On behalf of AOFAS, I want to welcome you to tonight's foot and ankle review webinar. Tonight's moderator is Dr. Sarah Gally. Joining her are Drs. Laura Atwater, Ajay Gurbani, Philip Locker, and David Ogie. You can find their full biographies and disclosures as well as disclosures for program planners in the program document posted in the chat box and in the AOFAS On Demand Education Center. 2023 webinars are provided free to AOFAS members and orthopedic residents, fellows, and medical students with funding from the Orthopedic Foot and Ankle Foundation, supported by a major grant from Stryker, and additional funding from Arthritz. I'd like to run through a few housekeeping items before we kick off the presentations. For technical difficulties, please try closing your browser and logging in the same way you did the first time. Registered attendees may earn two hours of AMA PRA Category 1 CME credit by completing the evaluation and CME claim form at the end of the webinar. 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We also invite you to become a surgeon training member of the AOFAS for access to journals and online resources, a global network of orthopedic foot and ankle specialists, and professional development opportunities. I'll now turn over the program to Dr. Galli to begin. Thank you. Good evening, slash good afternoon, those of us joining from the West Coast. My name is Sarah Galli. I'm an orthopedic surgeon in Madison, Wisconsin, and it is my honor to have this awesome group with us tonight to go over with residents some preparatory information for the OID test, which is coming up shortly for everyone, sorry to be the bearer of bad news. I want to thank all of our participants and all of our presenters for the time they've taken to put together this, and I want to encourage our participants to participate, first of all, and then also to provide feedback. We get further away from this test and you guys are taking it, and so we want to continue to make this content relevant and informatory for your preparation for the test, and so we welcome your input, feedback of what you guys see when you take the test to help us continue to make this an impactful lecture for you guys. And so without further ado, I'm going to turn it over to Dr. Laura Atwater, who joins us from Portland, Oregon, and she will be taking over probably the hardest OID topic, and we're going to just save the best for first with Halix Valgas while we've got you guys fresh and signed in. Laura, thank you. All right. Well, hopefully by the end of this, I'll convince you that bunions are surmountable. All right. All right. So Laura Atwater, I'm at Oregon Health and Science University. West Coast is the best coast. Nothing to disclose. Go to Foot and Ankle Fellowship. It's super fun and awesome. I went to Mercy. All right. So Halix Valgas, we all know when we see it. It's that deviated big toe. So what causes it? And I'm going to minimize this. Okay. So females more than males, but correlations you want to keep in mind are pes planus, basically pronation in the back leads to pronation in the front. And then also ligamentous laxity. You get hypermobility in the midfoot for the first TMT. And then that first metatarsal can start to drift immediately. And then there's hereditary factors. There is a family history, though. This is a multifactorial thing. Neuromuscular disorders, again, kind of goes along with the neuromuscular or with the ligamentous laxity thing. If you're floppy, the joints do what they're going to do. And then you also have inflammatory, like rheumatoid arthritis. And then Lu Xionui says toes like friends. And so, you know, if you were to cut off the second toe, that big toe, dollars to donuts would probably move over and find that third toe. The toes just kind of find each other. All right. So and this is just a picture of high foot Valgas or pes planus for those who haven't done a foot and ankle rotation. And here you can see a person with pes planus pronating and abducting a little bit. And that's kind of translating into pronation through that big toe. This is ligamentous laxity or tarsal instability. Or people also call this joint the first metatarsal cuneiform. We use them interchangeably. And you can see at the bottom of that joint there that with the arrows that it's wider at the bottom and the top showing you that that there's some instability there. You need to account for that and how you choose to treat this. So so what's going on? Part of what happens is you get this contracture of the lateral capsule. The medial capsule over that over that MTP joint gets gets very lax and stretched out as things start to get worse and worse. You get this rotation of the of the metatarsal. The location of all of those tendons start to start to change. The lateral sesamoid often becomes uncovered as things sort of deviate and rotate. The EHL will start to move laterally and it can actually accentuate the how it's Valgas and kind of accentuate that contracture because it starts to have an eccentric pull over the first MTP. And then you also get a secondary pathology or of the the second toe, which is a hammer toe, because basically the foot is a tripod that first MTP is supposed to be doing a lot of work. And when that migrates medially, the second MTP gets beat up because it's doing all of this work that it wasn't designed to do. So with the plantar plate that gets destroyed, the plantar plate is what kind of holds that proximal phalanx from popping up. And so when you overload the second MTP, the plantar plate sort of gets attritional damage. And then that second toe starts to pop up. So that's why those are connected. And you will see questions on that occasionally, that connection. Treatment, there are things that you can do to kind of make it feel better, but there's no device out there that will like fix it. The only thing that will fix it is is surgery, bony surgery specifically. So these are a couple examples of things. And again, correcting the flat foot is helpful. And then you can correct just sort of the position of the toe and pad the toe. All right. So the questions, the part everyone wants the most help with. So before we do that, let's talk about a couple key angles with how it's August. So this is the how it's August angle, which we all know. The second is the first and second intrametatarsal angle, which is sort of answering the question of how much is that first metatarsal deviating medially? This is the distal metatarsal articular angle, which residents have a really hard time with. And so it's asking the question is of is that cartilage surface of the first MTP perpendicular to that vertical axis of the first MTP? You can see in this picture here that that cartilage surface is sort of deviated laterally relative to the axis of the metatarsal. That's called a juvenile bunion, and those need to be treated slightly differently than a traditional degenerative bunion, which we'll talk about. And then this is the interphalangeal angle. Basically, is there some valgus between the two phalanges? And so the other question you need to ask yourself is congruency. So this gets back to that DMAA bugger we were talking about. So on the right, you have a congruent joint. You basically, if you were to open that up, you'd see healthy cartilage against healthy cartilage that those two bones in that joint grew up together. They are, they are simpatico. They, they, they glide nicely on each other. On the left side, you have basically, you know, the ice cream has fallen off the cone. That proximal phalanx started up over that first metatarsal, and there are degenerative changes that we talked about in the pathoanatomy slide. And basically, things just started to rotate and sublux there. So, so degenerative on the left, juvenile bunion on the right side. Non-congruent on the left, congruent on the right side. And you can see on both of these, there's something called a medial eminence. When we use that word, there's this little prominence of bone on the medial side where you have sort of the end of the cartilage surface, and then there's this little hump of bone. So that's where that little transition between the hemisphere of the cartilage surface, and then that medial hump there, that indentation. That's where I try to find when I'm trying to look at a degenerative um, uh, first metatarsal head to try to figure out like, where's that, that cartilage surface supposed to be? All right. So, uh, in, in the algorithm that, that I teach for this, there are basically four questions you need to ask yourself. You don't need to memorize a ton of stuff, but you do need to memorize these four questions. So first, um, is there arthritis? And when I say arthritis, I mean of either the first MTP or the tarsometatarsal joint. Um, is there instability at that first tarsometatarsal joint? Is there congruency of the first MTP, uh, what we were just talking about? And then finally, it's all of those numbers that intimidate us and drive us crazy, um, as residents and make this seem really, really hard. But really, you know, you can answer many questions. Just ask, uh, um, just asking yourself the first three on this list here. So hypermobility, again, I showed a slide earlier. You can see on this bladder radiograph, there's, uh, not just gapping plantarly, but there's actually translation, um, of that, that first metatarsal dorsally. Um, and you can see, uh, some subluxation of that first MTP on that AP radiograph, uh, hypermobility, um, uh, can also be, um, uh, correlated with second, uh, MT or second tarsometatarsal or metatarsal cuneiform, um, arthritis. All right. And so here's, here's the, the sort of the algorithm in pictorial form. So question number one, is arthritis present? If it's present at the MTP, this is easy. You just fuse it. So, um, there are special situation as well, where, uh, we basically know that over time you're going to lose if you do, uh, uh, uh, uh, a correction where you're not fusing the joint. So specifically cerebral palsy, gout and rheumatoid arthritis. Don't kid yourself. Just go ahead and fuse it. If you try to do something else, like it's going to recur. If you are, have arthritis at the first tarsometatarsal joint, also a very easy answer. You just do what we call a lapidus or a first tarsometatarsal fusion. If there's no arthritis, then you move on to question number two. And remember question number two was, is there hypermobility? So if there is hypermobility at the first tarsometatarsal joint, aha, again, we just fuse it. So, uh, to link things leading to fusion, both arthritis and hypermobility at the first TMT, um, if there is no hypermobility, we will do, uh, most of the time what's called a soft tissue release, which I'll show you in a second. So you never do soft tissue release in isolation. It's always soft tissue release plus something bony. Um, so question number three is the joint congruent. So if it is congruent, you have to do something called a bi-planar, um, or osteotomy or a medial closing wedge osteotomy. Basically you need to, um, uh, take that joint surface and make it perpendicular to the metatarsal, uh, or, or perpendicular to that, to access there. And I'll show a picture in a second. Um, and you can do that, uh, with either that medial closing wedge or a bi-planar where you're doing that in addition to the sort of a traditional bunion correction. And then if there's the MTD is not congruent, IE, it's, uh, uh, uh, it's a degenerative bunion. Then you start measuring your angles, right? So if, if you have a big IMA, which, uh, I would consider about 15 or above, um, then you need to do something proximally, um, that proximal procedure that can be a fusion that can be, uh, uh, a wedge osteotomy, but you need to do something proximal. Um, so, uh, like it says there, and then, uh, if that how exfalgus angle is really, really, really big, IE over 40, then you definitely have to do a proximal and distal osteotomy, just doing something proximally, uh, and bringing, kicking that first, uh, metatarsal over is not gonna do it, uh, uh, by itself. So if you have a how exfalgus angle, uh, over 25, but that IMA is narrowed, so you don't have something you need to correct proximally, then you stick distally. So HVA over 25, then you're going to do, um, uh, uh, uh, some kind of distal osteotomy, which we call a Chevron usually, um, or a scarf, uh, which is a rotational one of social unisex. Um, if it's, if it's not bigger than that, then you'll definitely just do a Chevron and keep it simple. All right. So this is another, another way to think about this stuff. If you're someone who likes to memorize numbers, um, uh, you, the slides will be posted and you can come back to this. Um, but basically like a bigger, bigger angles, get bigger corrections. Um, if there's widening at the first TNT, then you need to narrow it down. So this is a, a image from man's, uh, where it kind of tries to show all of the different bunion procedures on one page. Um, distally, traditionally we just do a Chevron where you move the whole head over. Um, you make a, a cut, uh, that was Chevron shape, hence the name. And then you just slide it, uh, laterally, which, uh, corrects the orientation of the joint. Um, the other thing that, um, is more powerful than a Chevron is a scarf where you basically make a Z shaped cut, uh, uh, or the lateral surface of the first minute tarsal and you slide everything over. So that's, that's a scarf and that's more useful for bigger deformities. If you get into the big IMA and you need that proximal work, then there's a whole bunch of ways that, that you can close down that IMA, um, in addition to a fusion. Uh, and then, uh, I want to point out that with an Aiken, if you have, they give you like a really, really big, uh, how it's August interphalangeus, um, uh, number, especially more than 10, they probably want you to add an Aiken, but usually in practice, we'll add that into, um, you know, sort of accentuate our correction to get a better causes essentially. Um, and that's an example of a proximal opening wedge osteotomy. So this is the modified McBride again, never in isolation, never