and Dr. Greg Guyton from Union will be moderating the session and giving the first talk. Thanks everybody and welcome. So I am gonna do the first talk. Do I just click on this or? So I need to get my talk up. Just click on it? All right, got it. Perfect. Okay. So, you know, the first talk, whenever you give a physical exam talk, it's always the one you start with. It's kind of the throwaway talk because most of the things we already know and there's gonna be some things we already know in here. I'm gonna try to do it in a way that speaks to kind of doing a physical exam along the lines of what are we going to do with the foot later and what are the questions we need to ask. There's my disclosures. And so I'm gonna start with the concept that I want to do a cavovirus reconstruction. So what are the things that I need to, the questions I need to ask and the questions I need to answer before I go on and do that reconstruction. So I need to know am I gonna do a fusion? That's number one. Do I need to worry about all this tendon balancing? Is there something that's just gonna make me do a fusion? What soft tissues do I need to reconstruct? And I don't mean tendons, I mean ligaments, soft tissues. What tendons need to be rebalanced? And then what nerves are working? And then lastly, and this is something that I don't think we've talked about enough, is what impacts your incision planning? Because these are potpourri cases. They have a lot of different procedures that one has to do in the process. The very first thing you need to ask is what's the diagnosis? And why are we here? Because cavus foot is a wastebasket term. It's an anatomical deformity. It is not a diagnosis. And we need to know what we're up to. What's the prognosis? So is it a degenerative neuromuscular condition that is going to have a defined outcome such as you see here with this unfortunate young lady? Is there a spastic component to it? And is that spastic component progressive or is it static? So for instance, is it traumatic brain injury with a static component? And if it's a traumatic brain injury, for instance, how old is it? Is it now a year out where it's going to be considered stable? Is it in the first six months where it's evolving? If it's a stroke, how far out is it? What are we looking at? And I'm not going to go into the details of each diagnosis here, but there are certain little pearls you need to take home. Now why am I showing hands on an early, early slide here in a cavus foot talk? Well, it's remarkable how often in your foot and ankle practice you will see undiagnosed to CMT. So there are around 150,000 CMT cases in the United States. It's probably a little higher now. But if you see intrinsic wasting in the hands, occasionally itopathic. Sometimes it's spinal root atrophy or a syrinx or something weird. But commonly it's going to be CMT. 60% of the CMT that is out there is CMT1A. That's the most common genetic subtype of CMT. We're actually going to go over that in just a minute. But the important thing to know is that 50% of those people represent new chromosomal recombination events. In other words, they don't have family with CMT. And I guarantee you, if you run a busy foot and ankle practice, you will eventually see a first presentation of CMT at some point. So open up their hands, see what their abduction strength is, and look specifically at their first dorsal interosseous if you see somebody that you suspect. The next one is, it's a simple thing, but always look to see if there's any hind foot DJD. And subtalar arthritis, commonly overlooked. It's actually remarkably easy to see in cavus because you get that beautiful view that lets you look right through the subtalar joint. So the subtalar joint is rotated into your position and you have a much better view of it than you do in a planovagus foot. So it's a little bit easier to see if there's any hind foot DJD. And of course, if you need to get a weight-bearing CT to make that determination, then do so. Is the ankle stable and is it fixed in verus? So these can be difficult questions to ask. Sometimes you have to think about doing a dynamic or a quasi-dynamic test. And I don't rely on stress views, but you might have to rely on a radiographic view to see if the ankle is reducible. The other point here is this is a rotatory drawer because so commonly in patients with cavus, the deltoid remains intact. And what's really failing are the lateral ankle ligaments. So it's based on a paper that I published and also that Physitco published some time ago indicating that a rotatory motion on the drawer test is actually a lot more sensitive for picking up subtle instability. But that's the pearl there. The other pearl is to have a high index of suspicion for perineal tendon pathology. If I see patients that have failed cavus foot reconstruction and failed in the sense that they still have pain, they still have problems. Probably the single most common problem is that somebody missed a perineal tendon problem along the way. So are the perineals intact? And for me, this is the number one reason that I might pursue MRI imaging on these patients. And if you do get MRI imaging, make sure you're getting a 3-Tesla study, something that you can really have a decent chance at following the perineals down. And we make a lot about pattern. We talk a lot about pattern. I'm going to tell you that you can't completely trust the patterns. We have classic statements that we always make. It's always easy to get up here and give a talk and say, well, you know, CMT, which is about half of what you're going to see, that's forefoot cavus. It's driven by plantar flexion of the first ray. There's a CMT patient on the left. And then you're going to see hindfoot cavus a little bit more rarely. Used to be polio, which of course was the overwhelming, not just cavus foot reconstruction issue in orthopedics, but one of the overwhelming issues in orthopedics until 1950. And then nowadays, when we see a hindfoot cavus with a high calcaneal pitch, it's usually an idiopathic case, although there can be other issues involved. So we think about the pattern because that does inform what we're going to do. This is the obligatory Coleman block test picture. You have to have one when you give a talk about physical exam. I'm also going to be honest. I probably almost never do the Coleman block test. And so this is one that has to show up in almost every chapter. And, you know, the classic thing is you're going to put the heel up on the block and let the medial column fall off the block and see what happens to the flexibility of the hindfoot. In fact, as you get a little bit better at it, you get to be able to do this primarily through your clinical exam to see how stiff or un-stiff the hindfoot is. And the Coleman block test cannot truly distinguish between, is it rocking at the ankle? Is it rocking at the subtalar joint? So it doesn't pick up all of the components of what might be included. But that said, you got to put the Coleman block test in that. Now we're doing a lot more weight-bearing CTs these days, and it's an important point. I do think weight-bearing CT has a lot of potential to assess cavus foot pathology, but it's also important to remember that weight-bearing CT, as it is done classically, is a static test. So you are really looking at alignment, but you are doing so without putting any force on that. So it doesn't give you any information about reducibility or flexibility. I found this to be very interesting. This was published just last year. It's in FAO, which is the online journal, so you can get get access to this. It's a very small study, but I actually asked myself the question, is anybody doing Coleman block tests or other quasi-dynamic tests with weight-bearing CT to actually assess flexibility? And it's a pretty darn good idea. Am I doing it? No, I don't have, haven't taught my techs how to do Coleman block tests, but it's probably a very reasonable idea if we're going to get down and dirty about trying to assess flexibility. And they looked at a whole series of different angles, the hindfoot alignment angle, the hindfoot moment arm, and the foot and ankle offset. And I'm not, this is not a weight-bearing CT talk, I don't want to go into those, but if you were going to learn about these, these are not just, these are not just 2D projections onto a 3D, these are actual three-dimensional constructs. So it's not like trying to look at a Saltzman view and come up with a hindfoot alignment, just projecting it onto a 2D alignment. The foot and ankle offset, for instance, picks the center of the talus and the center of the weight-bearing tripod of the foot and shows the directional offset. So I would encourage you to learn about these things. We don't know where they are, nor do we have standards for them yet, but this is probably the future. And lastly, you have to assess the severity of the deformity to determine the kind of the hindfoot correction that you're going to do. We're always looking for the unicorn, at least I think we are, when we're doing cavus foot reconstruction. Because this is what we love to talk about in book chapters. This is what we're looking for when we do, when we talk about the Coleman block test. We're looking for that isolated, fully flexible forefoot cavus. And does it exist, is the first question. And the answer is, not a lot. Because, I'll be honest, it's common that the patients come in that almost everybody that has symptoms has some level of contracture. At least that's my bias. And the other question is, does it matter? And maybe we'll talk about that when we get to the cases. And that's more of a philosophical question. In other words, if you do a little bit too much, is that a bad thing in the average CMT patient? What's the, what's the penalty? So if you do a dorsiflexion osteotomy the first ray, or you do a lateral slide, what's the penalty? How many over-corrected CMT patients have you seen coming into your office? It's a relatively rare thing. And that's a philosophical question that maybe we can talk about when we get to cases. What's the tendon balance? So this is the surgical algorithm, the classic surgical algorithm for CMT. So the anterior tibialis is the weak agonist. The intact antagonist is the peroneus longus. And the solution is traditionally given as a dorsiflexion osteotomy of the first ray. And that's an important learning point for the orthopedic resident, to be that concept that the peroneus longus is actually antagonist of the anterior tib in this regard, with regard to the first ray, and not the gastroc. The other important one though, is the balance between the longus and the brevis. And the rest of this table you can, you can just read for yourself. It's also in the, it's also in any of the classic book chapters on CMT. For instance, the peroneus brevis against the posterior tibialis is going to give you, the posterior tib is going to overpower it and give you inversion. And then the anterior tib with the gastro soleus is going to give you the foot drop. And then you'll have the hammer toes, which will result from the imbalance between the extrinsics and the intrinsics. But the balance between the longus and the brevis is an important point. And this was a point that wasn't appreciated for many years in understanding CMT, not probably until the 1970s and 80s. And it was demonstrated first on clinical exam. I would like to give Roger Mann, my mentor, some credit for that, although it's probably older than that. And then there's some MRI studies that demonstrated it as well, once we got MRI, that you actually saw wasting of the brevis, but maintenance of the longus as an important point. And it's an important point because it gives you something to do. You can do a longus to brevis transfer as a dynamic component, either in conjunction with a static maneuver like a dorsiflexion osteotomy, or perhaps in an early case as a maneuver all on its own. And this is something I do think is an important thing to do in the clinical exam, is try to isolate brevis and longus. I do try to do it. Whether it's reliable or not is hard to know, but you'll have the patient just press down with their big toe while not pressing down with the lateral side of their foot, and you can try to isolate longus strength. The other point that comes up is EHL sparing, and this is an important physical exam point for the same reason. It gives you something you can do. So not all cavus knocks out the EHL, and there is a type of, there's a pattern of CMT that spares the EHL. I'm going to talk about it in a second, but if the EHL is spared, you can do the old-fashioned Jones transfer, which is an IP fusion, and transfer the EHL either into the first metatarsal, as classically described, or into the dorsal midfoot as an option, which may be more appropriate than what I commonly do. But you want to look for EHL sparing, and of course drop foot you're going to be looking for, heel cord tightness, I'll zip through these so we stay on time, and the solution, of course, triple hemisection versus a strayer. Now, you've got to think about nerves. So what is their baseline sensation? We didn't think about this until fairly recently, and Christy Giovanni should get a lot of credit for making us think about this based upon both anatomic and some clinical studies. There is concern over the lateralizing calcaneal osteotomies and their potential for nerve injury specifically because they reduce the volume of the tarsal tunnel, as demonstrated on some MRI and cadaver studies. So the more anterior the osteotomy, the more you can shift it, and this is a simple trade-off, but also the higher the risk. So as you move it into the middle third of the bone, there's more risk, but more shift, more correction. As you move it back, there's less shift, but less risk to the nerves. And so it's important to assess baseline sensation, not just on general principles, but because we have this very specific issue. Now, if you look at the clinical follow-up of this, this is his paper along with Brian Den Hartog and some others, the middle third osteotomies were in fact more dangerous in terms of having nerve injury than the posterior third osteotomies. The important point about this, though, is there was no protective effect from tarsal tunnel release, so that is also a point of contention in the literature. So it does seem to matter for risk, but there was no benefit to doing a prophylactic tarsal tunnel in this paper, which remains our best paper on the topic. How do I deal with all the incisions? You're going to be thinking about that