoSponge or posterior drilling and/or you are going to use particular juvenile cartilage like the De Novo. If it's a large cystic lesion, you are going to go straight to back filling with osteochondral transplant procedure or allograft procedure. So again your OsteoSponge or your back film. So realistically this is a nice little algorithm that we can use to treat these patients. I think it's pretty accepted technique at this point and I have had decent results with it as decent it could be with this type of pathology. Unfortunately, more recent studies identifying people with osteochondral defects that are recalcitrant to treatment by and large are going on to ankle fusion and ankle replacement in dramatic numbers. So a large enough osteochondral defect, that's recalcitrant to treatment, these patients should be made aware as soon as you diagnose this pathology that this is a very hard-to-fix situation. Appreciate your time. We are ahead of schedule. Any questions comments or concerns? Alright. Thank you so much. Enjoy Las Vegas.
TAPE ENDS - [22:20]