do it in a congruent joint or a juvenile bunion, which go together. Um, and that includes, um, taking that media joint capsule and suturing it over itself to, to tighten things up. So let's do a question. So 18 year old female, um, has bilateral bunions, um, complaining of worsening pain, uh, failed all of the things. Uh, she has pain over the medial eminence, her hallux valgus angle is 32 degrees and her inner metatarsal angle is 17 degrees, which you're thinking to yourself, is that big or not big? Okay. That over 15, that's big. So, so I'm going to remember that. Um, so these are her x-rays, uh, you can see, uh, she, uh, does not seem to have arthritis or instability. Um, and again, she is a young person. So let's go through our algorithm. Um, and here, um, what I'm trying to show you, uh, I'm giving away the answer really is that she has a congruent joint here. Um, that cartilage surface is not perpendicular to the first metatarsal. So you're going to need to do something special. So going through the algorithm, there's no arthritis, uh, there's no hypermobility. So you're going to have to do something bony. Does she have a congruent MTP? Yes, she does. So you're going to have to do a biplanar, um, or a media closing wedge osteotomy to change that, um, DMAA. And so what I'm doing here is I'm first, uh, closing, um, closing the IMA down. And, uh, I apologize going back to the original question. The question stem was in addition to some form of proximal correction, what does she need? Um, so I'm already sort of baking in the proximal correction part. So there's a proximal correction. Um, so now you're going to do a biplanar where you're going to sort of translate that over, but what you really need to do is rotate that into the right direction. So now you can see that the cartilage surface is perpendicular, um, to the axis of the first metatarsal. Um, and I can answer questions about that in the Q and a session. So, uh, going through the answer twice is, uh, Aiken of the proximal feelings. That's never the answer. You always got to do something to the metatarsal distal Chevron wrong answer. Cause it's a big IMA biplanar. Yes. And to fusion, no, she does not have arthritis and distal soft tissue release alone. Again, always a no, no. All right. So another question here, uh, 45 year old female presents with, um, you know, eminence pain. She's failed all conservative measures. Uh, her IMA is 15, so kind of borderline, and her HV is 38, so not quite 40, but still pretty darn big. And so what is most appropriate from the following choices? And those are her x-rays. So going through things, does she have arthritis? Well, kind of, you know, like in real life, this is a patient that probably could have been offered a joint sparing procedure and a first MTP fusion, and I think both of those answers would have been reasonable depending on the patient's activity and goals, 45, kind of young. MTP is not the wrong answer, so that'll sort of depend on the answer choices. So we'll, for the purpose of this, we'll say, okay, what if the question person, question writer decides they don't have arthritis and they don't put MTP fusion as an answer choice? So if we decide that she doesn't have arthritis, or if on physical exam and they give this to you, like she has a negative grind test, which is how we evaluate for arthritis, she has no pain in her arc of motion with the first MTP, probably not going to fuse it, right? So we'll say no for arthritis. Is it hypermobile? No. We saw on the lateral radiograph that she has a stable first TMT. Is the MTP joint congruent? Absolutely not. You can see that cartilage surface, those surfaces are not lining up whatsoever from the way that they used to be. So now we're talking about angles, IMA over 15. So her IMA is at 15, so kind of borderline. So we're going to say yes for the sake of this argument. So we're going to, yes, we agree with the proximal osteotomy portion of this. And, and just to remind you, her HVA on this particular slide is over 35. And so both of those are kind of leading you toward something more powerful or toward a proximal osteotomy. So going back to the choices, one distractor that they like to give you is the Keller, Keller section arthroplasty, which is basically just taking away the joint surface and making it into just leaving soft tissue and sort of disarticulating it. Are we going to do a lapidus? No, because there's no arthritis or instability at the first TMT. Distal chevron? No, because this is a big deformity. Both the HVA and the IMA are big. Proximal first ventricular osteotomy with distal soft tissue release. Yep. That's probably the right answer. And then distal biplanar osteotomy. That's definitely not the answer because this is, this is a non-congruent joint and it's not a juvenile bunion. So we need to do something proximal. Other correct answers would be, other correct answers would be anything that, that, you know, it could be a proximal and distal combination or anything that, that is definitely going to give you some action at that proximal. All right. So those are my baked in questions. Complications, biggest complication of hallux valgus is recurrence. And if you don't correct it all the way under correct that IMA or the HVA, if you don't recognize that you have an abnormal DMA, things love to come back. And with the juvenile bunions, the earlier you operate, the more likely it is to recur. So you just got to tell your patients the truth about that stuff. When you have the risk of shortening, which can lead to a transfer metatarsalgia or pain under the lesser toes, because of they're just doing more weight. You can get AVN, you can get neuroproxia of the dorsal sphenocutaneous nerve, which is a favorite question. And then finally, hallux varus, how do you get that? If you over-resect that medial eminence, it falls off immediately. If you do an excessive lateral release and there's nothing holding it over there, it falls off immediately. And if you resect the fibular sesamoid, remember you have the tendon running through there. And so if that's not connected, you're going to get overpull of the medial and that's going to pull it over into hallux varus. And then finally, anytime you fuse these patients, remember non-union is possible. And, you know, even the best surgeons are going to get non-union some of the time. So keep that in mind when you choose a first CMT or a first MTP fusion for your recommendation. All right. Thank you so much. Sarah, you're muted. Thank you. Thank you, Dr. Atwater. That was fantastic tour de force of a very challenging topic. And definitely encourage you guys to download the slides after this presentation, and you can play these back as well to help you. All right. I've got a couple now for you. Okay. And so this dovetails nicely from Dr. Atwater's talk. First of all, just want to confirm if someone can that you're seeing my screen. Yes. Thank you. All right. So our first topic, we just started with hallux valgus. We're going to follow it with hallux rigidus, also known as big toe joint arthritis. Big toe arthritis etiology is all comers. It can be post-traumatic from a turf toe on a field. It can be microtrauma. See this a lot in our runners, especially our forefoot strike runners, seeing a lot more of that now that the minimalist running movement is becoming so popular. We also can see it as a follow-up of inflammatory arthropathy or from patients with gouty arthritis. With gouty arthritis, just remembering there's two different causative organisms, and they might show you those pictures with crystals and get you into some basic science. So remembering the appearance of both uric acid and CPPD. Big thing with questions when they're talking about hallux rigidus is wanting you to be able to differentiate impingement pain from arthritis pain. And we'll get into kind of how that presents because that is the key to these questions. So when you get a stem, it points you to a patient with big toe pain. You're first going to rule out other injuries. They're probably going to give you that in the stem. They're either going to give you a picture of an x-ray or tell you that they have an x-ray with arthritis change. Like all things, the OID wants to make sure we're a responsible surgeon. So they want to make sure we know when to pick non-surgical treatments. So don't always jump to surgery with these stems. And so for big toe arthritis, you're looking at a stiff or a rougher shoe. You might add a Morton carbon fiber plate to the shoe. You want to give the toe more room if that bump on the top is really painful. Activity modifications, anti-inflammatories, steroid injections, the things we do for arthritis. If they've told you that those things have been tried, they're either going to give you one of two types of patients. They're going to give you the patient that has a big bump, the bump hurts, and they get pain when they dorsiflex the big toe. They're pointing towards removing the spur that causes problems. That spur removal is called the chylectomy. They're going to give you another question stem. They're going to tell you the patient has positive grind. That was what Dr. Atwater was talking about, where when you load the joint and squeeze it and push on it, kind of the same way you do the CMC grind in the hand, they're going to tell you that the patient has mid-range pain, positive grind, and pain sometimes at rest. They're telling you the patient has arthritis pain. In that case, they're pushing you to choose MTP fusion. Some quick pearls about the different surgeries. Chylectomy is removal of the bump. The indication is pain related to the bump. Intraoperatively, you remove about 20 to 40 percent of that dorsal joint surface, as you can see pictured and highlighted. Advantages of this surgery is it allows early weight bearing, early range of motion because there's no bony work that has to heal. Big thing with these, I don't know if they test it, but I think it's a fair game thing, is it maintains motion, doesn't improve motion. I'm very cautious with telling patients that removing that big spur is going to give them dorsiflexion. It preserves, doesn't improve. The disadvantages of it is if you miss a patient with arthritis, their pain may persist. They still may complain of stiffness after the surgery. It's an arthritic condition. It can progress, and we know about 10 percent of these patients do progress on to a fusion. So talking about fusion, the indication is arthritis pain. A couple other indications is salvage of a chylectomy that still has pain. Patients that have had various resurfacing or replacement implants in the big toe. Patients with bunions and inflammatory arthritis, that's another one. And like Dr. Atwater said, there's certain bunions for big toe fusion may be the direction that they point you as well. Advantages of this procedure is it's durable pain relief, and it provides a stable first ray. The disadvantages is you obviously lose motion with a fusion. There's some theoretical risk of adjacent joint propagation of that arthritis, and then the non-union risk of fusing a joint, which is somewhere less than 10 percent. You can see pictures of that here. A couple big things with MTP arthritis that I do think are fair game with testing is putting the big toe in the right position. You don't want a Michael Strahan effect of the big toe with a big wide gap. You want slight valgus. You want neutral pronation. You don't want the lateral or the medial border of the foot of the toe, I'm sorry, lying on the ground. You want just that right amount Goldilocks of dorsiflexion. Here are some angles here, but I think the bigger thing is what you're seeing pictured, which is the foot plate test that we do intraoperatively to evaluate is the hallux toe gently resting on the ground when the foot is brought to neutral dorsiflexion. I think where the questions may come in is what happens if you get that position wrong. If you have too much dorsiflexion in your fusion, the IP has to compensatorily flex, and they develop a fixed flexion contracture of the IP joint, and then they develop a callus or pain on the tip. If you have too much plantar flexion, they under load underneath the IP joint, and then it hyper extends. So either way, you don't want too much, don't want too little. I include this slide, not so much because I think they would test these as proper answers, but they might be incorrect answers. And so understanding there are other treatments besides chiolectomy for the bump and fusion for the arthritis. There's some osteotomies that either decompress the joint or improve range of motion. So those are motion sparing osteotomies for very early mild arthritis, but notably, again, motion concerns. There's various resurfacing and implants for replacement. The big thing with those is they involve resection of bone, and so bone loss is a harder problem for a revision later. And so understanding that replacements and resurfacings involve removal of bone to place them, then when they fail, there's more loss of bone. So that has to be taken into account with the fusion. The resection arthroplasty, which Dr. Atwater talked about, really is a salvage for a very low demand patient only or a patient who has an ulcer where you don't want to place hardware. And this is essentially kind of like a girdle stone of the hip. You remove the joint and just allow soft tissue to interpose and the joint to be kind of a flying joint. They would give you the low demand patient, the patient with the ulcer, that's who they would be testing you on for that. And then last, something that I think maybe talked about a little more on tests in the future is the polyvinyl chloride implant, which is the small jelly bean looking device that you see pictured in the right, which is indicated for neutral alignment, no deformity, mild arthritis pain. I don't think they would test it, but if you're looking at it, they're going to be telling you about that patient who has some arthritis, but they refuse a fusion and they have neutral alignment. Those are the people that they might get you pointing in that direction. And so summary