for incision planning as you come up with your algorithm, and we're going to go through the algorithms as we go through the other talks. It's common that you have to do a Brostrom, a perineal reconstruction, and perhaps a Dwyer calcaneal osteotomy. There's some tricks that you can come up with. One, combine the trick one if you have a Brostrom and Dwyer combination. You can cheat the Brostrom incision a little bit more anteriorly. You can use a proximal tenodesis if you're doing a perineus longus to brevis tenodesis. You can do that tenodesis up in the, up above the SBR rather than down in the foot. You don't have to do that on the side of the foot and avoid some extra incisions down there. This one's done with an open Dwyer osteotomy, but the other option is to learn some MIS techniques. So the incisions don't matter nearly as much if you can do the calcaneal osteotomy through a small incision. So the practical pearls considered fusion based on diagnosis. Remember ankle instability. Have a low threshold for LDCO, a lateral displacement calcaneal osteotomy, even in conjunction with apparent modest flexibility. You have to put into your head what's the downside. And yes, there are some downsides, but I have a relatively low threshold for it. Assess the severity of the hindfoot deformity to help you choose the hindfoot procedure. Moving up in severity between a simple minimally invasive lateral displacement to a Dwyer or one of the other variations on the Dwyer or a Malerba, all the way to a subtalar fusion. And then look for the clinical tendon tears, especially the peroneals. And look for the critical tendon pathologies, those little one-offs that there are things that you can do things about and plan your incisions. So those are the practical pearls. That's the run through the physical exam. I'm going to give a two-minute neurology update, maybe three minutes, because that's part of my charge here. So the pathology and neurology update is going to be all about CMT. That's what you're going to see. That's what we're looking for. So CMT1A is a focal trisomy of the PMP22 gene. That's been known for a long time. It is the same protein, PMP22, which has a considerable role in keeping the myelin sheath happy and functional. We don't exactly know what PMP22 does. There's getting to be a little bit more understanding of it. What we do know is that if you get a focal trisomy, you get CMT1A. If you get a deletion of one copy of the PMP22 gene, you get hereditary neuropathy with liability to pressure palsies. These are the problem that was first described in Dutch potato diggers who kneel all day long and got drop feet, transient drop feet, and they were just described as having HNPP. I did a study some time ago to try to explain why we get EHL sparing and how can you put that together with something like this. Basically my theory, and to date I have no clinical proof of it because I'm not sure how I would prove it clinically, is that there are variations in perineal nerve branching. So perhaps the nerve that goes to the EHL comes off a little bit earlier and doesn't run around the side of the fibular neck. Something about PMP22 in the myelin sheath makes you more susceptible to compression neuropathy. Now where that goes, who knows, that's not a neurology update. That's been around for 20 years. CMT, we get a better understanding of CMT, and again I said CMT1A is 60% of cases, but it's a heterogeneous neurological disorder. There are other point mutations that have an autosomal dominant feature that affect myelination, and that's type 1. So type 1s affect myelination and are autosomal dominant, and there's now B through G. It might be up through H by now. Type 2 is variable severity. It's over 30 subtypes, and this is primarily with the axon itself. It's also autosomal dominant. Type 4 is much more rare. It's autosomal recessive, and it's demyelinating. Also has multiple subtypes, and then you will see type X, which is X linked has six subtypes. So there's a huge number of CMT subtypes, and to be honest, I practice in Baltimore, so I have the advantage of sending people to NIH if they have a weird subtype, and that's what I do, and I would suggest you take advantage of your neurology colleagues for some of these because they don't all show up with the same foot patterns. PMP22 is a glycoprotein in the internodal portion of the myelin sheath. Probably plays a role in Schwann cell death. The mechanism of disease is unclear. If you get a nerve biopsy on CMT1A, you see balls of Schwann cells that fail to make compact myelin. They make balls of myelin, and that's what these onion bulbs are on the micrograph there. There are now, this is the update part, the two slides, there are now a series of active and recent clinical trials for CMT1A, including some very early gene therapy studies. Unfortunately, it hasn't gotten very far. The one at the top is a gene therapy study. It's a phase one clinical trial, and it's a adenovirus associated injection of a protein called neurotrophin 3. Neurotrophin 3 stimulates myelination by Schwann cells, so that's the point, to try to upregulate Schwann cell. But obviously, you've got to be very careful if you're injecting genes that could upregulate production. If you look at the numbers, they planned three participants, and it was all the safety studies. That's all they were doing. They were injecting them into the gastroc, anterior tibialis, and into the quad. And even with three patients, they've currently suspended that study because the vector has not been produced. So we're obviously a very long way away from gene therapy for CMT. It's not going to come in the near term. So as surgeons, we are still going to have a role. We are not going to be out of jobs. I'm going to stop there, and let's move on. I think Chris Kaseya is next with a discussion on the subtle cave of varus foot. Thanks. That was pretty powerful to follow. So my goal is to talk about the subtle cave of varus foot. When do I slide the heel, and when do I do more? I have nothing to disclose for this specific talk. And this was actually a good introduction. So I'm not talking about the neurological part. This is the subtle cavus foot. And this will not be the people with CMT or any of the neurological deformities. So it's not the person on the right. It's the person on the left. And you cannot talk about subtle cavus feet without paying homage to Art Manoli, who basically taught us most of what we know about the subtle calus and cavus and what to do with it. And then Greg Pomeroy obviously followed with that. And it's a good article in 2014. And not only did he give us really good information, he came up with a few very nice phrases that everybody will remember, like the peekaboo sign of the heel turning in a little bit. So if you think about subtle cavus feet, for me, the question is, when do you move the heel for subtle cavus? The short answer is almost never, because at least 25% of the population will have a subtle cavus foot. It is just as normal to have a slightly high arch than what it is to have a flexible flat foot deformity. And we don't recommend to do a reconstruction for a child with a flexible flat foot deformity that's pain free. By the same token, we should not recommend to do additional procedures for the 25% of people with a slightly high arch and slight hind foot cavus. So this can obviously be either hind foot or forefoot driven. If it's hind foot, it might be due to a malposition of the calcaneus or the subtalar joint. It could be due to tarsal coalitions or previous fractures. Forefoot is mainly a plantar flexed first ray. And that can be structural or dynamic. Greg went through all the physical examination. So I'm not going to go through this again. This is the non-neurological group that I'm going to talk about. You will hear everything about the neurological group later. We want to know if it's flexible or rigid, bilateral or unilateral, bony versus soft tissue, and then hind foot versus forefoot. And this is the picture. It's the typical slightly in-toeing, slight hind foot varus, and slight forefoot adduction. That's the patients that I'm talking about. Otherwise, perfectly normal soccer player, no issues. But their parents is concerned about their high arches. So same thing, you have to talk about the subtalar mobility in the Coleman block test. I actually do the Coleman block test. It's not perfect, but I think it's a good test to do. And I love the idea of maybe doing this weight-bearing CT with and without a Coleman block test, because it takes five minutes extra. And that might give us very good information. It really still helps the flexibility of the deformity. And sometimes you can do this without the Coleman block test. You can just assume with your examination that you can do that. But if you look at this, this is a true mild cavus deformity with the hind foot varus. You can see the typical C sign if you look from behind. And you look at the outside, you only see the base of the fifth metatarsal, not the little toe. And then when you do the Coleman block test, that corrects. So now it's a straight line in the medial side. In the lateral side, you see the little toe. To me, that's a good Coleman block test. And whether you believe it or not, this actually still works OK. So if you have a way to do it, do it. It helps a little bit. My son, who's unfortunately a lawyer, asked me, so what's this tripod thing that you always talk about? So I said, well, let me show you. And then he was a typical lawyer, took a video of that, which is not a good thing. So if you have a plantar flexed first ray, the one that I'm moving, see what happens with the heel. So that's just simple. We know that's how it works. So plantar flexed first ray will give you hind foot varus. And the opposite is then also true. If you dorsiflex the first ray, then your hind foot goes into valgus. Very simple, and that's true not only on this tripod, but in real life as well. This is a fixed hind foot varus deformity. Oftentimes, this will be a secondary pathology, whether it's due to tarsal collision or some form of an injury. Because you can see the opposite side is normal. So we want to look at the forefoot declination, whether there's stiffness, whether there's toe deformities, which usually tells you it's neurological, not this idiopathic group. And then also muscle testing. Do the routine radiograph to see where your heel sits in relation to the foot. And then there are reasonable non-operative treatments for the people with subtle cavus and a little bit of symptoms, and mostly if you want to treat the parents, not the children. And again, from Art Manoli, the ART rival is the orthotic that is used for the subtle cavus deformities. And it works reasonably well trying to do the opposite of what we usually do with a medial ART support. This is a little bit more built up on the lateral side than with the recess for the first metatarsal. So it's easier for me to think about when to do what, if you think about clinical scenarios and just not try to make it a whole. So one thing is we have a subtle cavus with a fifth metatarsal stress fracture. So you obviously need to fix the fifth metatarsal stress fracture. The question is, do you do anything else? And in what population do you do anything else? Now, the reality of it is if it's an athlete somewhere between 15 and 50, I don't think if it's a subtle cavus and a first time fracture, you should do anything else but fixing the fifth metatarsal. Especially if it's a higher level athlete, if you start to add first metatarsal osteotomies and calcaneal osteotomies, I personally believe you change the direction of that player's career. Fix the fifth metatarsal, give them orthotic, and see what happens. If it goes on to a non-union and you have secondary problems, then you can think about additional procedures. And I would love to hear what you all think about that, but that's my approach. I fix the fifth metatarsal and move on. So if you think about additional procedures, so let's say it's a subtle cavus and the exam is normal. Other than fixing the fifth metatarsal, I do nothing other than maybe custom orthotics. Depending upon the sport, most people don't like these heavy arch rival type orthotics because it just doesn't fit in the shoes that they play. You still want to know if it's forefoot or hindfoot because that will determine the shape of your orthotic. If your exam is abnormal, the most common by far will be peroneal weakness or peroneal pathology. And then the question is, if you do something else, do you do first metatarsal versus calcaneal osteotomy? So the next group is the subtle cavus with peroneal tendinosis or tear. And the question then always is, was the cavus there before the peroneal issues, or is it because of peroneal issues? And I think that's when it's good to look, obviously, to the opposite side as well. Because oftentimes, you get a peroneus brevis tear and slowly over time, you develop the slight hindfoot varus. So this is one with a peroneus longus. You can see the peroneus brevis is still intact. And remember, like Greg said, the peroneus longus is a plantar flexor of the first ray. So theoretically, if you tear your peroneus longus, it will help your cavus, especially if there's a little bit of flexibility in your midfoot. If you have a fairly rigid cavus, it will not over time help. But you'd remove that plantar flexion power on the first metastasis. I don't think you should repair a peroneus longus rupture in the slight cavus. If you do anything with it, you should transfer it. And you can either do a peroneus longus to brevis or put your peroneus longus in the cuboid or the calcaneus so it becomes an e-verter. Because again, subtle cavus for me is more a problem in the younger athletic population. And it's hard for me sometimes to violate a perfectly normal peroneus brevis by doing a tenodesis of longus to brevis. Because no matter what you do with that transfer, you violate the peroneus brevis to some degree. So if the peroneus brevis is perfectly normal on MRI when you look at it, I actually transfer peroneus longus. So if peroneus brevis is perfectly normal, I transfer peroneus longus either into the cuboid or into the calcaneus. So that you keep its function, but you make it an e-verter and not a plantar flexion of your first ray. Again, that's not written up anywhere. So it'll be interesting to see what you feel about that. So if it's peroneus brevis that is injured, different than longus, they are different scenarios. So this, to me, is the simple one, where peroneus longus is normal. There is clearly pathology to peroneus brevis. But it's not torn. So this is simple. You repair it, and then you do what additional procedures you think is necessary. I briefly mentioned before, you always have to look at your lateral ligament complex and test it. Not look at the MRI. Because if you do an MRI on all of us that are older than 40, it will show that you had a previous anterior telofibral ligament injury. That's just part of the deal. You should not treat every MRI tear with surgery. You should examine them. Because otherwise, we will do 95% lateral ligaments unnecessary. So look at forefoot, look at hindfoot, and decide if you need to do anything else. This is different. This is a complete peroneus brevis tear. Peroneus brevis tear, peroneus longus is intact. So with this, we know we don't want peroneus longus function, because that's counterproductive. It plantar flexes the first ray and will give you hindfoot varus. So in this case, I will tenude these brevis to longus above the distal fibula. And then distally, you move peroneus longus to the fifth metatarsal. So you make it a peroneus brevis function. So either they're not a plantar flexor. This is the real issue. If you have a subtle cavus, but then you have both longus and brevis out. Because to try and repair, that's not going to work. So depending upon where you're trained, you either will do allograft replacement and put in the fifth metatarsal. Or you can take FDL or FHL from the medial side and put into the fifth metatarsal to replace peroneus brevis. If we look at the forefoot cavus, you can see that plantar flex first ray. There's first metatarsal in purple. And with that, you do a dorsiflexion osteotomy. So the most common procedure that I do for a subtle cavus is actually dorsiflexion osteotomy of the first metatarsal, much more than calcaneal osteotomy. Let me see if I can take the sound away. So this is one. So if you correct the hind foot, you can see how the forefoot is plantar flexed. And in that case, there's many ways that you can do it. This is just a straight up and down dorsiflexion osteotomy. You can make it, what I do more often, a long oblique to give you a better stability of that osteotomy. But this was a simple dorsiflexion osteotomy. And what I like about that, you can start with any closing which osteotomy start fairly small, close it, and see if you have enough correction. Most often, it's a pure first metatarsal cavus. Occasionally, maybe in 5% or 10% of cases, when you have your first metatarsal where you want it, your second metatarsal, there's two plantar flex, and you have to move that as well. Now you can see it's in a much better position. And let me see if I can. So if we think then about calcaneal osteotomies, this was first described by Dwyer in 1955. And Dwyer is a lateral closing which osteotomy. There are good articles about what happens when you lateral slide versus closing wedge or a combination. And it was mentioned before, the issue with the lateral slide, that you can get tarsal tunnel issues. So if I do a calcaneal osteotomy for the subtle cavus, I usually do a combination of a Dwyer and a lateral slide. Because I think it puts a little less stress on the tarsal tunnel, and you can also get a better overall correction of your alignment with that. So simple schematic illustration of that, where you take the lateral wedge, slide it, and improve your function. So this is a hind foot varus. You obviously need to make sure that you protect your sural nerve. You can actually see the sural nerve here. It's just dorsal to the incision. Make sure that you clean off enough soft tissue that you can get some form of fixation in there. And then same as with the first metatarsal osteotomy, start fairly small and go bigger with your wedge as you correct your deformity. Make sure that it's loose on the medial side without cutting through the calcaneal nerves, and then close it. And you can see when you close this osteotomy, it automatically also translates a little bit laterally. And then you can use whatever fixation you want, whether it's screws or staples. And you can see how much it improved the hind foot alignment by a fairly small dwire, and then a slight lateral slide. That's what it looks post-op. And in cases where the calcaneal pitch pre-op is high, but that's more the situation in the severe deformities than subtle, then I think you should slide your calcaneus up a little bit as well, because that automatically lowers your arch. Very important always to evaluate the lateral ligament instability in any of these cavus deformities, less so in subtle than in the more severe than you will see, because oftentimes there will be a chronic instability. And I will have a low threshold to repair this, and also a low threshold, especially in the neurological ones, to do some form of suture tape augmentation, because there will be always this tendency to continue to have a lateral instability. So in summary, the subtle cavus, very seldom a neurological origin. Custom orthotics might help, and you should determine if it's forefoot or hind foot driven, and then treat that accordingly. Usually osteotomy is very seldom. You do tendon transfers, because it's not a tendon imbalance like the ones that you will see in the next talk. Thank you. Sure. You can introduce yourself. Sorry. I'm Paul Fortin. Thanks, Greg. So we're going to talk a little bit about, step it up just a little bit and talk about more severe deformities. I think Greg pointed out, well, I'd just like to, for the residents in the room, the younger physicians, point out that distinction, a lot of times with these sections on cavo verus, you're either a lumper or a splitter. And we're, in this session, a lumper, because we're talking about cavo verus in general. And I think it's really important to differentiate that CMT specifically has a whole host of its own nuances that are differentiated from cavo verus itself. So what to fuse, when to fuse, and how to fuse. These are my disclosures. If you look at some of the current literature, this is as recent as 2018, it would lead you to believe that more advanced deformities always ultimately culminate in arthrodesis. And I think that that's a misconception. I think that with some basic principles of deformity correction, not always, but often, a lot of these complex deformities can be treated with selective arthrodesis or sometimes no arthrodesis. So I'm not a big fan of algorithms in general. I can tell you in 30 years of practice, I've never done a JAPAS osteotomy. If I did, I didn't recognize that I had actually done it. So like Chris had talked about, we could all agree on this being a very salvageable, at-risk, subtle cavo verus that really has a remarkably good outcome and really salvage of this joint with something relatively simple. And 15 years ago, we would go to the course, and all we'd ever learn about was a calcosteotomy and a dorsiflexion osteotomy the first. And that was kind of the initial stages of a recognition of an entity that now I think that we've embraced. Probably, in my opinion, one of the more complicated conditions that we treat, really highly variable. But if you break it down, I think you can make some inroads in terms of understanding it. So as an adult foot and ankle surgeon, unfortunately, this sort of thing is way much more common, at least in my practice. And these are super-challenging problems and not always resulting in great outcomes. So seemingly, you know, relatively mild cavovirus, medial peritalar subluxation, some evidence of overload on the fifth metatarsal, and, you know, I went to the course and they told me I need to do a calc osteotomy and a dorsiflexion, a medial column osteotomy, a tendon transfer, and it, you know, admittedly looks better, but not always great. And all too uncommonly, this is what we end up with, and this, unfortunately, has happened to me on multiple occasions. And if you're very careful and discriminating about your results, I think that you'll find that this is kind of what you end up with more often than not. And I don't have all the answers for you because I still struggle with this, and I still have patients that I think I do everything on, and they still have a virus hindfoot. So if you look at some of the more often quoted studies on cavovirus, especially as it relates to CMT, this paper keeps on coming up. This was out of Iowa. They had a series of 25 patients. They did peroneus longus to brevis, tendon transfers, dorsiflexion osteotomy the first, and plantar fascial releases. So the kind of classic joint spearing operation, they had a very low incidence of arthritic changes at long-term follow-up at 26 years. But interestingly, and this is not in the abstract, this is in the body of the paper, 80% of them had a virus hindfoot. And this is a totally different demographic than we operate in, and these were kids that admittedly had a better chance of a good radiographic and clinical outcome. And not that their outcome wasn't good, but their radiographic parameters didn't necessarily follow that. Some of the other literature, if you dive into it, and again, this is often buried in the body of the paper, significant incidence of persistent virus. So I think that we still have a lot to learn. With adult caboverus, we're oftentimes dealing with situations like this, arthritic and very stiff joints. And I think if you look at clinical, what I consider clinical causes of failure, what a failure looks like, persistent virus, like we talked about, lateral overload that may or may not be coexistent with heel virus. You can have neutral heel alignment and still have lateral overload from the spun-up forefoot equinus. And cavus, rarely but occasionally, residual cavus can be a pathologic condition and a cause of failure. Some of the other things that you commonly see are lower extremity malalignment that's been unrecognized. A big one that we'll talk about a little bit more, in my opinion, is inadequate soft tissue release. It can be dysplastic bone structure. The bones are shaped differently. They don't move well. You can do a release, you can do an osteotomy, and you can't get them to go in the position that we want them to go in. Bruce and Georgian and others described this and talked about inherent virus, inherent virus being conditions where there's lower extremity malalignment. And the subtalar joint itself has an abnormal axis, so you just don't get it to spin back around. Inadequate tendon balancing, you can have ongoing neurologic deterioration. Multiple reasons for failure, and Dave's going to talk in more depth on that. So it's important to understand, and this will be reiterated, that cabal virus looks a lot different. These are all cavus feet with a varus hind foot with multiple different etiologic causes, all that need to be treated differently. If we want to sub-segment the CMT patients, I think that it's very interesting and important to kind of like break down that anatomy because it's really important in terms of how you approach these things surgically. So what I call the neurogenic cabal virus, it doesn't have to be CMT, but the neurogenic cabal virus is much like a club foot. The navicular is medialized, oftentimes abutting the medial malleolus, the hind foot obviously is in varus, and this is really the important part right here. You get reciprocal supination of the transverse tarsal joints. The cuboid comes to rest, plantar to the navicular, and you get compensatory spin or pronation of the forefoot. That's really complicated and it's super hard to completely treat, particularly in the adults. So you have to be able to evaluate the deformity, and it's important to make a distinction between this sort of foot, which is somebody with what I want to call medial peri-taylor subluxation or peri-taylor deformity, and this sort of foot, both of these in CMT patients, both of which are treated markedly differently. So you have to ferret out the components of deformity. You have to evaluate the soft tissue tolerance for correction. Some of these have poor soft tissues, and unless you're going to take bone out, if you're going to do it acutely, you're going to run into wound problems. As was pointed out, you have to look into the various aspects of the neurologic status. Spasticity is one of the ones that really is a wild card that will affect your results, whether or not they have arthritis. And one of the things that is commonly touted at these meetings is whether or not it's fixed or flexible, the Coleman block test or, you know, is the hind foot flexible. I would suggest everybody take a look at this. I'm not a big fan usually of consensus statements. It's, you know, an opinion poll more than anything. This is really good. This is, I'm not sure who spearheaded this. It was Glenn or who did this, but this was really a good consensus statement. And among other things, they point out that the terminology fixed or flexible really is something that should be assessed after the soft tissue recession and after you've released everything. And a more appropriate terminology really should be whether it's reducible, partially reducible, or irreducible. And I would suggest that even if it's irreducible, that doesn't necessarily preclude a joint sparing operation. And really, again, in my opinion, the medial release is the key. Regardless of whether you're going to fuse it or not, you have to be able to do a medial release. In that segment of the population with cavovirus that have a neurogenic cause or have that peritailor disease. Historically, this is all we did. We did a plantar fascial release through a small incision. And oftentimes, the posterior tibial tendon would be harvested and that would suffice as our medial release. An example of the shortcomings of that, this is a patient of mine from, I can't remember when, that history of CMT, not horrible disease, but pretty significant medial peritailor subluxation. I had gone to the course. They told me I needed to do a calcaneal osteotomy, a dorsiflexion osteotomy of the first met. I did a plantar fascial release and a longus to brevis tendon transfer. I was led to believe that that's the way you treat this. And I never did anything more than that. And not too surprisingly, it's left with, you know, pretty significant residual deformity. Different variations of calcaneal osteotomies have improved our ability to correct hind foot verus. And I think that those that involve some bone removal allow us to better coronal plane correction. And I think that, as Chris pointed out, when you translate the heel