with regard to how it's rigidous, if they have bump pain, choose the chialectomy, remove the bump. If they have impingement pain, pain with dorsiflexion, again, remove the source of the impingement, choose chialectomy again. If you get pain with grind, choose fusion. If you get an obliterated joint space on x-ray, choose fusion. If a patient refuses fusion in one of these scenarios, no one resurfacing or implant option is superior. I think if they were pointing you that direction, they would only give you one to select. And so it'd be the patient that for some reason has arthritis, but they are refusing fusion would be the way the question stem would read. And then if someone, they show you an x-ray that has some sort of metallic or silicone implant in there, and they've lost all this bone, the answer is going to be a distraction using a bone block, either auto or allograft fusion of the big toe joint. And again, just to highlight, if you're saving the joint, the pre-op motion predicts the post-op motion. So a couple of questions here, a 40-year-old businessman presented with two years of worsening big toe pain. X-rays show he has joint space loss and extensive periarticular calcifications. He has mid-range pain that is worse with dorsiflexion. He has a strong family history of gap. He has tried insets and true modifications. What intervention offers best chance of reliable and durable pain relief? And so with this, I wanted to highlight a couple of the things in the stem that point you towards choosing MTP fusion as the correct answer here. One mid-range pain, arthritis pain. They have gout, which goes kind of along with inflammatory arthritis. And then they also highlight durable pain relief. We know the chylectomy and resurfacing options tend to have a shelf life associated with them. And so everything about this question stem is pointing you to select fusion for this patient. Okay. Jumping into kind of probably one of the next tour de force topics for your OID preparation is what was previously known in my residency as post-stratipial tendon dysfunction, but it's now been renamed progressive collapsing foot deformity. I think for the purposes of the OID still, it is relevant to talk primarily about the posterior tibial tendon and some favorites when it comes to the OID is testing with regard to its biomechanics. So understanding the role that the posterior tibial tendon plays in gait. We all have seen the little gait man. We all hate that one, but there are some things about it that are particularly relevant and I want to go over them here. So the posterior tibial tendon, it fires concentrically and inverts the hind foot during terminal stance. What that does is when it contracts, it takes you from a flexible hind foot to a rigid hind foot. It locks your transverse tarsal joints. That gives you the rigid lever arm that you need to lift your heel off the ground and go into toe off and allow your calf to then become the main acting force of further propulsion in heel lift. So the PTT or posterior tibial tendon initiates it during terminal stance to allow you to lift your heel so that then the calf can be the primary muscle driver of lift off or of propulsion through. What it then does is relaxes just prior to heel strike to then allow your transverse tarsal joints to be flexible. These topics here are very big fan favorites for the OITE to understand the relationship between gait and pathology. Understanding how the pathology further goes on is the posterior tibial tendon stabilizes your arch. So when you have posterior tibial tendon dysfunction or progressive collapsing foot deformity kind of given away in the name, you're going to lose arch stability from the loss of that restraint from the posterior tibial tendon. So some ways they might give you that question stem as a patient has arch pain. They may give you an MRI or a question stem that talks about spring ligament pathology. They may even ask you an anatomy question of what does the spring ligament connect and then you can answer that it goes from the sustentaculum to the navicular and it supports the medial arch. They may talk about a patient that has calf fatigue and ask you why. The reason the patient has calf fatigue is because the calf is having to do all the work of not only propulsing but initiating heel lift off because that posterior tibial tendon isn't working. It's not locking the transverse tarsal joints and because it's not locking the transverse tarsal joints it's a less efficient mechanical arm. Another thing that happens in fallen arch is the calcaneus drifts into valgus or drifts laterally. So when the calcaneus drifts laterally it can abut upon the fibula and so patients can present with subfibular impingement. So they may have some pain medially over the posterior tibial tendon but they may also have some pain laterally which is hinting you that the calcaneus may be abutting on the fibula. When you start losing the calcaneus and drifting out laterally you start losing the support of the spring ligament. The tailor head then drops and that's where we come into talking about some of the other clinical presentation aspects. So first of all when you're examining this patient you always are going to examine both feet standing barefoot and you're going to compare one foot to the other and you're going to look at is there hind foot valgus as you see when they're standing and then you're going to ask them to go up into a calf raise. One it's important can they that's helpful but then two you're looking at what happens to the hind foot when they go up into calf raise and so does their hind foot valgus correct into varus that tells you that the posterior tibial tendon fired the posterior tibial tendon inverted and locked the hind foot so that they were able to successfully initiate heel off. Those are components of the standing exam that you're looking at. Then you're going to proceed to your sitting exam you're looking at do they have a calf or an achilles contracture that is evaluated with a test called the silver skeel test. You're going to look at if they have first ray hypermobility telling you is there instability in the columns. That's kind of done with a piano key test as you can see on the left going up and down. They're also going to ask you or potentially point you to understanding what is compensatory supination. I have a slide that we'll get to that in a little bit later, but what they're also looking at is when you neutralize the hind foot, similar application to the same photo on the left, the hind foot is neutral and that medial column, the first ray, sits still elevated. So after you correct them out of valgus to a neutral ankle, the big toe still sits elevated and all those things come into what question stems may get at. When patients can stand, we get standing x-rays. When you're examining the posterior tibial tendon or progressive collapsing foot dysmorphia, you want ankle and foot x-rays to examine and properly stage this condition. A couple angles, thankfully they're a lot more simple in the progressive collapsing foot disorder. You're really looking at talus coverage or its opposite, talus uncoverage. As you can see in the picture on the left compared to the right, you're also looking at the degree to which the medial column collapses by looking at an angle between metatarsal and the talus and that is called Muri's line. Those are two important angles that we use in terms of guiding treatment. First of all, like we talked about with hallux rigidus, start with conservative treatment. First of all, an asymptomatic flat foot can be a normal variant and no treatment is indicated for an asymptomatic adolescent or adult with a flat foot. So choose no treatment if they give you an asymptomatic adolescent or adult with a painless flat foot. Not every flat foot is dysfunction of the posterior tibial tendon, hence it's why it's been renamed progressive collapsing foot deformity. A good OID principle in general is don't operate on asymptomatic things or things that have not tried bracing. Bracing and posterior tibial tendon dysfunction for the flexible flat foot is some type of insert or a special hind foot control device called a University of California Berkeley labs insert. When you're dealing with a rigid flat foot or someone with ankle arthritis, you're going to talk about an Arizona gauntlet. All right, flow charts. Flow charts are the theme of these complicated OID topics. So you have a patient with posterior tibial tendon dysfunction or more commonly now progressive collapsing foot disforming. You want to think, are they pointing you towards a flexible or a rigid deformity? If they're pointing you towards a flexible deformity, you're looking at tenosynovitis alone, which is stage one. You're looking at arch collapse deformity that's flexible in stage two. You're looking at hind foot rigid deformity in stage three, and then you're looking at ankle valgus deformity in stage four. Stage four is very tricky to test, and I think they're going to stay away from it with the OID because it's still so controversial. So I want to highlight really just stage two and stage three. So stage two breaks into two groups. Is the talus covered or is the talus uncovered? How much is that foot abducted is what they're testing here. And so if the foot is not significantly abducted and the patient has failed conservative treatment, they are pointing you to doing a varus producing or medial displacement calcaneal osteotomy and a flexor digitorum transfer. If they're talking about a patient that has a positive too many toes sign or a lot of abduction deformity or a lot of talus uncoverage, then they're telling you to do a stage 2a treatment plus a stage 2b treatment where you add the lateral column lengthening to revert that significant abduction and then still do the soft tissue procedures that we talked about. If they give you a patient with a rigid deformity or arthritis on x-rays and a collapse arch, they're then pointing you to doing a fusion procedure. In general, the principle is fuse what hurts. Usually that's talked about as either a double subtalar and talonovicular or a triple arthrodesis adding the calcaneal cuboid to that. Like I said, stage four is controversial, but I think the big thing with the various treatments that are out there, as you can see a lot of hardware, the biggest thing I want to highlight is where they might test it is trying to get you to pick an answer that avoids a pantalar fusion. Avoiding fusing the tibia to the talus and then the talus to the navicular and the calcaneus. Looking at question stems, if this was tested, the big thing would be as a question stem trying to point you towards preserving the ankle through either a deltoid reconstruction or an ankle replacement and then doing soft tissue procedures elsewhere. Just looking at question stems to try to answer that question. Big theme, busy slide. If they give you a question stem with a flexible deformity, you're not going to do fusions. You're going to choose osteotomies and soft tissue balancing procedures, usually FDL tendon transfer. If they're giving you a rigid deformity, a rigid question stem, you're thinking about doing fusion procedures of those deformed joints. A couple other pluses that they can test about, because like we said, not every flat foot is the same. Not every flat foot is the posterior tibial tendon. So if they talk about a patient with compensatory supination, the hind foot's reduced and then the foot assumes this picture in the lower left that you assume the first ray is elevated. If they have a stable medial column, you're going to do a cotton or a plantar flexion cuneiform osteotomy to bring that toe down. If they tell you the patient has first ray or medial column instability, then they're pointing you towards doing a first TMT fusion to provide that correction of the deformity. If they tell you about a patient that has an Aquinas contracture, well, you want to know, is the Aquinas from their gastroc or is it from their Achilles? The way you determine that is through a silver-skilled test. So if they tell you a patient had a positive silver-skilled or their ankle gained dorsiflexion when you bent the knee, then you're going to do a gastroc lengthening. If they tell you the patient had Aquinas and it didn't improve when they bent the knee, then they're telling you to do a tendo-Achilles lengthening. Another question that I saw one or two years ago introduced on the OID was a question stem that gave you a patient with a fallen arch, but the apex was in the midfoot. They had bad TMT arthritis. And so what they're pointing you towards there is recognizing this isn't the posterior tibial tendon, this is the midfoot. So fuse those midfoot arthritic joints. Same thing if they give you an x-ray where the apex is at the NC joint, fuse the joint that's arthritic and deformed. And so that's where kind of going back to that last slide, rigid deformity, evaluate where the deformity is. Most commonly it's your hind foot joints and that's where double and triple arthrodesis come in. But don't just jump to that. Look at the x-rays, read the question stem if they're pointing you towards different aspects of the deformity. This is that supination thing we were talking about. This was a very hard concept for me as a resident and it's not easy to understand. And so I wanted to try to go. So this is looking at the kind of Dr. Atwater talked about this, the foot tripod, the foot rests on the metatarsal head, the fifth metatarsal and the heel that forms the tripod. So what this picture really tries to show is the foot falling into valgus. Well we don't stand on our inside arch and our lateral part of our foot doesn't stand up like this, our foot compensates. So in order for our foot to not walk on our instep, our foot supinates to bring our lateral column of our foot down. That's what happens in chronic flat foot deformity. So what happens then is if you correct their hind foot valgus and they're flexible, well they stay level on the ground. But let's say that that supination became fixed because they were there for such a long