in a cephalad direction, and rotate it, you can oftentimes neutralize the verus pull of the Achilles. Most patients with CMT, I would say all patients with CMT, don't really have Aquinas. They don't have gastroxolias contracture. They have limited ankle dorsiflexion, but lengthening the Achilles or doing something to the Achilles oftentimes is neutralizing the verus pull of the Achilles rather than lengthening per se. The medial release is really the key to correction, in my opinion. It starts with this, and there's a million different ways you can do this. This is just a short video on how I like to do it. The posterior tib is harvested. The important part is right here. The important part is a circumferential release of the talonevicular joint capsule, the superficial deltoid, the spring ligament complex, the anterior, middle, and posterior facets of the subtalar joint are all released. Oftentimes, I put some type of distraction device on there to mobilize both the subtalar and the talonevicular joint. And then oftentimes, we'll do an FDL tendon transfer, and then the posterior tib is transferred over laterally. So an example of how that can be effective. This is somebody that had, one of my pediatric colleagues had done this procedure, relatively straightforward, six years after this. They have recurrent deformity. You can see how there's still medialization of the navicular, the hind foot's still in verus. They had had the typical calcosteotomy, tendon transfer, plantar fascial release, residual deformity, recurrent ulceration over the fifth metatarsal. And with a relatively simple procedure, more extensive medial release, tendon transfer, and lateral column derotational shortening, the foot is put in a reasonable position. And you can see how not only can you correct the hind foot verus and the medial peritalar subluxation, but you can unspin the foot and derotate that through the calcaneocuboid joint fusion. That's an important part of it. So what about something that gets a little bit more difficult? This is, you know, your typical 60-year-old that his wife's been looking at him with this funny-looking foot all his life, and he finally gets sick of listening to her, and he comes into the office and says, you know, Doc, can you do anything to my foot? This is a more severe deformity, and if you ferret out the aspects of this, you know, the different parts of this deformity, it's mostly peritalar, right? The tibiotelar joint's in pretty good shape. He's got this significant, almost clubfoot-looking, medially displaced navicular. The hind foot's in a ton of verus. His ankle joint's in pretty good shape. He's still got a stable ankle joint. And if I follow my algorithm here, it says that, you know, I should do a triple or a Cole or a Japas osteotomy. And I would tell you that if nothing else, if you start out with a medial release, it at least gives you an idea of what the next step is. So in this case, we start out with that medial release. You release the tail navicular joint capsule, the posterior tibial tendon, the spring ligament complex, the subtalar joint, and then you can decide what the next step is going to be. In his case, it's a tendon balancing procedure, a limited arthrodesis where you derotate the spun-up forefoot through the calcaneocuboid joint and correct the forefoot adduction by shortening the lateral column. And even in a more severe deformity, you have reasonably good restoration of parameters of his foot, albeit he still has cavus. And in my experience, residual cavus in most people is not a big issue as long as it's a balanced cavus. Interestingly, in many of these more significant deformities, after you do this correction, because many of these patients have external tibial torsion, you end up with a foot that's pointing east and west instead of north and south. That's not necessarily a bad thing for people that have flexible deformity. It can be more significant in fixed deformity. Just a quick example of that. Somebody that's had previous correction, she has residual deformity, you're going to do a biplanar wedge to bring her out of adduction. And as you do so, you're going to uncover the external tibial torsion that sometimes has to be dealt with, particularly in a more rigid deformity. So in this case, you do a biplanar midfoot osteotomy, a rotational osteotomy of the tibia and fibula to correct the external tibial torsion. Gradual correction with a frame is occasionally, not commonly, but occasionally helpful, particularly in multiply operated patients or those with poor soft tissue, those with potential neurovascular compromise with acute correction. And it avoids shortening. You know, many times if you're going to take on these big deformities, you take out a lot of bone. That's really the basis of a lot of the old-fashioned JAPAS, coal osteotomies, is you just take an osteotome and you keep on taking bone out until you get the deformity corrected. You don't always have to do that. If you have the right patient, it's amenable to gradual distraction techniques. An example of that, this gal had had multiple surgeries. She actually is one of these rare Charcot-Marie-Tooth patients with peripheral neuropathy and a sensory neuropathy that acts much like a diabetic. She's not a diabetic. She has CMT. She's had fellowship-trained foot and ankle surgery and operated on her like six times. She's got residual deformity. Most of it's peri-taylor deformity. And it has this open wound that she's had for three years. An amputation certainly is a reasonable option. This is what her spun-up and markedly abnormal metatarsal looks like. And in her, gradual distraction just allows you to kind of pull it apart. You pull the foot apart, then you bring her back, and you fuse her. And her, you know, the frame acts as a means of wound management in addition to distraction that facilitates you being able to correct the deformity a little bit easier. There is substantiation for use of small pin fixators. I'm not here to promote small pin fixators. I can just tell you that it's something that does have a role. This is another example of how it can be used. This is kind of switching over to the non-CMT cavovirus. Equinus, again, is not a big problem in patients with CMT. It is a big problem in patients with post-traumatic equinovirus or cavoequinovirus as a result of compartment syndrome or other disease processes. So residual equinovirus in this setting in my hands is treated, again, with small pin fixation to correct the varus, then correct the equinus, and then subsequently do the tendon balancing procedure. Occasionally, it can get much more involved than that. Somebody with residual equinovirus, flat-topped talus, and really all you want to do is get the foot plantar grade, and there's a means of doing that with a fixator and a supramalleolar osteotomy. As I had mentioned, residual cavus is rarely pathologic, at least in my opinion. Isolated sagittal plane deformity is usually well-tolerated as long as it's balanced. And really, you have to make the, if you're going to take it on and if you think that it's pathologic, you need to make an assessment of whether or not shortening is acceptable. If you don't mind having a short foot that potentially has to wear a different shoe size, you can do a biplanar osteotomy, and you don't have to mess around with an external fixator. An example of that, somebody that already has a pretty short foot because of the calcaneal or because of his cavus, and he just has metatarsalgia. So the cavus is actually the cause of his problem, a biplanar wedge, relatively easy straightforward procedure that corrects his adduction, and it gets his foot plantar grade, and he probably puts an extra sock on because his foot's a lot smaller than it had been. Somebody with poor soft tissues, it's a burn contracture, residual cavus, refractory metatarsalgia because of his cavus, his foot's already small. And in my hands, this is something that's taken care of more appropriately with not taking more bone out, but just doing a small incision, osteotomy, bringing the foot up, and getting him off his metatarsal heads. Carl's going to talk more about this. I think that CMT and cavovarus, I think the take-home message is that regardless of whether or not you're going to do a joint sacrificing definitive procedure such as a fusion or a replacement, tendon and osseous balancing is oftentimes necessary in conjunction. Somebody, that x-ray that I'd shown earlier with significant varus hind foot, ankle arthritis, that in addition to the definitive procedure on the ankle, you have to get his foot plantar grade. And that's done through a combination of soft tissue balancing with tendon transfers, as well as the osteotomies that we just talked about. So I think that these are nuanced cases. I don't have an algorithm for you. Somebody hopefully smarter than me will come up with one. There will be a cookbook that you can follow. I doubt that will happen. And I think that you have to be prepared to be challenged. Thank you. All right. So we're going to move on. Carl Schweitzer is going to talk to us about the difficult problem of ankle arthritis in association with cavus. The best part of giving a talk up here is you get to take your mask off. My charge this morning was just to lower the IQ of this ICL session, so I happily obliged. It was actually to lower the age. These are my disclosures. I just made a bunch of enemies in the front row. Practice in North Carolina and Raleigh, when I see patients like this, I tell them, well, you got fleas and ticks. You got the varus ankle and the cava varus foot. The Bob father told me if you can understand the cava varus foot, then you understand most of foot and ankle. And I think that listening to these talks today, you can really start to understand the complexities and what it takes to think about these cases with preoperative planning and then really good execution to get the deformity corrected. Today, we're going to focus on the bottom two points. So not to overload you with literature, but the key is get it to neutral. I think the total ankle literature shows that no matter if you're starting with 30 degrees of varus, 20 degrees of varus, if you get it to neutral, they do about the same as someone that started off with three degrees of varus or a neutral deformity. And that helps to limit edge loading, early failure of a total ankle, limit early failure of your cava varus reconstruction and soft tissue reconstruction. So these were, I started to put a list together of essential tools. I called it a toolbox. I guess it looks more like a tool chest. It's pretty large. But these are some of the things you need to think about, a lot of which have been highlighted already by Paul and others. But spurs and loose body excisions, particularly in the lateral gutter that may prevent you from derotating your talus and reducing it, medial gutter osteophytes that are draped underneath or that the deltoids draped over top of and tensioning, a deltoid sleeve release and peel, and that can be superficial and deep, a lateral ankle ligament reconstruction that may just be a barostrum with anchors. It may involve allograft. It may involve tenodesis, depending on what your soft tissue status is. As we highlighted, a medial release, I think, is really critical. It keeps you from having that foot and ankle that's mostly corrected, but then you still have that residual adduction. So release selectively of the TN joint, spring ligament, perhaps the medial hind foot ligaments as well. A posterior tib release, a Z lengthening, a transfer to the peroneals or through the interosseous membrane to the midfoot. And if it's certainly severe in some of these paralytics, release and lengthening of your other flexors as well. An anterior tib transfer to the lateral midfoot. That can be done in part or in whole. Peroneal tendon reconstruction work, longus to brevis transfer, allograft reconstructions, flexor transfers to the peroneals, plantar fascia release, Achilles lengthening, various osteotomies, arthrodesis, and finally, total ankle replacement. And there's things to consider with implant selection, I think, with that, and even considering role, particularly in some of the congruent deformities for pre-op CT guidance and planning. So terminology, it's always good to start with terms that are understood. So congruent would be less than 10 degrees, difference between your distal tibial plafon and your talus, incongruent deformity, varus degenerative would be greater than 10 degrees between the plafon and the talus. There's other deformities, obviously, to consider. A lot of these patients come in with knee deformities, proximal tibial deformities, and I always think work proximal to distal, and so getting that corrected first. Obviously, supramalleolar work, ankle deformities, which we're going to highlight mostly in this talk, and inframalleolar deformities at the hindfoot, midfoot, and forefoot. So in terms of congruent, we're talking about an intra-articular deformity, and that's basically through erosion of your distal medial tibial plafon. Incongruent tend to be more extra-articular, is how they term it, and it's more associated with lateral ankle ligament instability, contracture, and tightness of your deltoid ligament, and your medial midfoot hindfoot structures as well, including your posterior tip tendon. More associated with increases in varus tailor tilt, medial malleolar erosion and flattening, or what they term horizontalization, say that three times fast, of your medial malleolus. And you also want to check your lateral gutter, particularly in these incongruents, there could be a spur or loose body that's preventing your reduction. It's a very simple thing that you can fix right off the bat to help derotate your talus in the mortis. And you can also have some degree of distal tibial plafon erosions in these incongruents. That's not just selective, just to the congruent deformities. As Paul said previously, I mean, flexible and rigid are the terms we learned in training, and I think, again, go back to that consensus paper, the better terms are reducible, partially reducible, and irreducible. And really, not every, you know, rigid deformities are not necessarily as common as you think, and I think you can't really call it that until you're intraoperative and you've done your stepwise kind of selective releases, then you can determine rigidity. But the true rigid ones are the severe degeneratives, irreducible hind foot deformities as well. So I mentioned the Bob father, I trained in Charlotte, so I got