time. Well then you correct the hind foot by posting it up medially as kind of this picturely shows. Well then the first ray is up. So you got to bring the first ray back down. So the way you bring the first ray back down is either with that cotton osteotomy or with the first TNT fusion. So a lot of information covered. These slides will be available. But just some test taking pearls. Always try non-op stuff. First for stage ones and twos flexible deformity, you're going to try a boot maybe acutely or an orthotic, a UCBL or a medial portion orthotic later. If they're giving you a rigid deformity that hasn't yet tried conservative treatment, then you're looking at an AFO or an Arizona gauntlet. Operative questions, when they're looking at a flexible deformity, they're looking at you to understand is there tailor coverage or tailor uncoverage or abduction. And that's what's going to drive your treatment there. They're going to maybe question some forefoot supination, in which case you add an osteotomy. Stage three, you're always going to pick the apex of the deformity. Most classically, that's the subtalar and the talonevicular joint. Something that hasn't been tested in a handful of years, but I think still might show up is if they're giving you a patient that has really terrible skin, they're trying to point you towards a patient that has high risk of skin complication. And they're in this contracted valgus position. You don't want to make an incision laterally. So they may point you towards an option that involves a medial approach, double arthrodesis. So they're going to give you a question stem that points you towards a high risk wound complication patient. And instead, you're going to choose an approach that allows you to still fuse, still correct deformity, but do it through a medial incision. And then, as I said, stage four, which is where your valgus progresses into the ankle, is still controversial. But I think the biggest thing to know is try to avoid the pan-tailor fusion when you're selecting your answers. A couple of questions. This is the picture I wanted to bring back. So a 67-year-old female has a flexible flat foot deformity that is undergoing surgical correction. Following correction of her hind foot valgus and FDL tendon transfer, the patient has this picture, persistent deformity. What additional procedures should be considered? So the patient's valgus of their hind foot has been corrected and their medial column is still elevated. So you need to bring that medial column down. The way you bring that medial column down is through a medial cuneiform plantar flexion or cotton osteotomy. You're not going to do a fusion because it's flexible. You're not going to lengthen a tendon to bring it down. You're not going to lengthen the lateral column because they don't have abduction. And we don't do this osteotomy through the metatarsals. So that's just one where they're testing to make sure you know where the cotton osteotomy is done. It's not done in the metatarsal. It's done in the cuneiform. Next question. 57-year-old presents to your clinic with the radiograph shown. He has attempted therapy, orthotics, and even bracing. He has a rigid deformity and an Achilles tendon contracture. So in addition to tendo-Achilles lengthening, what surgical procedure would you discuss? So you have a good workup. You have ankle and foot x-rays. You don't need any more workup. He doesn't have valgus at the ankle and he doesn't have valgus of the tibia. So you're not going to do a varus producing supramalleolar osteotomy. That's a distractor. You're, they're giving you a rigid deformity. So you're not going to do soft tissue or osteotomy procedures, which are the next three. So they are pointing you here towards a rigid deformity, gets a joint sacrificing procedure, a double or triple arthrodesis. Okay. We got through that one guys. All right. We're on to Achilles tendon disorders. So a couple of things with Achilles tendon anatomy, they sometimes like to do this on MRI cross sections, but first understanding the Achilles is the terminal tendon attachment of the gastroc and the soleus muscle onto the heel. It has a very broad distal insertion. It's bigger medial than it is lateral. There's two bursa, one superficial and one deep. And then some adjacent anatomy that might get talked about with complications or understanding or cross sectional imaging is that the sural nerve runs lateral and that your plantarus runs medial. Two real things that get tested for the OITE purposes is the acute form of Achilles disorder, which is a rupture in the chronic, which is tendinopathy rupture. It's frequently a male weekend warrior between thirties and fifties. Usually it's an eccentric load, but not always. Exam is done prone. You're looking for increased resting dorsiflexion, a Thompson test, which is a calf squeeze and seeing what happens and a palpable defect. If you're examining these early, you're always going to get an x-ray because you want to see if there's calcifications in the tendon or an avulsion. And then if you're unsure about the diagnosis or you're unsure of the location, then you can consider getting an MRI or an ultrasound, but it's not critical to making a decision about treatment. This is what gets tested. The difference between operative and non-operative. I think still it's debatable, but for the most part, the studies come out with fairly equivocal results, but they want you to understand the differences. There's lots of techniques for operative treatment. None have been proven superior. The pro that likes to get tested is that decreased re-rupture risk and that it has straightforward post-op protocols. The con is you're doing surgery in a tenuous area. There's a risk of wound complications. There's risk of blood clots. Non-operative, the buzzword they want you to recognize is functional rehabilitation. The pros is that you avoid surgery. The con is there's still a risk of blood clots. It still happens. And then the other con is the increased re-rupture risk and the strict eligibility criteria to be included in treatment. Sorry. A couple other nuances that may get tested is why do we get x-rays? Because you want to make sure they don't have this picture here. They don't have something that's going to create impending skin breakdown. And then you want to look at, is it a small piece or a big piece? And that will drive, do you fix it or do you advance the tendon and repair it down to bone? With chronic ruptures, the things they want you to recognize is how big is the defect and what are your options in terms of treating it? Small defects, generally that cutoff is less than three. You're going to do a V-wide advancement of your calf. If it's a larger defect, usually that again greater than three, they're going to point you towards an Achilles turndown, an FHL transfer, or an allograft reconstruction, or some combination of those. All right. Tendinopathy. On to the next one. It's a spectrum of disease. The big thing is it often gets itis afterwards, but they've done microscopic studies and there's actually no evidence of inflammatory infiltrate in the tendon itself. The insertional type is often associated with calcifications at that insertion. They may have a Haglund's, which is a squaring, particularly of the superior lateral prominence of the calcaneus, or they may have an insertional calcification, which is much more distal. This is less responsive to therapy than its counterpart, mid-substance tendinopathy, which is where it sounds like mid-substance. The buzzword for non-operative treatment of this condition is eccentric exercises. So the buzzword for non-operative treatment of an Achilles injury was functional rehab. The buzzword of non-operative treatment, Achilles tendinopathy, eccentric exercise programs. Busy slide. Two things I want to highlight. First of all, never inject an Achilles tendon. It's associated with rupture. Again, this highlights the two different kinds. Tendon versus insertional. Big thing when you're assessing this is you get an MRI. When it's refractory, you look at how much tendon is involved, and how much tendon is involved is a big driver of what your treatment options are. And so if they have non-insertional with greater than 50% tendon involvement, you debride the tendon and do an FHL transfer. If it's just less than 50%, you just do the debridement. Come over to the other side with the insertional variety. Greater than 50% in tendon, add the FHL. Less than 50% tendon, don't add the FHL. Still treat the spurge, still treat the calcifications in the tendon. That covers that variation. The other variation, they might point you to someone that has a contracture of their calf. So they may be pointing you to adding a gastroc lengthening at the same time as your treatment of their insertional or non-insertional variety. You may see some that point you towards PRP or shockwave therapy. I don't think that'd be tested because that's still controversial, but just knowing that those treatment options do exist out there. So Achilles tendon disorders, our summary. OP versus non-OP, still debatable. OP has wound risks and a lower re-rupture risk. Non-OP, remember functional rehab, but still some suggest that there is a higher re-rupture risk. Achilles tendinopathy, big thing, buzzword, eccentric exercises for non-operative treatment. Sorry, ruined the surprise. A 78-year-old male presents to you in clinic two months after having an ankle injury with a pictured MRI. His past medical history is notable for being hospitalized with pseudomonas pneumonia six months prior, and he was treated with six weeks of moxifloxacin. In addition to tendon repair, you should discuss all of the following with the patient except. So you're going to talk to him about, this is a chronic rupture, two months. He was on a fluoroquinolone antibiotic for six weeks. So first of all, just because he had a pseudomonas pneumonia doesn't put him at increased risk of a surgical site infection. So that's the not correct thing, but I want to go over the correct ones. So this is a chronic rupture. So you're going to talk to them about an FHL transfer because it's chronic. There may be a gap. You may need a gastroc lengthening to bridge that gap. When you do an FHL transfer, there is increased plantar flexion strength of the ankle when you add that FHL transfer to it. And then last but not least, his injury might be related to the course of antibiotics, the fluoroquinolones that were used to treat his pneumonia. So this kind of gets at a couple different things about the basic science and treatment of Achilles tendon injuries. Next, 45 year old police officer presents to your clinic with three weeks of worsening heel pain and the x-rays shown. He attributes this to when the police department changed their boots. He points to the bump on the back of his heel. You rule out an Achilles rupture by your exam. What is the best next step in treatment? So he's only had three weeks of symptoms and you've ruled out a rupture. You're not going to jump to surgery or an MRI. You're not going to put steroid near his Achilles. You don't need foot x-rays to answer more questions about this. And you're not going to put a lift in his shoe. You're going to do an eccentric program for this insertional Achilles tendinopathy. All right. Last but not least for me, this one's a fun one. Diabetic foot and ankle conditions. We're going to talk about ulcers, fractures, and Charcot and try to move through this quickly. So diabetic foot ulcers, their etiology is neuropathy leads to intrinsic imbalances, which creates Aquinas and Clottos. Neuropathy also leads to autonomic dysfunction, which leads to drier, more fragile skin. There's also a high association with peripheral arterial disease, which is associated with bad immunity and healing. All of that points to the development of ulcers. Ulcers are bad. They have a high risk of progression of deep infection. They tend to come back. They're associated with a much higher risk of amputation for that patient within the year. They have a mortality that's associated with them because it indicates the severity of their disease and they're expensive to our healthcare system. When you're working them up, do they probe to bone? If they give you a question stem that says probe to bone, that is highly sensitive and specific for osteomyelitis. So if you think they have osteomyelitis, get x-rays and an MRI. Get vascular studies, and this algorithm helps outline when you should get it. So you're either looking at their ankle brachial indexes or their toe brachial indexes. It depends on if they have atherosclerosis or not. Ultimately, if those are below threshold, you get a vascular consult. Vascular will help evaluate in more ways than just toe pressures, but understanding that toe pressures of those thresholds, sometimes 40s use, sometimes 55, but those different thresholds indicate healing potential. So less than poor healing potential, greater than healing potential. And then last, if you're working them up and they have an ulcer, you're gonna get deep appropriate cultures and sensitivities to guide treatment. Busy slide, but this highlights what we're doing with the treatment of diabetic foot ulcers and how we break the cycle. So if they have a deformity, surgery can address the deformity. If they have poor biology, optimize their biology. A1C goals, arterial consults, nutrition. If they have an ulcer, you wanna prevent it from becoming infection and amputation. So you do wound care and casting. And then if you see a patient who has lack of protective sensation and diagnosed with this, you want to prescribe them an orthotic. The answer is a full length or accommodative orthotic. And you wanna make sure they have routine foot care. All of this is the goal of preventing someone with neuropathy from developing an ulcer or someone with deformity from developing an ulcer and ultimately undergoing amputation. So a couple of things that get specifically tested. These metatarsal head ulcers, they have a deformity from an imbalance in their intrinsics that leads to overload of the metatarsal head. You try to