this from the Hodge father. And so, you know, he likes to think about things simply, and this really kind of struck a chord with me in terms of algorithms when we're thinking about varus, degenerative ankle with a cave varus foot. And so you have ankle reducible, foot reducible, ankle irreducible, and foot reducible, and then the ones that kind of make you nauseous the night before, the irreducible foot and the irreducible ankle. But you don't want to get your cart before the horse here, so remember your indications and relative contraindications for total ankle arthroplasty. I listed some of the more common ones we think about as moving them away from an arthroplasty procedure. Infection, arterial disease that's not reconstructable, poor soft tissue quality, Taylor, avascular necrosis, Charcot, insufficient bone stock, moderate to severe peripheral neuropathy, dense neuropathy, and paralytic deformities. These things can all derail good outcomes. So let's start with the simple one, the first. This is the congruent, the reducible ankle, reducible foot. And so we think about this, as we said, this is medial distal tibial plafond erosion. These tend to be milder deformities in general compared to some of the other ones, and really your distal tibial cut is going to correct most of your deformity at the level of the ankle. It's a interarticular deformity. You're going to resect more lateral than medial. You want to try to minimize resection, you know, based on your ligamentous status. You don't want to get into a situation where you don't have enough metal and plastic to stabilize things. And I said you're going to resect more lateral than medial distal tibia, and typically these have less of a need for a lateral ankle ligament reconstruction, and really I don't find that I often have to touch the deltoid ligament in these cases. I found that these can be, you know, have pretty predictable results using pre-op CT guidance for my total ankle. This is most always done in a single stage. The order is your total ankle, post-year release, and then potential cabovaris work. I think the TN medial midfoot release is really critical, perineal tendon reconstruction, dorsiflexion osteotomy, first metatarsal, and various calcaneal osteotomies that you could perform depending specific to the deformity that's there at the hind foot. So this is a 54-year-old female, healthy hiker, works as a bakery manager, long-standing history of chronic lateral ankle instability, pain at the medial ankle, perineal tendons, lateral foot, has a milder subtalar joint pain that's present. These are her weight-bearing radiographs. MRI shows some perineal tendon pathology and a lateral stress fracture or stress reaction at the fifth metatarsal base, and this is her CT scan. And so for her, I find that with these types of congruence, it's nice to do pre-operative CT guidance. I think it really helps to determine your distal tibial cut, get that exactly right, and that's what drives the procedure. I think if you have that right, everything else kind of falls into play. And so here is doing the total ankle, did an Achilles release, a medial midfoot release, perineal tendon reconstruction, and then brought the medial column up with a dorsiflexion first metatarsal osteotomy. She's about a year out. She's doing well. She's hiking, and her pain's gone. She's well-corrected. You can see that medial peri-taylor subluxation that she had pre-operatively is fairly corrected here, and her AP miris on her weight-bearing X-ray is neutral. Next category, so kind of stepping it up in level of complexity, this is the ankle irreducible and the foot reducible deformity. This is your incongruence. And so a little bit more work here as we highlight. These have more taylor tilt, more tightness medially at the deltoid, more attenuation of the lateral ligaments. They can have some medial plafond erosion at the tibia. You get these morphologic changes at the medial malleolus, this horizontalization of it. You have medial osteophytes, the deltoids draped over lateral gutter, pathology that's blocking your reduction, loose bodies, and osteophytes. They have more anterior taylor subluxation, and you have to keep that in mind using laminar spreaders to minimize your resections, and they can have tight medial structures. So for this, I prefer more of a robust intramedullary-based ankle replacement system. Most always doing these single stage in the order is really converting this incongruent to a congruent ankle, and then you just go down the congruent pathway that we talked about. So this is a 66-year-old hunter-fisherman, 20-year history of his foot turning in multiple sprains, failed injections and bracing, pain in the foot and ankle, told by two other orthopods that he needed a fusion. His exam, he was partially reducible or correctable, tight achilles, and this is his motor function. This is his standing front and posterior views, showing the deformity. These are his weight-bearing ankle radiographs here, showing an incongruent deformity without significant amount of distal tibial erosion. Lateral radiographs showing supination of his foot, overpull of his posterior tib and medial structures with that medial peritailor subluxation that gives you that adduction deformity. CT, some selective cuts here. You can see the osteophytes immediately. You can see a loose body and osteophyte off the lateral tailor body in the gutter. These are going to be really important to identify and address. Spend a lot of time preoperatively looking at these CTs. I think planning is really critical here. You got to have all your steps in line. So plan for this patient was an intramedullary-based total ankle replacement, achilles lengthening, a medial midfoot release, and a transfer of his posterior tib tendon to the perineals, perineal tendon transfer, possibly a lateral ankle ligament reconstruction, calcaneal osteotomy, and bringing his medial column up with the first metatarsal osteotomy. It's been highlighted. It's really critical to plan out your incisions, and so as you get more comfortable doing some of these tendon transfers, you can start to work through a little bit more smaller incision, but as you can see, you can get these spaced out pretty well across the foot and ankle. And so we begin, achilles lengthening, a medial midfoot release. Here we're harvesting the posterior tibial tendon, bringing it up posterior medial above the ankle. We're going to swing it using a large Kelly clamp along just the posterior tibia, not to entrap any nerve vascular structures, and I'm not going to set it at this point, but I'm just going to keep it in a moistened gauze until the end of the case. And then here we're approaching our anterior ankle, addressing the medial osteophytes that are tensioning our deltoid ligament, and then really aggressive lateral gutter work. So remember this person had a loose body and a lateral tailor osteophyte as well that needed resected. This really allows you to start to derotate your talus, and that's critical. I don't pass go unless I get it neutral, otherwise there's no point in doing the rest of the case. And so here you could argue even a little bit overcorrected, but in any event, I don't have a fluoro shot showing, but it's really important to use two laminar spreaders, one medial, one lateral, to distract and tension your ligaments, and that is going to help minimize your resections when you're doing your total ankle, and that's going to be really important so you don't end up out of poly. So here we have it pinned. It's now a congruent or neutral deformity, and now we're going into the frame. And at this point, this is a relatively straightforward total ankle replacement. We have the joint distracted. We're doing our cuts, and then we get the metal and poly trials in. Then we're going to start stressing the ankle, and you can see there's some residual inversion stress. And so at this point, I take the poly liner trial out and then work towards just doing a barostrum. This patient had pretty adequate lateral tissue, and so anchors were fine here, but if not, you can always rely on tinnitus or an allograft, and we can talk about that as we go further in terms of whether you might want to stage that with a cement spacer as well. Anyway, retrialing, now we're stable at the ankle. You can see there's a smaller poly in there. That's a 12-millimeter poly, and then I'm going to go ahead and finalize my lateral ankle ligament reconstruction. Now I'm going to go ahead and set my posterior tib tension, respecting kind of Blick's curve relationship and doing a pulvertaft into the peroneal tendons. I'm also going to go ahead and transfer the longest to brevis and then tenotomize the longest distally. And now we're starting to look at the hind foot and move into the foot, because the ankle is now neutral. So you can see there's a residual hind foot varus. For this, I prefer, or my lateral calcaneo-osteotomy of choice for this patient is just a sliding, closing-wedged wire, and then you can also proximalize that distal fragment and reduce any calcaneal pitch. You can kind of dial these in appropriately. Obviously, there's other calcaneo-osteotomies you could consider. Malarbo or Z can also get a good de-rotation of your hind foot as well. So now we're pretty neutral. The forefoot's plantigrade. We're not going to have to do anything with the first metatarsal. And so six months out, this patient's happy. They're neutral. They're pain-free. Relationships look good on weight-bearing radiographs. So this was just to go back, pre-optiformity on the top, post-op on the left. Pretty well corrected. The patient's no longer walking on their lateral foot. Last one, ankle irreducible, foot irreducible. These are tough. You definitely don't want to start off doing total ankles and capovarious and starting with this one. So this is your highest level of difficulty. I think this is reliably done in two stages. I rely heavily on an intermediately referenced ankle replacement, like we highlighted for the middle category, and then osteotomies and fusion. Stage one, generally, to correct the anklevarus to neutral using the tools we talked about. So gutter debridement to derotate the talus. And typically, these come with more deficient lateral ligament complex. And so for this, I'm going to use an allograft or a tenodesis. And then I'm going to put an ankle cement spacer in immediately to hold the ankle so it can heal. All that ligament reconstruction can heal and neutral. And then we're going to go ahead and do the rest of the tendon transfers, all the tools that we highlighted. Likely, with these rigid ones, you're thinking about a triple and midfoot osteotomies. You're going to let that heal for about three to four months and then get a CT. As you know, to do total ankle after that, a lot of some of these hindfoot screws have to come out. So you've got to be healed. And that CT scan will happen. And then we'll proceed with stage two, which is your intermediately referenced ankle replacement and any remaining correction that you need to dial in. So this is just going through staging. The first category, always one stage. The middle category, most always one stage. And what else do you have to two-stage beside the irreducible foot and ankle? You know, I think you have to think about your surgeon experience, your comfort level with these deformities, what's best in your hands. I think that there's no substitute for being honest with yourself. Total ankle replacement and any type of hindfoot arthrodesis, like a subtalar arthrodesis, I think that can be a lot to the talus and the blood supply. And I think I prefer personally to stage those, although some will choose to do it in one stage. And then any gross lateral ligament laxity or insufficiency that's going to require you to do something more than just your standard brostrom, whether that would involve allograft. And I think that's nice, so that can heal with a cement spacer in to keep the ankle neutral and come back and do a relatively more simple ankle replacement in stage two. So that was a lot on ankle replacement. What about the non-total ankle candidates? A lot of these cases have been shown. These are more your neurologic or paralytic deformities. You're going to bring along your same tools that we talked about, and this can be combinations of ankle fusion with cavovirus reconstruction and soft tissue balancing, or TTC and cavovirus reconstruction. Most always, I find, able to do this in one surgical session. The goals here is really to only fuse what you feel is necessary to get things corrected and neutral. And you want that patient to be pain-free and brace-free, or in some situations, braceable. And you also want them to be ulcer and infection-free. A lot of these people come with superficial ulcers laterally at the foot. So a variety of options for this. This is a 70-year-old CMT patient with a prior triple malunion, and we basically tackled this by doing a realignment ankle fusion and then a cavovirus reconstruction around the hind foot malunion, along with medial midfoot releases and a posterior tip transfer. Got them relatively neutral. You can see, I think that AP foot correction is pretty dramatic. We've reduced the adduction and supination to the foot, and things look a lot more balanced at this point. Here's a 79-year-old idiopathic cavovirus, ankle virus. And you may say, well, why didn't you do an ankle replacement on this one? He was scheduled for it, and then a week before, kind of got some cold feet and opted. He said he just wanted the security of just having to do one procedure and not having an ankle replacement potentially fail. And so opted for a TTC orthodesis with the other tools that we talked about to correct the foot. So I think the concepts remain simple. The surgeries can be hard. When you're looking at deformity correction, just get it to neutral. If it looks like virus on the table, that's because it is, and you got to keep going. You got to know when to stage. You got to be honest with yourself, and you got to be reasonable with what you can do in one setting versus two. I think there's no substitute for meticulous pre-op planning and then good surgical execution to carry out what you planned. Know the algorithms. Know the sequence. Know the order of steps you're going to go to, and you got to really be comfortable with all these tools. You have to be able to do all of them, and I'd recommend cutting your teeth on the simpler deformities to start with. References. Thanks, OrthoCarolina family, for putting this meeting. It's going to