accommodate and offload it. If they develop an ulcer, you try casting. That still doesn't work. Very, very good evidence shows that a gastroc or an Achilles lengthening procedure decreases recurrence and improves healing of these ulcers. Charcot, we don't fully understand the etiology, but it's this microtraumatic or microvascular disease that leads to a red hot swollen foot. It's often confused for infection, but there's no sores. And when you elevate the leg, the redness goes away. If you suspect it, they give you a question stem or someone's in your clinic with a red hot swollen foot, get x-rays, get them in a cast, get them off their foot, even if their x-rays are negative. And then you wanna optimize them. So similar to what we were doing about A1C vascular and nutrition, you wanna get them in a good space with their diabetes and their health. And then treatment acutely, you're casting and offloading to prevent collapse. And if it's stable or chronic, you're trying depth rocker bottom shoes and full length accommodative orthotics. When it progresses to surgery, that means they're gonna tell you about a patient that wound care casting fails. They have an impending ulcer. They have a foot that can't fit in a shoe or they have an active infection. You're doing a big reconstruction, a big fusion in these. And you wanna go in general, a joint above their deformity to give you good stable bone to build into. So you see these x-rays where you're going a joint proximal to where the deformity was in the midfoot here. Lots of hardware or you use an X-Fix. And the theme often in the care of diabetic patients is you need prolonged non-weight bearing, prolonged immobilization. Goals is to produce an ulcer-free, infection-free foot to allow the patient to resume their ADLs and wear commercially available feet. Neuropathic fractures, the last thing they like to test. They're gonna give you a buzzword of a painless dislocation or a delayed presentation to your office. Just because a patient has diabetes, even poorly controlled, does not mean you're gonna choose non-operative treatment. You're gonna choose operative for these. This is similar to fracture care of a hip fracture in an elderly patient. These do poorly when we don't fix them. They fall apart. They develop charcot. So you want rigid and robust fixation. One of the sayings is double the hardware, double the immobilization, and never use flexible fixation in these. So last questions. 63-year-old female with diabetes presents with the following non-healing ulcer. She had a previous charcot reconstruction. Her A1C is 6.3. Her nutrition is optimized and she has palpable pulses. Despite this and wound care and casting, her wound has not healed. What treatment is associated with increased wound healing and decreased recurrence? They gave you palpable pulses. She doesn't need vascular angiography. They're not telling you anything about infection. It's not gonna be antibiotics. They're not giving you x-rays that show a joint that's a problem. So you're not gonna do a color resection. But what you are gonna do is do a gastroc lengthening to improve healing. Because what did we ask? Increased wound healing, decreased recurrence. So you want a gastroc lengthening. All right, last but not least. 61-year-old female with diabetes and neuropathy presents to your clinic four weeks after being fixed while on vacation. Her incision's benign, but her foot is red hot and swollen. What could have helped to prevent this catastrophic collapse? It's not antibiotics. It's not bone health. It's added fixation, added stability of this neuropathic female's fracture. Delayed fixation doesn't change that and closure with suture instead of staples doesn't change that either. So thank you guys for bearing with me. I'm gonna stop my share. And we are gonna have Dr. Locker switch us from chronic conditions to fractures. All right, can you guys all hear and see my screen okay? Looks great, Phil. Everyone, I'm Phil Locker. I'm one of the current foot and ankle fellows. I'll be reviewing foot and ankle trauma a little bit different pace from what we've been here before, a little more straightforward, I think. I just wanted to thank the AOFES and the Young Physicians Committee for the opportunity to be a part of this webinar. I have nothing to disclose outside of the fact that I'm a fellow, so just a year ahead of some of the residents on the call, but I did pass part one of my boards. So a brief overview, go over some test taking strategies and then the various foot and ankle fractures. And so, like I said, I'm one year out in fellowship. So the closest to these exams compared to other people on this panel. So I thought I'd just go over my thoughts about exam and test taking. And as you guys probably imagine, OID and boards are not exactly like real life, but unfortunately you have to go through them to get to real life. And so things I found helpful really just doing questions, questions, and more questions. It really is just pattern recognition after a while. I liked res study and ortho bullets and that's, I think it's all you really need. Outside of that, podcasts, Nailed It Ortho is really good. It's one of my chief residents helped set it up. And I think it's a really quality information as well as the AOFES, OTA, JLS, ortho bullets. And then my residency paid for the AOS board prep course, which I also thought was good. And then my last year in going into boards, I really just made a massive data sheet of recurrent tables, graphs, and kind of things that you see here, the flow charts that you're seeing on this webinar. So just stuff you can look back at. And then if questions you keep on getting wrong, I would just explain it in my own words so I can just review it at a later time. And then one other thing to kind of keep in mind is looking at last year's data, only a 2% fail rate for first time test takers. And I think the very fact that you're on this webinar probably means that you're gonna be okay. So I just, keep your head down and keep on studying. You should be okay. So getting into it, first, Lisfranc injuries. It's a spectrum of injury that involves a Lisfranc ligaments, usually from an axial load on a hyper plantar flexed foot. The Lisfranc ligament connects the medial cuneiform to the second metatarsal. So that's an easy anatomy question to go over. Additional articulations involved include the tarsal metatarsal, intermetatarsal, intertarsal. And it can be classified as either fracture or ligamentous. Sorry about that. The exam buzzword you wanna look for is plantar ecchymosis. And then on x-ray, you're just really looking for instability. And you usually see that through bilateral weight bearing films and abduction stress views. And so you really wanted to look at the relationship between the cuneiforms and the metatarsals. So your medial cuneiform should match up with your first. The middle cuneiform should be with the second. And then the lateral cuneiform should line up with the third and the cuboid with the fourth. And then on the lateral view, you're looking for any sort of dorsal displacement. You can consider an MRI and ligamentous injuries and then CT for fractures. So treatment's very basic. I don't think they'll really make you decide any kind of in between. But for clear fractures, you wanna think about fixing arthrodesis for ligamentous and chronic. If you see a flex sign, that means a ligamentous injury. So I lean towards fusion. And then if there's any fourth and fifth TMT involvement, pinning because the lateral column's a little more mobile. What they're really gonna test on is the outcomes. And so you need to decide. The studies have shown that fixation and fusion have equivalent outcomes with the big difference is there higher rates of secondary surgery related to hardware removal with fixation. And then some complications that go over is post-traumatic arthritis, painful hardware foot deformity, which you see here in the picture. You see pes plano valgus and then forefoot abduction. And then infection in non-union can occur. So moving on to calcaneus fractures, two big types that you wanna distinguish right away are the TUM type, tuberosity abulsion type and the intraarticular joint depression. So the big things you wanna know for the tuberosity is it's a surgical emergency due to the soft tissue compromise that can happen. So you really just wanna fix as soon as possible. And you're gonna plantar flex the foot to help reduce the foot to that displaced tuberosity fragment. And then for your intraarticular calcaneus fractures, you're gonna get x-ray and CT. On x-ray, you're gonna look for the height length and for the alignment and depression through Bowler's angle and the critical angle of Gesane. And then CT scans is pretty much universally gonna be done. And don't forget to look at the soft tissue window for your perineals. And on CT, the Sanders classification is done on the widest point of the posterior facet. All you really need to know for the exam is that you have a higher type, there are worse outcomes and it's more combination. So the goals for fracture, for calcaneus fracture treatment is you wanna restore the articular surface heightened with really just the overall shape of the calcaneus and avoid infection. There are numerous techniques for treatment, non-operative, open with limited perks, sinus, tarsy, extensile, lateral, and primary arthrodesis. I think there'll be fairly clear cut about which technique, but they really want you to know really is who is at risk for poor outcomes. And it's everyone you would expect, men, workers, comp, laborers, smokers, lower angle, vasculopathy, and then open injuries. And so going into the complications a little bit more, so when you get subtalar collapse and loss of your angle, you're gonna get anterior impingement and the treatment would be a bone block arthrodesis. If someone postoperatively has issue flexing their great toe, it could be from an aberrant systentaculum screw damaging the FHL because it's intimate relationship of the FHL running underneath the systentaculum. And then with extensile lateral approach, you wanna look out for wound complications and several nerve injuries. And then other complications include increased heel width arthritis and then perineal injuries. Moving on to talus fractures. So three main body parts to think about for the talus is a lateral process, which you see in snowboarders and it's due to forced dorsiflexion, axial loading and inversion with external rotation. Just think about someone with a seemingly like a bad ankle sprain mechanism that's not getting better, significant swelling and a little bit more distal than the fibula. Think about the lateral process and then neck and dome fractures. And the blood supply is a commonly tested subject for the talus. You have the posterior tibial artery which feeds the tarsal canal and then the deltoid branch which is preserved during osteotomy. You have your anterior tibial artery and then the perforating perineal artery. And so that supplies the artery of the tarsal sinus. And so artery of tarsal canal and artery of tarsal sinus sound very similar. So it's an easy test subject just to know where their respective arteries are actually coming from. And diagnosing, you have x-ray and CT scan. On CT, you usually see varus, deformity, medial convolution and then you're gonna look for other associated fractures. The Hawkins classification is based on additional dislocations. And essentially when you get to Hawkins 3 and 4, studies have shown nearly 100% chance or risk of AVN. And then the treatment for talus fractures, like anything else, if it's dislocated, you wanna reduce in the emergency department or the operating room. Open reduction for talar neck fractures, the standard of care really is a dorsal dual approach because it's easy to look at one side and think the reduction's on and then you go to the other side and it's way off. And then if it's extruded, there are case series and protocols to have a successful replant. And so complications like all of the fractures is what they really kind of focus on. And so post-traumatic arthritis, specifically the subtalar joint arthritis is the most common complication. And then also a common complication is AVN. And so you wanna look for the Hawkins sign, which is actually a good thing, which usually shows up at six to eight weeks. And it's this lucency in the talar dome, which indicates vascularity. And other complications include malunion. And then another important commonly tested question is the risk of complications is not increased with delayed fixation. And then lastly, going on to fifth metatarsal fractures, it's broken down into the three zones. So your zone one or your tuberosity is your pseudo-jones. And that's typically the mechanism is a plantar flexion and hind foot inversion. Jones fractures are your zone two, which is in your relative vascular watershed zone. And then zone three is a more chronic. And then your treatment is also based on zone. Zone one, you could be treated just like an ankle sprain, protected weight bearing. Zone two and three really depends on the patient. You can make them non-weight bearing. And if they say anything about them being in sports or college athlete or professional athletes, consider fixation because the higher rate of non-union and fracture rate, the more reliable return. And then again, complications, another focus. So non-union risk factors are zone two and three. Metabolic causes, specifically vitamin D. You want to look for any sort of signs of subtle cavus to be having a little bit more lateral column overload and then early return to sport. Treatment related complications. The sterile nerve is like two or three millimeters from the tuberosity. So that can easily be injured during fixation. And then more fixation complications relate to screw placement. And so it's a straight screw and a curved bone. And so you can easily get distraction at the fracture site. The ideal point is this high and inside position. And then if you get too short of a screw, there's no compression. And then smaller than 4.5 screws have high increased