be a great meeting together. Thanks for John Kwan, Ken Ellington for including us and including me on this ICL. Appreciate it. All right, we're going to move ahead. Dave Thurdarson is going to tell us what to do when everything else has failed and we need to fix salvages. Great. Thanks, Greg. So, following up on Carl's comment, I'm going to increase the age here, but I'm going to further decrease the IQ of the talk. I'm no longer a journal editor, so you'll notice there's no references for this. This is just principles and some cases. Do I click on this? Is that? Oh. So, hopefully what you'll do is you'll do a good exam like Greg's done, like he talks about, and address the problems the first go around. This is not a talk on Chris's types of failures. It's not to sublocate his foot we're talking about here. I don't have extreme examples like Paul has in here. This is, and it's really more a C&P focused thing, because those are the ones that tend to develop progression, or I think are just the more common sources of these problems. So, failure of K-1 virus correction is typically almost always due to under-correction. Like Carl was just saying, if it looks like virus on the table, it probably is still virus. It's usually a residual static deformity, sometimes a dynamic component to it. Rarely it's over-correction, and as was alluded to earlier, it's typically if you have a slight over-correction, it's probably not going to be much of a problem anyhow. So this is a patient, just to show, it's a typical patient, 30 years old, with a hindfoot K-1 virus, a little delayed onset. It is a CMT patient, and did the standard sort of correction, which I think that's kind of the go-to, or at least the traditional go-to, peroneus longus brevis tenodesis, your lateral side calcaneal osteotomy, plantar fasciotomy, and included a Jones because the patient had a claw toe, to improve the dorsiflexion strength, and it's not the folks that talked, but this patient's really their only complaint was, hey, I've got, you know, some residual clawing in my toes, but the patient did well, and that's the standard thing for the not as severe deformity, but again, it's, you know, one, two, three, you know, four, four things we did here, and it's usually a combination of things when you're fixing these. But what about the residuals? So again, the static deformity, at least in my hands, and I'm not talking about the extreme cases like Paul talked about, is usually treated with the static part with osteotomies. The media release can be very helpful. I've actually been doing that more recently, and most recently, I did a media release on a tail or neck malunion, not with a cable varus due to that, and it can really, really help. If the plantar fascia wasn't released previously, obviously, it can help that, but you can add that to your procedure. A very, very stiff joint or with arthritis, probably a fusion is a way to go, but again, these things don't always require fusions. This isn't a talk primarily about fusions here, and it's usually a combination of deformities, and there's usually heel varus almost invariably, and that's probably the most notable part causing the failure. There can be cavus, but oftentimes, a cavus is not as big a problem, and if they have metatarsalgia, sure, then maybe the cavus is a big part of it, and then that midfoot, hindfoot supination, there can be a problem with that spinning that Paul was alluding to earlier. So, for the fixed residual heel varus, if subtalar joints are not arthritic, somewhat mobile, residual revision calcaneal osteotomy will oftentimes get the job done. I personally find that it's often difficult to get enough correction with these really severe heel varus problems with just a slide, so I'll do a combo slide and a Dwyer closing wedge to get the thing to go over, and you can also rotate that, so you bring the infraspect, the calcaneus, even further out laterally, it can help get more correction. Now, obviously, the subtalar joint is arthritic, or if it's super stiff, then I'd probably just do a subtalar fusion. Those cases prevent predominantly resecting lateral bone to get your correction of that heel varus there, but if you can't get it all with your joint preparation, then go ahead and add a calc osteotomy to it also. So, here's a patient, severe CMT, severe cable varus, unstable ankle, and while it's not a failure, this is somebody who's had a lot of weakness going along with this, and in this case, I did a fusion, but I found when I was first doing these cable varus corrections, I was so focused on the source of pain, this patient complained miserably about the ankle joint that, okay, we go and we do a TTC fusion, correct the heel varus, get the ankle fused, and the patient will do fine, but don't forget the forefoot, so do that in one stage, as Carl was just alluding to, and Paul, you add the dorsiflexion osteotomy, otherwise, this patient would have failed. They would have had callous and pain and metatarsalgia over that first met head. I don't typically do or even try to do a total ankle, but we can talk about in the discussion section about some of the other speakers may have done a rebalancing and then a replacement in this case. Now, what about the mid or high foot residual supination? Again, depending on the degree of stiffness, you can do a derotational osteotomy. I typically do it just through the cuneiforms and cuboid. You can even resect the tail and vicar joint if it's a severe arthritic hind foot. If the cave is excessively high, I'm not particularly concerned about shortening the foot. My goal is to get a plantigrade foot that doesn't hurt, and if it's a little bit short on the contralto side, I'm not worried about that, so you can do a wedge resection. And again, add those soft tissue procedures. The plantar fascia wasn't cut previously. You can cut it if the medial capsule hasn't been released previously. Go and release it. So here's a case of a 40-year-old periodontist. She had severe ankle instability. That was her main complaint. She really didn't have any ankle pain. You can see the joint space is narrowing there a little bit, but her complaint was just instability. She couldn't stand, and you can see on the lateral the significantly plantar flexed first metatarsal. So on her, this is my procedure. I did the standard, I did the dorsal flexion first, metatarsal osteotomy, calc slide, added a brostrum. She was quite loose, but she was better, but when she healed up from this, she was all said and done. She still felt a little unstable. She was a lot better than she had been, and you can see here, though, that there's still a lot of cavus there in the foot, and slid her over probably about a centimeter, 1.2 centimeters. Despite that, she still is at best straight, but probably in a touch of varus. Now, it's not a heel, but it's not a weight-bearing view. You can see she's still over there, but I don't know I could have translated that a lot further, but I only did a slide here. This is not a closing wedge. So in this case, we wanted to fully correct that. So plan for a wedge resection. You wanna get the varus out by taking more bone laterally. You get the cavus out by taking more bone dorsally, and then revise the calcaneal osteotomy. So here you can see, and I saw Paul's slides where he uses a lot of fixation. I found when I'm cutting through this cancellous bone, it likes to heal, so I'm oftentimes just using Simon pins through the skin or a single screw, and they seem to heal pretty readily, and it makes it a lot easier with regard to fixation. So did the wedge resection here. You can see where he took the bone out, so now we're pretty well aligned. Actually, we've gotten a lot of that cavus out, and then you can see revise the calcaneal osteotomy. On this one, I slid it a little bit further, but I actually did a wedge resection this time to pull the heel out of further varus, and maybe because it's a two-stage surgery, there was no nerve injury on this one, and the ankle is very stable, and she's quite happy with this. Added some arthroplasties over lesser toes because she also had claw toes. And you can see that things are pretty well aligned here. Not a particularly perfect x-ray, but again, slid the calcaneus a little bit approximately, get some attention off her gastroc soleus also. So one year, she's quite happy. She's got a balanced foot, but of course, this is a CMT, so she has a contralateral problem. And this was alluded to earlier about nerves and all that. So I learned my lesson for the first side. Okay, the calcaneal osteotomy, a slide wasn't adequate. If I take her a centimeter, centimeter and a half over, I'm probably not gonna fully correct that. So I'm gonna go ahead and add the wedge resection with my slide at the same time. Obviously, dorsiflexor first metatarsal. And I got her corrected. This one, I went ahead and slid it, wedged it, let it translate a little bit further dorsally. That got some of the cavus out. She was actually very nicely balanced on the table, and I added the lesser toes at the same time, added the dorsiflexion first metatarsal osteotomy. However, she did well. Here she is a year post-op, but she had a numb bottom of her foot for about the first three months, and it recovered such that by about six months, it was all done. So that problem does exist, and I think that, I don't know, I did not do a prophylactic tarsal tunnel release, and as was alluded to earlier, that may or may not have made a difference. But during those first six months, when that sensation was recovering, the plantar aspect of the foot, I was thinking probably I should have done that, or at least I would have felt better having done that. First grade, if it's plantar flex, obviously correct that with the plantar flexion now, with the dorsiflexion osteotomy now. Residual mechanical instability. When I'm doing a primary procedure, typically all I'm doing is a brostrum. Now granted, if the patient had no ligaments whatsoever, sure, I'd do some sort of suture tape augmentation or something like that, but I think that the vast majority of the stability the patients recover during the surgical correction is by correcting the bony deformity. They have a completely imbalanced foot. It doesn't matter what you do to the ligaments if you don't correct the deformity, but conversely, once you get that deformity corrected, to throw a brostrum in there where you just reap the ligaments up only adds five minutes to the case, and it's not a big deal to add that. Now if they previously had the deformity corrected and they still have a lot of instability, then certainly I'd do some sort of allograft ligament reconstruction, dealer's choice, Chrisman, Snook, Evans, or whatever. If there's ankle varus and arthritis, then sure, you can consider an ankle fusion or even a replacement. Now, the other part of the problem, those, you know, check their stability, check their ligamentous laxity. Part of the instability a patient may have may be functional only. It may be poor proprioception. It may have a significant neuropathic component, and there's nothing you're gonna be able to do surgically to help with their lack of proprioception. But if you do have weak eversion and you've not fused any of those joints, then go ahead and do your splenus-longus brevis transfer if it wasn't done previously. And as alluded to previously in other talks, if both perineals are ruptured and you have no proximal elasticity of the muscles, then you can do an allograft reconstruction, or occasionally I'll do an FHL or FDL transfer to the lateral side of the foot. Now some of these patients come in, they're well-balanced, their stability's back, but then they got the drop foot, and it may be that you failed to correct at the initial surgery or the disease has progressed and now they have weak dorsiflexion. And those are ones where you can just, I typically will just do a posterior tibial to dorsum transfer. So here is a patient, this is a fixed cavovaris, a lot of ankle instability, but minimal ankle pain, despite having essentially bone-on-bone contact there. But this, so she got, I did a triple on this one, did an Evans because she had no ligaments whatsoever out there laterally. And whereas she was stable, and she was happy with this, contralateral side had a different mix on that side. She had fixed equinovaris, but she also had a foot drop, but she didn't have the ankle tilt. So on this one, did a one-stage procedure. So she has fixed cavovaris, you can see, she can't get to neutral, you can see the adduction in quinus and varus, so, and she also has that IP flexion traction there. So she was somebody that we did the triple orthodesis and TAL, so we get the foot to neutral. Did a Jones procedure to try to help that, but I personally have been never overly impressed with the amount of dorsal flexion strength to get from a Jones procedure, just transferring the HL to mid-foot alone. So went ahead and did the posterior tibial to dorsum transfer. So here's the patient, interrupted with the correction, you can see, got the patient to neutral, you can see the various incisions for transferring it. She heals up, here she is at six months, and she's got a solid fusion, and these one-stage things could actually work reasonably, well, this is her sixth week, so she hasn't even moved her foot yet, and you can see that you asked her to dorsal flex, and she can already get to neutral, even though she's been locked up in a cast for six weeks. So in conclusion, the usual problem with the cavovaris problem is under-corrections, rarely over-correction. Address each component of the residual to form the appropriate osteotomy or fusion, or even soft tissue releases or reconstructions to get the foot plantigrade. Repair the lateral ankle ligaments that are lax, and definitely balance the foot with tendon transfers as needed to get a balanced foot. Thank you. Let's see, why don't we have, Carl, why don't you come up to the front here. You'll wanna, we don't have a place for you to see the screen, so we can just sit here, and I guess we'll just pass the microphone around. But let's go out of here. So what I thought we'd do, we'll go through some cases. I do wanna entertain questions from the audience, too, so why don't I start with some cases, and then let's just hand the microphone up here in the front. And Paul, you wouldn't mind coming up to the front, too, because that way we'll all be in the same general vicinity. So, all right, so what I thought we'd do, we got about half an hour. Let's go through this one fairly quickly. This is a 17-year-old male. He's CMT1A, he comes to my office, he's got ankle instability. So the first question I have to the panel is does subtype of CMT matter? Do you care? Chris, do you care? No. I probably should, but I don't. All right. Anybody care? I think you need to, I mean, it comes, for me it comes down to a good, all right, for me it comes down to doing a good neuro exam. I'm not familiar with all the subtypes, admittedly, but there, as you pointed out, there are subtypes that are associated with more profound muscle weakness and sensory disturbances, as well, that you need to know about. So I only care when I match the subtype up to the age. So if I have a, if I have one that I know is gonna have a profound rapid decline and they're young, then I do worry about that, and I worry about possibly I'm gonna do a little bit more. But on the other hand, if I have a CMT patient that's showing up with perhaps a less severe deformity that's in their 40s that has a type two that's not gonna be one of these more rapid progressions, then I have less concern. I also have less concern over the other side. So I have some, I think it matters only in if you match it up to the age and where they stand in terms of their progression of deformity to their age. Now this is a fairly typical thing. His primary complaint is ankle instability and lateral ankle pain. So we've talked about this as kind of the cookbook approach if there is sort of a cookbook approach. What would the panel do if you just had to come up with this off the, I'll tell you, his ankle is congruent. He's got a varus heel. He's got a little bit of a, on a Coleman block test, he doesn't quite reduce. I'll skip to the chase on some of this. So what are you gonna do? Carl, what do you wanna do with this guy? Send him to Baltimore. No, I think that for this, as a neurologic CMT, definitely thinking about calcaneal and first metatarsal osteotomies, depending on the specific exam on the table. Longus to brevis transfer, and then addressing the ankle instability. Okay, so incisions. What do you wanna do for incisions on one like this? We've got a lot of different things that we can do. We've talked, you showed a slide that was about as busy as this, and I don't pretend that people wanna be able to read that, but you've got a congenital cavus foot, you've got ankle instability, you've got neuromuscular deformity, and you have all of these things. This is your bag of tricks, and you gotta accomplish them. So how do you wanna do the incision planning on this one? First, I'll assess for pain and think about an MRI to look at the perineal tendons. I don't wanna miss that, and that's gonna direct, that's really where decision making with incisions comes into play. So if there is perineal tendon pathology that I'm gonna address, whether it's a repair or perhaps needing like an allograft if it's about rupture and not reconstructable, I'm gonna probably make more of a utilitarian lateral incision that can do the brostrom and the perineal tendon work. I'm gonna space that out from my lateral calcaneo-osteotomy incision. I'm not really an MIS person at this point, but that may be a good indication. There was a paper out of Charlotte that talked about the safety of that lateral extensile ankle incision and a lateral heel slot incision, and that is safe to do if you can get them spaced out and move the lateral ankle incision more anterior. The other incision placements, pretty standard. They're usually out of the way of the other ones. So what about this one, stretching a long extensile incision and trying to do everything through the same goal? Anybody wanna argue for that one? In other words, trying to get the calcosteotomy through that. I've done that, and I've always regretted it. I mean, I did probably two or three times. I just cheat that incision anteriorly and cheat my calcaneo incision posteriorly because you're coming at a really weird angle to get at your calcaneo-osteotomy, and you're really running a high risk of buggering up the serral nerve, so I've gone to two incisions. But I like your MIS approach. So pretty much every time I've done that, I've seen serral neuralgia or I've seen some problem. Yep. Well, if you did an MIS approach, you would still potentially have problems doing tibial neuropathy from a calcosteotomy. So, well, let's be clear. The rate of tibial neuropathy from calcosteotomy, even in Chris's work, is very low. It's not particularly high. I will tell you that in the series of MIS I've done, I have not seen that problem. So it is a relatively uncommon problem. I don't want to pretend that it's a high rate, whereas the rate of stretching a long extensile incision and pulling back to do a serral, that's remarkably high. So I think the point of what I'm getting at is, and I think the panel would agree, it's not a good idea to try to do it all through one incision. You could go medial, make a medial incision to do the calcosteotomy, and it's actually easier to push the calc part, the tuberosity part away from you than it is to pull it towards you. Well, I suppose you could. I don't have any experience with that. I would tell you, as in terms of our data, if you have about a four centimeter skin bridge between your two incisions, that works out pretty well, even if you do a long incision. If you do an MIS incision, you don't have to worry about it. The tricky part gets if you have to do much more extensive perineal work. So the concept of cheating your incision anteriorly works pretty well if you have perineal tendons that you can mobilize and you're doing a brostrom. If you have perineals that are badly scarred, that are down in there and you actually have to get in there and sort of dig them out or work out all your perineals, then you're gonna be doing a lot of dissection behind the fibula with your primary incision. And to me, that's one of the better indications for an MIS slide, even though with an MIS slide, you won't get as much correction. You don't have to worry about the incisions nearly as much. Thank you. So this is what I did. I did a brostrom, a dorsiflexion osteotomy of the first ray, percutaneous LDCO. This was not a severe deformity of the calc. Remember, the kid's 17. I did a longus to brevis transfer. I did not do a plantar fascia release. I did not need to do an Achilles or gastroc lengthening, and I did not do a medial release. Again, this is a 17-year-old. So I guess my feeling is that you get in these younger patients, if you're working an earlier CMT, I actually love it when there's an excuse to operate on them early. Does anybody else share that? I mean, I was happy to see this guy came in with ankle instability. It gave me a chance to do some things that might give him a better chance of avoiding trouble in the future. Anybody else share that attitude? Glenn, you're sitting back there. Do you share that attitude, or do you try to worry? Operate on them as soon as you know them. I would encourage anyone to operate on these patients as soon as you know they're not going to be doing well. And you know that fairly early. You'll know that at 14. You'll know that at nine years old. Yeah, so that leads to the corollary of this question, and I had it on another slide, but we'll skip to it. His brother has CMT1A, also genetically known, because now we have a genetic test for CMT1A, has a plantar flexed first ray, doesn't have ankle instability, but has a little bit of lateral ankle pain. Is there an indication to do a peroneus longest to brevis transfer in the brother? And that's an open question. Anybody on the panel want to weigh in? Carl? I would probably just start them off with an orthotic and see what benefit they get. If it helps, and then they prefer something more permanent, I'd offer them surgery. Well, that's an easy answer, but that's skirting the issue. Glenn? It's hard to operate on someone who's not asymptomatic. That's the problem. I would not operate on that person, but I would probably do it truly myself or a member of the family and say, you make sure to text me when things are going wrong. I do exactly the same thing. I don't. I did not. I don't operate on asymptomatic patients, but I say the minute something is a reasonable excuse to do this, then I think it becomes more reasonable to do. Vic Macro from Stockton. You skipped those four other hammer toes that are heading towards claw toes. What do you do with those? So again, for me, it becomes the unicorn question. You know, the flexible claw toe that we do girdle stone tailor transfers on, and if you ever have them, it's in these young CMT patients. So it becomes an option. And then the older CMT patients, I fuse the toes. And I'm going to say I fuse the toes. I don't do arthroplasty. I would love to hear what other people say, because if you have a neurogenic claw toe, and these neurogenic claw toes, where they're all four like that, and you try to get by and do arthroplasties, there's such a remarkably high incidence. I'm talking about older patients with CMT or with any of the spastic conditions. They come back with either a nonunion through the attempted arthroplasty that has deformed, and a straight nonunion's fine, or they come back with DIPs turned down. With the modern small cannulated screws, I'll put small cannulated screws in them, and I'll fuse both joints in the toe, and I walk away with the neurogenics. I'm pretty happy with that. Chris? Yeah, I totally agree. I think you should fuse the toes, and then what I also do, because it's intrinsic, but also extrinsic imbalance, I will move extensor digitorum communis to somewhere in the midfoot. They use it as a dorsiflexor of the ankle, and also make it a dorsiflexor of the ankle. So, Paul, did I make a mistake by not doing plantar fascia release or not doing a medial release in this kid, and what's the threshold for that? You know, I don't really have an answer to that, but I would be interested, you have a lot of insight, Greg, into the neurology of this, and could I just ask you to take a step back, and you sort of gave the answer away here and said this is a neurogenic case. I think that what I and maybe some of the other younger physicians struggle with is say this kid just came in with ankle instability, and you don't know, just can you go through your thought process on what do you try to ferret out, what's your workup of somebody that's got this type of foot first presentation, and how do you proceed? I know you got a lot to cover, but I just appreciate your insight. I mean, the first thing to do is look at the other foot, which I think we don't do enough, and see if they have an identical opposite foot, and see what the shape of the opposite foot is, because most idiopathic cavus, which is what we're usually dealing with, is a mild varus deformity. This kid came in with a really plantarflexed first ray that was driving the equation, so it's the same physical exam concepts. I tend to agree with Chris, is that in that most of the patients that are younger athletic patients, in terms of their brostrom, in terms of their fifth metatarsal fractures, I give them one pass. Particularly the athletes, like if I get a collegiate athlete in sport in the middle of their career, I give them one pass, and I fix their lateral ankle ligament instability, because foot deformity is not exclusive of doing remarkably well in sport. It's important to remember that Carl Lewis had remarkably high arches, and then Usain Bolt has Plano-Valgus feet, and two of the fastest humans on Earth that both have opposite foot deformities, and it doesn't make rhyme or reason, and you gotta not mess with their feet when they're doing well. You have a question? Oh, I had a question on the last question, so no problem. Thank you for the nice session, anyway. What do you mean by the patient is adolescent with the cave of virus deformity, and you see if he is asymptomatic, you won't treat? Is symptoms only pain if the patient is in virus and is walking on the outer border, and the deformity is progressive, but he has no pain. He's 12 or 13, and has no pain, but he hardly can put his first tree on the ground, so do you operate or not? I think you've embarked onto the philosophy of medicine talk here. That's the problem. You know, if it's predictable that that patient is going to do badly, and there are some patients you clearly know they're gonna do badly, it's the same thing when you deal with Plano-Valgus feet. So if you see the Plano-Valgus foot that's kicked out 60 degrees at the talonevicular joint, you know where that's going. Sorry, Glenn, you were gonna make a point. Just one comment about the lateral ankle instability. First of all, this is a great symposium. Thank you very much. I learned stuff. This last week, I operated on my 600th CMT case. That's a lot of CMT cases over 30 years, and just two observations. One is when it comes to the instability, right? You'll see instability in CMT patients, in my experience, in older patients, you know, 40, 50, 60. That's when you're gonna see lax ankle. You're not gonna see lax ankles in younger patients, by and large, if they have CMT, and that's their problem, because they're too impaired. Nobody who can just walk six blocks because of their CMT is gonna have ankle laxity at the age of 20, in general. The people who you're seeing with ankle laxity young are people that have a cable varus foot. If you have to make a generalization, maybe others would disagree. I guess I would be careful, because this was a kid who was athletic, who happened to have a bad ankle sprain, and I've seen plenty of people with CMT play college sports. Absolutely. So, and nowadays, they go out and they get ankle sprains, and then you have the whole constellation, but you have to take the neurology into account. But that's really someone you're treating with a cable varus foot who happens to also have CMT, right, as opposed to someone who's impaired by their CMT. I don't know that I can make that distinction. The only other one quick thing I wanna say is Paul's comment, and I saw a lot of heads shaking, I thought is just so subtle and so important. 