rate of complications. So going over some quick practice questions. First one is a 40 year old and an MBC. Shows up to the emergency department with this exam and x-ray. The treating surgeon proceeds with arthrodesis over fixation. What are the expected outcome? And so you see some diastasis at the Lisfranc enteral and then plantar ecchymosis. So you should be thinking about a ligamentous Lisfranc injury. And so we know that ORF and arthrodesis have similar outcomes. And so we're gonna be looking for things going through each one. Higher wound infection rates, no difference. Improved functional outcomes, again, no difference. And then decreased need for subsequent operation. So that sounds good because less likely to have to remove the hardware. And then they have a similar risk of traumatic deformity. And then last one is 50 year old male, smoker, diabetic. Sustains accommodated intra-articular calcaneus fracture following a fall. On-call surgeon elects for non-operative treatments. And so what is a patient unlikely to experience in six months? And so going through, tight shoes can definitely happen because they've increased heel width. Reduced dorsiflexion can happen because of the loss of your subtalar height and you get anterior impingement. Difficulty on uneven ground can come from subtalar arthritis. And then pain with eversion can come from any sort of perineal pathology. And so the correct answer is none. Thank you guys. Here's my email address. Feel free to reach out if you have any questions about anything I talked about or anything related to residency and fellowship. Be happy to help. Thank you. Dave, you're muted. Oh, thanks. Yep. So I'll be talking about canvas foot and then we'll move on to perineal tendons, and then we'll do ankle arthritis. I have no disclosures for the talk. So, in a cable varus foot, the most important part of this is really identifying the cable varus foot and usually in the setting of perineal tears or chronic instability. With that, you know, while the hypha is in varus, there's no adequate eversions or shock absorption, so you get increased stress and you're more prone to perineal tears, stress fractures, and so forth. And so a lot of these questions for OIT, we'll talk about fixing the hypha varus or the plantar flex first way. Here's the example of extreme form of somebody with cable varus foot deformity. The problems that can arise is perineal tendons, most obvious, you can get tears, tendonitis, subluxation, stress fractures, especially Jones fractures, like Dr. Locker just mentioned, sesamoiditis, that's the plantar flex first ray, you get callus formation at the first met head or on the fifth met head due to the cable varus foot and recurring ankle deformity and varus ankle arthritis. Common block test is something that comes up very frequently and you kind of, they won't test directly about the test, but you will need to know how to treat the results from the test. Essentially, it determines whether the heel is fixed or flexible and is it a forefoot driven or hindfoot driven. What you do is you put a block on the heel, essentially, and you take the heel out of varus or is it fixed? You kind of let the first ray drop over the edge and then you see if the hindfoot is it fixed or is it flexible? If it does, if the hindfoot is flexible and it corrects and then it's a forefoot driven, if it does not correct, it's a fixed hindfoot deformity and so you correct the hindfoot and it is a very commonly tested test. If it's a forefoot driven hindfoot varus, then typically it is a plantar flex first ray, it's got a supple hindfoot and the usual treatment is a closed osteotomy of the base of the first metatarsal and this will correct that deformity. If it's a fixed hindfoot varus, then you fix the hindfoot, usually it's a lateral displacement calcaneal osteotomy, or you could combine that with the Dwyer osteotomy, which is a lateral closing wedge calcaneal osteotomy, or you could do both. Radiographically, these patients typically have an elevated Mary's angle, they have a compensatory forefoot pronation, so you have an elevated cuneiform fifth metatarsal distance. The hindfoot varus will result in open sinus tarsae in the lateral view. The fibula is posteriorly translated, or it looks like it is, and then you'll see the double talar dome. You'll never be able to see that nice, perfect lateral view of the talar dome. And then you'll have an elevated calcaneal pitch. Nonoperatively, you can treat it with ankle brace, lateral heel pose, which is a very common tested topic, AFO. And obviously in terms of operative treatment, you kind of treat the deformity, whether that's a forefoot or a hindfoot, and usually in the study of other pathologies, such as ankle instability, perineal tears, subluxation. So a lot of the questions will look into whether you can identify whether there's cavus deformity and what you need to do in order to treat that in combination with something else. One of the most commonly tested deformity for cable varus is Charcot-Marie-Tooth. It's a hereditary motor sensory neuropathy involving the PMP22 peripheral myelin protein. It results in weakness and atrophy of the intrinsics, tibia and peroneus brevis. Of those three, the foot intrinsics are the first ones to kind of become weak. And as a result, the ankle flexors and the longus retain their strength and causes the very typical deformity such as equinus, as the tibia is weak, gastric soleus or plantar flex, and contract the Achilles tendon. These patients typically have cavus foot because the longus is not affected and it's overpowering the tibia. The hind foot varus deformity forms because of the posterior tib, again because the brevis is weak. And then the claw toe formation occurs due to intrinsic foot function loss. That is usually the first to lose strength again and overpose everything else in the foot intrinsics. Soft tissue procedures for this typically includes a plantar fascia release, but that's not singular. You have to do it in combination of multiple other three surgeries. You typically have to lengthen the Achilles tendon to correct the equinus contracture. In terms of the forefoot, you may need to do EHL to first match transfer. That's usually in combination with IP fusion and hallux. Claudy Jones procedure to treat the claw toe of the hallux. Typically the longus is transferred to the brevis or you can transfer the fifth mat at the base and that can help elevate the first ray. Posterior tib to the dorsum of the foot, typically the cuneiform to treat the drop foot. And you can combine that with forefoot to treat the claw toe, such as shortening the osteotomies, the metatarsals, PIP fusions, or grotosome tailors. Boney procedures include hallux claw toe, such as the Jones procedure I mentioned, the modified Jones. Dorsiflexion and osteotomy of the first metatarsal to treat that plantar flexed first ray. If they have metatarsus adductus, you can do mytho-osteotomies to correct that, or you can dorsiflex the metatarsals if needed. The hindfoot varus is typically treated with a lateral closing wedge called the Dwyer or lateral displacement osteotomy. In severe stiff deformity or arthritic deformity, a triple typically works very well. I do have questions, but I am going to save them for the perineal brevis talk. So we'll go and move on to lateral ankle instability and perineal tendons. Again, no disclosures. So ankle sprains. Hey, Dave, we're still on your CAVUS. Oh, are you? OK, sorry. That's OK. Just wanted to give you a heads up. Ah, thanks. There we go. All right, guys. Sorry about that. So ankle sprains are fairly, it's not the most common topic, but the most important part is really to not take the operative option. For OIT purposes, and also for just clinical purposes, ankle sprains are treated non-operatively for the most part in acute settings. There is a grading, 1, 2, and 3. It does not affect the care. So whether you have a grade 3 or grade 1, you would still treat that non-operatively. Same thing goes for distal fibrillation fractures. They do like to trick you to show a fracture there and make you pick the operative option. Again, that is treated non-operatively. The most important part really is to kind of rule out any associated injuries, such as fifth metatarsus fractures, calcaneal fractures, and perineal tendon tears. Again, non-operative treatment with or without immobilization, such as a brace or a CAMBU. And then early immobilization is the most important. Physical therapy is also important to start perineal strengthening and proprioceptive training. Those are kind of the buzzwords that you need to know for that. Range of motion exercises as well. And then, again, you never operate on the acute sprains. Now, that's different from chronic ankle instability, which we'll talk about. MRI is typically not done in the acute setting. Typically, you wait at least six to eight weeks after ankle sprain in order to consider MRI, unless you're suspecting something else, like a fracture, perineal tears, or other pathology, or if they're having severe pain with weight-bearing for an extended period of time. And what many people don't know is that ankle sprains certainly can't last many months, and that's why we typically don't advocate for MRI early on. Now, chronic ankle instability is a whole different beast, so to speak. It involves multiple ankle sprains, and so the ATFL and the CFL is typically lax and gives out, and patients typically have a positive drawer test and tailor-toed test, kind of like this x-ray shows. Now, from an OITE setting, really, you need to rule out whether there is a cable varus deformity, the ankle and the foot. From a non-operative treatment perspective, you could do PT and embrace. Abrasion procedure is typically the most common surgery done in patients with connective tissue disorders, such as Ehlers-Danlos. Then you typically do an allograft reconstruction, and then you have to kind of identify the underlying cable varus deformity, like a hypovarus, and if they do have that, you have to make sure that you pick the option, the surgical or treatment option that includes treating those deformities. Perineal subluxation is commonly tested. It involves the perineal tendon dislocation or repetitive subluxation from the lateral malleolus, secondary to disruption of the superior perineal retinaculum. Typically involves rapid dorsiflexion and an inverted foot, and you activate the perineal tendons and rupturing the SPR. You have to realize that there are associated conditions that you may have to treat, so that includes perineus brevis or longus tears, ATFL, CFL injury, and again, you have to identify the cable varus foot deformity. Typically, you can treat this, well, for a perineal subluxation. If you catch it acutely, you can treat it non-op, but typically it only works about 50% of the time, and the booth, non-weight-bearing mobilization, typically it is an operative injury involving SPR repair, typically a groove deepening, and identifying any other deformities such as perineal tears, it's in the synovectomy, and also correcting the varus deformity of scene. Perineal tendon tears, they are associated with multiple ankle sprains and cable varus deformity. They usually have pain over the perineal tendons with decreased eversion and pain with resisted eversion. It's a typical MRI image of a tenosynovitis and tear to the perineal tendons. Treatment-wise, if it's a small split tear, you can't treat it non-operatively with protective weight-bearing, PT, or early mobilization. If there is a high-grade tear, less than 50% from an operative standpoint, if they feel non-operative management, typically you can debride it and retubularize it. The typical board answer is if it's torn more than 50% or if there's significant tendinosis, then you would do either a tenodesis, where you attach one to the other if the other one is salvageable. If they're both bad, you do an allograft reconstruction. And if the tendon both have severe tendinosis or high-grade tear chronically, and there's no excursion intraoperatively, you would do a tendon transfer such as an FHL. Again, you have to treat the hind foot for various cavus foot deformity, and they love testing that and including information about cavus foot. And so you have to make sure you identify that. Here are some questions. 22-year-old male soccer player stepped on another player, sustaining an ankle injury. His pain overlying the lateral ankle ligaments reports no fibular perineal pain. What is the most appropriate treatment at this time? Non-weight-bearing for operative treatment, lateral ankle, MRI of the ankle, weight-bearing is tolerated, ankle brace, appropriate substance training. This patient has a typical lateral ankle sprain or inversion type, and the typical answer is the non-operative treatment. 18-year-old soccer player, inversion ankle injury five days ago reports lateral ankle pain, swelling, and distal fibular tenderness. Exam shows a positive JOR test. X-ray shows an injury with a small distal fibular avulsion fracture. What is the appropriate step in treatment? Ankle arthroscopy, remove the fragments, lateral ligament repair, RAF with syndesmosis, MRI of the ankle, stress evaluation, weight-bearing is tolerated, PT, preceptive training. A is not the right answer because for these acute injuries, even if it's a diversion fracture, you treat it non-operatively. This question doesn't really show a syndesmotic injury. In acute sprains, you don't get an MRI. And since this is more of an inversion type of injury, you don't really need to do external rotation stress review to look for syndesmotic injuries. So as a result, the answer is E again. 35-year-old female troll running when she twisted her ankle on a tree resulted in pain and discomfort. Five months later, she reports clicking and popping sensation, especially with activities. Her symptoms continue despite non-op treatment. She has strength that's five out of five to inversion and other range of motion. She's hesitant to ever her ankle against resistance. MRI shows this, where it's the most appropriate step in treatment. On this MRI, if you look very carefully on the lateral ankle, you can actually see that the peroneus longus is subluxated. So this is consistent with peroneal subluxation. Typically, in a chronic setting like this, it is the operative treatment. And as a result, A would not be appropriate. C would not be appropriate since it does not address the underlying issue. They may have a tear, so you may have to do it. But as a result, D is not the right answer because it doesn't, again, treat all the deformity. And so B would be the most appropriate treatment. 46-year-old female capable of various foot deformity. Insidious onset. So stable anterior jaw and over the peroneals. Weakness to eversion and fixed. High foot various deformity. There's a high-grade peroneus brevis tear. What is the most appropriate treatment for this patient? PT, medial heel post. That typically would not be the right answer since medial heel post is for treatment of pes planeus for flat feet deformity. B may be the right answer, but this patient has a fixed high foot deformity, so it doesn't address any of the bony abnormalities. So B will be the wrong answer. C does involve repairing the tendon and calculating the osteotomy, LDCO. So that is most likely the right answer. And D is maybe the right answer, but this patient shows high-grade tear. Doesn't really tell you any information whether the tendon is salvageable or severe attenuation of the tendon. As a result, FHL transfer is typically not what you would do for this. And so as a result, C will be the most appropriate answer. 55-year-old female with lateral-sided ankle pain and chronic instability. Exam demonstrates tenderness, again, over the peroneals. Part of the drawer, high foot varus deformity. Hormone block test reveals the flexible high foot varus deformity. Patient continues to have symptoms despite non-op treatment. What is the most appropriate surgical management? A, ankle arthroscopy and brochure and procedure. Again, it doesn't necessarily address all the abnormalities. Also, it doesn't address the bony issue of cable varus foot. FHL transfer to the fifth met. Plantar inflection, first met osteotomy, and brochure and procedure. That would be wrong as you would want to dorsiflex the first rate, not plantar inflex. And also, the FHL transfer is typically for salvage. So that is, again, gives you a clue that that may not be the right answer. D, sort of C, brevis repair. Transfer the longest of the fifth met. Brochure and procedure and dorsiflexion, first met osteotomy. That is most likely the right answer, as the TTC fusion would be not appropriate for this type of pathology. The longest to fifth met transfer, again, would address the plantar inflex first rate, help it elevate, and improve the eversion of strength and stability to the ankle. MRI of the ankle with the chronic lateral sided pain. What is the anatomic factor? Anatomic factor may predispose this patient to recurrent injury. APTTD, most likely not. That will probably help. Equinus contracture, not necessarily. Ankle impingement, no. Behind foot varus, certainly that would put continued stress to perineal tendons. And then metatarsus premus elevatus would be the wrong answer. First met that is elevated is typically protective. If it's plantar inflex, that is an abnormality. So the D is the right answer. All right, so we will move on to ankle arthritis. The etiology of ankle arthritis is not as common as the hip and the knee. Ankle chondrocytes produce more protoglycans in the ankle, and so there's better potential for repair, and compared different types of cartilage, such as the knee, ankle cartilage actually has increased resistance to loading and less sensitive mechanical damage. The most common etiology of ankle arthritis is trauma, but it can also include inflammation, such as rheumatoid, infection, and chronic instability. And the most imaging-wise, you do need to get standing x-rays of the ankle to determine whether there's severe or survives deformity. Now, if there's, you can get a CT scan if they have severe deformity to assess, to evaluate for structural defects, assess for adjacent joint arthritis, and the MRI to look at AVN of the tailors if that's suspected. And also, which I didn't write on here, you could get a long cassette view to look at kind of the overall mechanical axis of lower extremity. We're going to jump straight to treatment for ankle arthritis. Typically, it's non-operative management includes medications, activity, and modifications. From OIT perspective, the most important thing to know is braces, so a soft brace, such as ASO, but more commonly, a rigid AFO, such as the Arizona brace, which is tested frequently. And then shoe modifications, such as a rocker shoe can help decrease the mechanical stress to the arthritic ankle. Cortisone injections, though injections typically is not the right answer when looking at OIT. And you can use ambulatory aids. Surgical options includes arthroscopic open debridement, but that is very specific for anterior impingement or some sort of impingement. Like the knee arthroscopic or open debridement of arthritic ankles does not result in long-term improvement. So it is a very narrow spectrum in terms of picking that as a surgical option. You can also include tibial calcaneosteotomy and varicervalgus deformity. The gold standard is still in arthrodesis, especially in a young population, but certainly ankle replacement is much more common nowadays. And there are historical treatments, such as distraction arthroplasty or allograft replacement, which you may see in the answer choices, but typically they have very high failure rate and not the right answer. Anterior ankle impingement, that can be bone or soft tissue, anterior sciatic joint pain. Usually they have tenderness to palpation, especially dorsiflexion range of motion typically cause anterior pain, decreased dorsiflexion with bony issues and pain with dorsiflexion. X-rays will show anterior osteophyte, and you can get an MRI to evaluate for synovitis, adhesions, fibrous tissue, ganglion cysts, and so forth. Non-operative treatment includes a heel lift that can decrease or increase the dorsiflexion of the leg relative to the ground, injection, rocker shoes, activity modifications. And these kind of limited anterior ankle impingement, you can consider arthroscopy and debridement, but again, you do not want to do arthroscopic debridement in patients with more generalized arthritis. It's very narrow to do that for arthroscopic debridement of arthritis. In terms of mild to moderate ankle arthritis with varus or valgus deformity, you could consider a tibial or calcaneal osteotomy. That would help correct some of that varus or valgus deformity. It's not as predictable in severe arthritis, but it can preserve the joints rather than fusing it. It's typically part of a staged procedure, as most of these patients will need definitive treatment sometime in the future, whether that's a fusion or a replacement. The goal of these type of corrective osteotomy is to redistribute the weight-bearing stresses to the non-arthritic area. So from a tibial osteotomy perspective, if they have a varus deformity, you could do an opening wedge of the medial aspect or a lateral closing wedge. If a valgus deformity, you could do an opening lateral wedge or a closing medial wedge. And either of these, you may have to do a fibular osteotomy. Calcaneal osteotomy involves a lateral displacement calcaneal osteotomy or a lateral closing wedge for varus deformity, with or without lateral ankle ligament reconstruction, such as subrostrum from chronic instability. Valgus deformity is typically a medial displacement calcaneal osteotomy, with or without deltoid reconstruction if there's instability there. As I mentioned earlier, distraction block arthrodesis is a historical treatment, and typically we don't do that at this time. What involved was putting an external fixator and then distracting it, and over time, there could be increased residual space due to cartilage formation. But again, that's typically the wrong answer. Ankle fusion is still the gold standard. You can do it in many different ways. There's many indications, such as severe arthritis, failed ankle arthroplasty, septic joint neuromuscular deformity, and so forth. Fusion position is routinely tested. Remember, it's neutral plantar flexion, slight valgus, 10 to 15 degrees, neutral to 10 degrees external rotation, and you got to make sure that the talus is placed underneath the tibia. Applications include adjacent joint arthritis, mainly the subtalar joint, nonunion can also occur, and then malunion, painful hardware, and then if you do a pantalar or even the talonevricular, or if you include other arthrodesis, certainly you will lose more motion. Ankle replacement from a board perspective has a much more narrow treatment window. Involves ankle arthritis with mild to moderate deformity, reasonably mobile, about 60 years or older, lower normal BMI, multiple joint arthritis, rheumatoid arthritic patients, usually comes up in the OIT in board to pick ankle replacement, and no neurovascular impairment, no infection, no severe neuropathy, Charcot AVN, that's diffuse or paralysis of anatomical muscle formation. Relative indications include obesity, weak bones, age, labor, diabetes, smoking, and severe deformity. Typically from a TAA versus a fusion, they have a very similar outcome. Some studies do show that there's increased function with them compared to a fusion. It does retain some more normal range of motion and more normal length, and may not result in adjacent joint arthritis as fast as compared to a fusion. Survivorship is fairly good in the short term. These are more the earlier generation. Certainly the newer generation implants may have better results, but there is obligatory secondary surgery that's typically needed, such as soft tissue or osseous impingement, cyst formation, and polyexchange. Predictors of outcome includes deformity. The bigger the deformity, the decrease in survivorship, and certainly adjacent joint arthrodesis in patients who have an ankle replacement with a subtellar fusion, especially in a younger population. These patients typically have less survivorship. That's thought because of decreased motion from the hypofusion. Interoperative complications of ankle replacement involves medial malleolar fracture, which is the most common malposition in implants and lack of ligament balancing and continued edge loading, such as various valgus deformity. Short-term complications include wound issues, infection, although deep infection is rare, DVTs. And then long-term complication includes infection in older implants, such as agility syndesmosis nonunion, subsidence of the tailor implant, aseptic loosening, HO, impingement, and polywear. Average procedure would be, if possible, revision. Typically ankle fusion would be the appropriate answer. If there's not enough bone, you could do a TTC fusion with a femoral head or a cage. If it's infected, you would stage it with an antibiotic cement spacer, and followed by revision surgery, whether that's a fusion or a replacement, and severe wound issues or infection that fails multiple surgeries, then BKA. And then in severe arthritis with a significant deformity, then you would typically choose a TTC fusion. These include AVN, ankle and sub-telogen arthritis, severe hypodeformity. There's many ways of doing it. Typically the retrograde IM nail would be the most appropriate way to do it, as that is more of a low-sharing device, and if possible, preserve telenevricular joint. Quick questions. Patient undergoes successful ankle fusion, but has continued gait abnormality during ambulation. What is the most appropriate shoe modification to try to improve the patient's gait? Medial heel pose typically won't necessarily help with this. Arizona brace just make it stiffer. Same thing, C, with the lateral heel pose will not help. D, makes it again stiffer again, and that's the right answer is E, a rocker bottom deformity to improve motion. What is the most common long-term complication after ankle fusion compared to ankle replacement? Osteomyelitis? No. Wound dehiscence? No. Adjacent joint arthritis? Radiographically? Yes. Non-union hardware irritation? No. So correct answer is C. 70, 60-year-old female with diabetes, peripheral vascular disease, significant ankle and subtile joint arthritis. What is the most appropriate treatment? Now there's multiple clues in this. They're talking about vascular issues, diabetic, older person. Typically, you would look for a fusion option, so that would be A or C. Typically, injection. Some PRP is always the wrong answer in these situations, and because there's ankle and subtile issues, you would do a TTC fusion. 