80% of the patients that I've operated on have an Achilles contracture, right? What's his name, you say that, Art. So they all need Achilles lengthening. And it's not because of an Aquinas, because the talus is not plantar flexed, it's in neutral, right, or dorsiflexed. So you can't extend much at the Achilles, so you can't, you don't have an Aquinas contracture, but the Achilles inverts the heel, and you're not gonna get good corrections on these people unless you correct the contracture, in my experience, that's inverting the subtalar joint, which is Paul made that comment, right? And it's controversial, but I just wanted to support what he said, thank you for it. All right, yeah, let's head in a different, oh, I'm sorry, Jim. Why do you do the Jones procedure instead of an FHL tendon transfer? So the Jones procedure in this case was an effort to try to get a little bit more dorsiflexion, because this kid had a weak dorsiflexion. It's a philosophical question, because one of the questions is, where do you plug the Jones in? The Jones was traditionally decided to, I mean, it's a way of freeing up the EHL, and the point being that he's using it as an accessory dorsiflexor. Also, if you bring it up, if you release it from that, it's not clawing the toe, which in effect drops the metatarsal head, so there's a secondary drop of the metatarsal head. You're correct, an FHL transfer could accomplish that, but wouldn't do anything for getting your dorsiflexion out of it. So the degree to which an EHL can help you, whether you plug it into the first metatarsal or the midfoot, who knows? I tend to plug them into the midfoot now, because I think it's a more direct place to work on. The original Jones procedure, as described in polio, was something different. I do want to get to some other points, and we're running low on time. So Carl, this walks into your clinic, and you see these x-rays, your resident shows you these x-rays. You feeling pretty good? Nothing too worrisome? Just say yes. And then. Looks great. That's the same patient. That's just to show you how much a neutral cavus can show you, can be pretty darn good on an AP foot and on an ankle. So this patient has never had surgery. What disease does this patient have? Polio. Polio, yeah. And one of the clues is that the toes are straight. So there's only a few things that are gonna give you this magnitude of a neutral cavus, and it's almost certainly gonna be polio, or it's gonna be one of the other progressive neuromuscular disorders typically associated with spasticity. And those don't give you straight toes, because they'll have issues with the foot intrinsic. Polio's a knockout, and can leave, in some cases, can leave the foot intrinsics, particularly if it happens very early, not imbalanced, and they'll still have these kind of massive deformities from the gastroc going on. So this is polio. She's never had surgery. So, 72, polio from 1952. So if you were gonna come up with something to fix this, if her foot is now unshoeable, what are your, well, I gave you some options there, what are those things you could do? Terrible question. Oh, that's me? Yeah, why not? Oh, thanks. Sorry. That looks shoeable. I disagree. All right. I'm gonna find a shoe. They can be remarkably more shoeable than the thought. I thought it's, I think it's important to go back and look at it from time to time. Go back and think about polio for a couple of reasons. You will occasionally see these patients, and you will see some that come in from the third world. The other thing is, it gives you some options for dealing with some of these really terrible deformities, because we didn't just invent the wheel. We may think we did, but we didn't. And so the Samuelson osteotomy is a crescentic osteotomy. I've drawn it out there. That would allow you to rotate the heel if you needed to get this down. That's one of the older operations for very severe hindfoot cavus. The Steiner stripping is just an extensive plantar fascia release developed for polio by Arthur Steiner, who's the original Iowa chairman. And then the midfoot osteotomy. We've thrown around the terms Cole and Joppas all day long, and I think it's important, because we talked about not having done one, but actually, Paul, you showed one, and Dave showed one, showed a Cole osteotomy. Didn't label it as such, but I want people to know what a Cole is. So that's a Cole osteotomy. It's done through the distal aspect of the navicular and through the cuneiforms, and you just take a wedge out. And for something like a polio patient, that would be an option, and this is an old historical operation. A Joppas is a V-shaped osteotomy that really belongs in the historical waste bin. But the Cole osteotomy, there are patients that you're gonna do a Cole or a Cole-like osteotomy on. They're gonna be salvaged conditions. This is gonna be something different. All right, so here we are. Chris, this one's for you. It's 1997. I want you to put yourself in the shoes of a young orthopedic resident. You're at Iowa. You're working with Charlie Saltzman. You happen to know this guy really well. He's a 75-year-old physiologist and author of textbooks. He has a mild cavus foot. By the way, that's me in the far back left corner there. And he got polio in 1947. He has a worsening drop foot. He's having trouble walking. It's harder to brace, and amazingly, because polio's a knockout, he still has perineals in his posterior tip. He makes his own spring leaf AFOs using a lathe, piano wire, a sock, and mail-order hushpuppies. And he's done that for 40 years. The greatest generation is not a myth. So, these are your options for my dad. He's got transferable strength by traditional criteria. What do you do? So, the post is still good. The post-tip is five minus. You could conceivably do it. He's getting weaker in the anterior tip after all these years. Yeah, so with that little bit of background, I would be totally fine trying to do a post-transfer. If there's no muscles left, then you'd basically do a fusion. But I think the post-transfer is totally acceptable. So, the answer was larger gauge piano wire, which is what he did. And the main reason he did it is because at this point in time, this is in the late 90s, we were getting a better understanding of what post-polio syndrome was. And so, I would advise for post-polio, when they start to show late weakness 30 years out, if they're showing weakness in one motor unit, there's a considerable chance that they're gonna start to show weakness in adjacent motor units. And so, it's a dicey thing to do tendon transfers. The concept of post-polio is that you get motor unit loss because it kills single neuron units. And then, the remaining motor neurons sprout and they can end up covering about seven times as many muscle fibers as they used to. So, each individual motor unit is covering a lot more motor units than they used to. And you can end up with, the thought is that it undergoes metabolic fatigue, that there's actually only so many firings that those muscles have, and that you may end up with inability to function. So, my father was heavily involved and knew some people about that, that contacted them and he decided to get thicker piano wire. Would it have worked? It might have worked for a while. But, so that's where we are. All right, shoot. I was gonna show one more. This walks into your office. Dave, are you happy? Got a little pain under the fifth metatarsal? No, I mean, happy, we wanna treat him. I mean. Well, there's the lateral. These were traps, but we're out of time. So, we don't, this is not a cavus foot, but it's one that has varus. It has a varus hind foot. And now, we always talk about metatarsus adductus in combination with bunions, but we never talk about it when we do these cavus talks. But, it's a pretty significant component for some patients, particularly old club feet. So, I guess the question here is, what's your threshold for fixing metaductus? And, what do you do? Well, that's, so, what, is his big toe symptomatic? I mean, he's. No, his pain is lateral forefoot pain. His big toe is asymptomatic. Yeah, I'm very reluctant to do multiple multiple metatarsal osteotomy because I'd probably leave the metatarsus adductus, but correct it through the midfoot osteotomy just because I think I'm gonna have more predictable healing through an osteotomy through the cuneiforms and cuboid than I am by cutting each metatarsal sequentially. Because he's overloading the lateral border of his foot, I'd probably just do a rotational osteotomy and take a little more bone out. Laterally, get some adductus out. But, that'd be hard pressed to leave that big toe alone, too, though. I mean, it's, I mean, if it's compliant, I mean, the first thing I'd do is I'd put him in orthotic with pressure relief out there. Oh, we've tried that. And, so, the problem is he'd keep getting stress fractures on the lateral border of his foot. And, so, that's really where we are. We're almost out of time, so I cut to the chase. I did a combination of what you said and addressed his toe by doing a first through third TMT fusion, but also medialized the base while doing that to allow me to bring things back over. Because I think if you do this, you have to medialize the base. If you're gonna go big, you have to go big. You have to medialize the base a little bit to try to correct it. And, then, fourth and fifth metatarsal osteotomies, which is always dicey because you're cutting right into the area of a metaphyseal-diaphyseal non-union on the fifth. And, I did both his sides and it worked out. Perhaps I got away with something there. So, but I thought I would show a quick metaductus case before we cut to the end. So, there's his other side. One last one here. This one's for you, Carl, because it's about ankle arthrodesis. 50-year-old with prior arthrodesis in situ. A prior triple arthrodesis in situ. You can see his ankle is shot. And, he's got ankle DJD. Let's presume, we're not gonna, just to skip to the chase. We're gonna do a derotational transverse tarsal osteotomy to correct this mal-rotated hind foot. We're gonna have to do, we're gonna have to deal with his ankle. There's sufficient bone stock to do one of your ankle replacements. But, we've got different diagnoses. So, I wanna know, are you gonna do a total ankle or a fusion in an old club foot? Neurologic function. Neurologic normal, it's a club foot. I'm not trying to pick on you, but this is a total. 70-year-old, I mean, potentially. I mean, I think it's a discussion of what their expectations are, how fast they wanna be able to recover from one stage versus two. This would probably be, if I'm thinking arthroplasty, I mean, this is gonna probably be staged. I mean, recognizing that if you fuse his ankle, he's got a block of wood down there. It's more than a pan-tailor. Right. The choices are a total ankle or a fusion. All right, well, that's fair. What about CMT? Will you do a, and Paul, I think you showed one like this. Will you do a CMT total ankle? Yeah. Okay. He's got enough function. Chris, you're shaking your head. No, because especially depending upon what type of CMT, it's a progressive disease. So if you do a total ankle, they will eventually be weaker as well. So I will fuse them. Dave, you're the only one who hasn't weighed in yet. If he has function, if he can dorsiflex, plantar flex, you said the guy's 70 or something like that? No, let's say he's, yeah, we'll call him 70. Well, if he's old enough, I don't think he's gonna, if he hasn't lost at all by then, I think he'll have enough function. I'd probably do a total ankle. But I'd do a two-stage, I'd like crawl, I'd definitely get the foot rebalanced before I did a total. I'd not do that all in one setting. Let's move up the chain a little bit. Now he's got a remote traumatic brain injury, RECP. So it's a static encephalopathy. Now he's got a little spasticity. Who's gonna do a total? I'm trying to get to the point where everybody's gonna fuse or amputate. So let's see, Paul, would you, he's got a little spasticity, but he can still volitionally move that ankle. He's still got up and down. That's a tough one. I mean, that's a discussion with a patient, and you tell them that this might be the next step towards an amputation as an alternative to an amputation. And if that's how it is framed, it's a different discussion, I think, with the patient, if you're doing a total ankle as an alternative to an amputation. Obviously, for purposes of test-taking and whatnot, and the standard answer would be if the spasticity is the wild card, and if there's significant spasticity, you gotta fuse it. I just have to say, I think with a lot of these deformities, I think the discussion should not be ankle replacement versus amputation. I don't think that's the reality. There's a lot of ankle, you know, I do a lot of ankle replacement, so I like that. But there's a lot of ankle fusions that do perfectly fine. You can give them a rocker-bottom shoe. I think you're wrong if you go into that discussion and say it's amputation or replacement. All right, we're at the end here. So Friedrich's ataxia. It's an older patient, so it's a late-onset variant, but Friedrich's, a progressive neuromuscular disorder that eventually makes them non-ambulatory, but they value transfers. It's a big deal. So what are you gonna do? I'm trying to get somebody to say fuse it. Soon as I get to fusion. All right. I think so, I think Friedrich's is one of the ones that I fuse, even in younger patients, because it's a progressive problem. They're gonna end up in a wheelchair. They don't do well with amputations because they can't transfer, and it's just where we need to get. All right, I had to get to this slide. This is the last slide, it's my thank you slide. If you know what, if you've ever been on FlightAware and followed, now all FAA planes, the FAA follows all airplanes. So I got in an airplane, I'm a pilot. I got in my airplane and I wrote, I decided we're gonna do a thank you slide for all my talks. So I got up there. My son brought along a young lady that he was trying to date. She got up in the front. We traced out thank you on a tablet GPS, and we flew up over Gettysburg, and we started doing these. And every time you turn, it's a 60-degree turn, it's a 2G turn, and if you look at the number of turns in there, you wonder why the K is messed up. That's because my navigator threw up as we were coming around the back of the K. And I said to her, as we were coming back, when we did the bottom of the K, I said, are you okay? And she said, I guess so. And I said, we got a lot invested in this. So we're not gonna write Y-O-U, but we did it, she agreed to a U. And then we made it back to Baltimore. It didn't work out with my son after that, but I got a great slide. So thank you very much. I appreciate it.

cavovarus deformities

foot deformities

ankle deformities

underlying cause

treatment approach

soft tissue release

tendon balancing

osteotomy techniques

alignment and balance

complications prevention

polio

congenital deformities

neurologic conditions

osteotomies

tendon transfers