62-year-old female with RA, long-standing arthritis, multiple non-op treatments such as injection reduces pain, but this patient has stopped responding to it, examines she has pain along the joint, moderate deformity, x-ray shows severe arthritis with adjacent joint arthritis and subtile joint and midfoot, but she's mainly symptomatic, again, as the question sent indicates, in the ankle joint, confirmed with injection. What is the most appropriate definitive treatment? A would not be the appropriate treatment because she is asymptomatic in the other areas, and so you necessarily wouldn't have to do a subtile fusion. Pantelus fusion would just make her very stiff. Functionally, it would be a pretty low result for her. Ankle replacement would probably be the right answer for this patient as the main pain is in the ankle joint. There's no pain in the surrounding joint. She has multiple joint issues, and she responded well with non-operative management without any severe deformity, so C is the right answer. D, E, and F, again, would not be the right answer. Ankle fusion would not, in this situation, I mean, you could. It's not a wrong answer, but certainly, from a board perspective, with adjacent joint arthritis, you would be worried about causing increased pain in the subtile joint if you locked the ankle joint, so you necessarily wouldn't do that. All right. Thanks, guys. Thank you so much, and last but not least, Dr. Gurbani is going to bring us home. All right. Sarah, let me know if you can't see my screen or hear me. You're good on both accounts. All right. Perfect. All right. Thank you, guys, for sticking around. I'll try to get through this last bit pretty quickly to get us out, hopefully, on time, so I'm just going to do a quick review on ankle arthroscopy and osteochondral lesions. I have no relevant disclosures for this talk. We'll talk first about ankle arthroscopy, some basics of, you know, some of the indications and setup and some of the risks involved, and so for indications of ankle arthroscopy, some of the most common reasons we do it are osteochondral lesions, bony or soft tissue impingement, synovitis, loose body removal. Some less common indications maybe are purely for diagnostic reasons, you know, somebody who's had chronic pain, undiagnosed, and then some talk about ankle arthroscopy and ankle fractures, you know, depending on your beliefs on that, and so anterior ankle arthroscopy is our most common approach for ankle arthroscopy, and this is, you know, kind of our utilitarian approach for most lesions and most things that we do, so we'll talk a little bit about the setup with this. So for ankle arthroscopy, you can do anterior ankle arthroscopy without traction, but I would say that most commonly it is done with traction in utilizing a setup like this, where you have proximal counter traction with your thigh in a holder. When you are placing that, you wanna be careful for avoiding pressure on the popotiofascia. You can drop the end of the OR table to bring your view of the ankle more in line. So when you put it into traction here, you can see that dropping the OR table down will allow for easier use for your ankle arthroscopy. Typically, we are doing a non-invasive distraction, so with the foot strut, and then this device is placed sterilely on the outside of the table here. There is also an option to have the foot strap around your waist. I've not done that personally. I would say that this is more common, but certainly that is also utilized. And then again, there is the ability to do ankle arthroscopy without distraction. And some of that depends on what kind of lesions or what you're addressing through the surgery. And so what's our approach here? You can locate your portals using a needle. It's not always necessary. I personally go straight to incision, but it's certainly accepted and reasonable to use a needle to establish your portals first. The classic teaching is a nick and spread technique. So just incising the skin alone and then spreading subcutaneously with a hemostat or some other device to get into the joint. The goal of that is to reduce the risk of neurovascular injury as you're entering. And then typically use a blunt trocar to enter so that you again, reduce risks of placement and cartilage injury as you're entering the joint. As far as portals, the intermedial portal is typically the one that's established first. That's the one that you use to visualize the joint where you are making this portal is at the level of the joint line, just medial to the intertibial tendon. So you feel your medial malleolus, you feel your tibia tendon, and at the level of joint line, there's a soft spot right between there. And that's how you typically enter the joint. The saphenous nerve and vein are at risk with placement of the intermedial portal. What you typically establish next is your anterolateral portal. This is just lateral to peroneus tertius at the level of the joint line. I personally do this and it's common practice to establish this under transillumination from the intermedial portal so that you are able to visualize the superficial peroneal nerve and make sure it's not at the level of your incision. And that's the most common nerve injury with ankle arthroscopy. And so you definitely want to be careful and make sure that you are trying to visualize it and staying away from the superficial peroneal nerve with your anterolateral portal. And that's commonly tested as far as the greatest risk of this portal and highest risk of neurovascular injury with ankle arthroscopy is to the SPN nerve. And then as far as diagnostic arthroscopy, these are all the anatomic structures that you can look at. And typically, classic teaching is to go from medial to lateral. So you start at the tip of the medial mal. You can see your medial gutter, your deltoid, follow the talus and go towards the central talar dome, central tibial plafond, looking for osteochondral lesions, and then take that to the lateral side, get into your lateral gutter. You can see AITFL. You can also turn your camera and look anteriorly at the anterior gutter. You can look at the syndesmosis. This is where you can do your syndesmotic drive to sign. If you are looking for syndesmotic instability, that's where you put a three millimeter probe. And if that fits there, then you're confirming that you have syndesmotic instability. And then looking at your trifurcation with the talus, fibula, and tibia, and then your AITFL. And so that's anterior ankle arthroscopy. Quickly gonna go over posterior ankle arthroscopy, which is less common. Some of the indications for it are posterior impingement, releasing the FHL, posterior osteochondral lesions, and posterior ankle synovectomy in cases like PBNS. You can also utilize this for subtalar fusion to get to your posterior facet. So the setup for this is prone position. And important thing that they sometimes test is you have to visualize the FHL tendon. The reason why you're doing that is if you're visualizing the FHL tendon, you know that you can be on the side of that to protect and prevent injury to your neurovascular gondola. As far as establishing the portals for these, they're on either side of the Achilles. And so you wanna hug the Achilles and be close to it. The lateral, the posterior lateral portal is at the tip of the lateral malleolus, or just proximal to that. And then the medial portal is at the same level, just hugging the Achilles. And if you're only addressing ankle pathology and not going to subtalar joint, you can cheat these a little superior. And then switching gears a little bit, just to quickly review some of the key points for osteochondral lesions. So some of the epidemiology for this. So osteochondral lesions are typically secondary to trauma. Estimates for the incidence of this are upwards of 50% of ankle sprains or 70, 75% of ankle fractures have some sort of chondral injury. Obviously not all of those are symptomatic. So not all are detected or even go on to be clinically relevant, but that's some of the estimates that we have. Medial osteochondral lesions are more common than lateral osteochondral lesions. Lateral are more likely to be associated with an acute trauma, whereas medial is more repetitive microtrauma. Medial osteochondral lesions are more likely to be deeper and to extend into the subchondral bone. And then talus osteochondral lesions are more common than tibial osteochondral lesions. The talus has thinner cartilage. And then this is also true for why the talus is more susceptible to osteochondral lesions than the knee, for example, is thinner cartilage in the talus, or that's a thought at least. So patients will come in with pain, sometimes mechanical symptoms. And so what kind of imaging do you get? You always start with x-rays. And oftentimes for osteochondral lesions, you can see an indication of this on x-ray. If they have negative x-rays, but you are suspecting of an osteochondral lesion, the most sensitive imaging to get is an MRI. In practice, we are getting this, or I would say most people are getting this for practically all osteochondral lesions anyways, but sometimes they will test, you know, what's the most sensitive imaging in terms of negative radiographs for an osteochondral lesion and that would be an MRI. CTs are also utilized often for osteochondral lesions, and that's typically to better evaluate the subchondral bone or cysts, and especially for surgical planning, that can be helpful as well. So how do we treat osteochondral lesions? Non-operative treatment. If you see one acutely, it's non-displaced, you could treat this with immobilization. More often, we're seeing these in a chronic scenario. The initial treatment you can start with is a typical activity modifications and sets bracing injections. When we start talking about surgical management, this is somewhat controversial and, you know, the details of it, I don't think they will test you on too much, but generally speaking, this is one of the protocols that's been published and it kind of goes through the characteristics of the lesion and then also the size. And I think that's how they may test you on this is primarily based off of the size. So when we're talking about osteochondral lesions that are less than one to 1.5 centimeters squared in terms of their size, so 10 by 10 millimeters or 10 by, you know, 15 millimeters or so or less in size, those are ones that we're typically treating with some form of marrow stimulation, whether that's microfracture or just a breathing vent or drilling, but some sort of marrow stimulation. And that number, the one to 1.5 centimeters squared, it's a little bit, depends on your beliefs on that. You know, if you're on the upper end of that or lower end, but if there's telling you a lesion that's smaller than that, and especially has not had prior surgical treatment, then you are typically looking at some sort of marrow stimulation procedure. When we're looking at the larger lesions, that's where it gets into a little bit of the weeds that I don't think they'll test you on too much, but these ones you're typically using a graft of some sort. And the decision on what type of graft depends on the presence of cysts, also the location. So if it's in the shoulder, a standard OATS plug may not be appropriate. You may need to use an AL graft at that point. And then if it's large enough that you can't use an OATS plug, then you may be looking at a larger AL graft. And then finally, as far as cases where the cartilage cap is intact, and they should give you some hints of this, either by the imaging or by the question stem, if there is an intact cartilage cap, those are ones that you can treat with retrograde derelict. All right, so that was a quick review there. Just a couple of questions quickly. What structure is most at risk when creating the arthroscopic portal seen in this image? So this is the area of the anterolateral portal. And so like we discussed, the superficial perineal nerve is most at risk with anterolateral portal. And this is also the most common nerve injury with ankle arthroscopy. So they may ask it in that way as well. And so either one of those would be, the answer would be the superficial perineal nerve. And then during anterior ankle arthroscopy, which portal is typically established first? So the anteromedial portal is the one that's typically established first. And that's because it's the safest. And then you can do your anterolateral portal under transillumination, like we said, to reduce risk of SPN injury. The patient presents to your office with a lateral tailor osteochondral lesion compared to medial lesion. What is true of lateral lesions? So lateral lesions are typically smaller in size. They're typically more commonly associated with trauma and then less likely to be posterior than more anterolateral. So the answer is they're less likely to have subchondral cysts. So the medial ones are more likely to be deeper and have subchondral involvement. And then final question here, patient presents after an injury four years ago, physical therapy hasn't helped, MRI reveals medial tailor OCD lesion. What is the most appropriate management? And here, the main thing is just the size. Like we talked about, this is under that one to 1.5 centimeters squared size threshold where you might be looking some larger procedures. So we're able to treat this with ankle arthroscopy and microfracture, so a mirror simulation procedure. All right, that's it for me. Thank you so much, Dr. Gurbani for bringing us home. I know we're flirting with kind of, well, flirting with slash running out of time. For any of our resident participants that have questions, we're happy to hang out and answer, but I understand your time is precious. It's a late night, especially for our East coasters, and it's probably dinner time for our West coasters. So if there are any questions though, please unmute yourself and feel free or use the Q&A. And like we said, we will also be posting all of this material and a recording of this will be going out as well, I believe within the next 24 hours or after 24 hours, I apologize. And just going to put a plug out there while we give people a chance to kind of get their questions together. You know, this is put on, and I want to say thanks to our speakers and to the AOFAS for making this a thing. It's been a lecture since I was a resident, and it really reflects a commitment to resident education and wanting to bring good content to you and wanting to expose you to the community and wanting to bring good content to you and wanting to expose you guys to the wonderful specialty that Foot & Ankle is and some of the wonderful people that are involved in the field who we are so lucky to have here presenting with me. All right, we've got a Q&A. The lectures will be on the AOFAS website. Residents can join, and then on that website, same place where you registered for this lecture, they will be posted on the, it's no longer called the Physician Resource Center, but I think it's now called AOFAS 1, and that will be where it is posted. All right, I'm going to take the silence as either y'all are tired of hearing about it from us, there are no questions because we answered them all so perfectly, or you're ready to go to bed or eat. So we will end things. Thank you guys so much. Thank you to AOFAS for the support and our administrators that are in the background supporting this as well. And last but not least, thank you, Dr. Gurbani, Dr. Odole, Dr. Smith, and all of you and thank you, Dr. Gurbani, Dr. Ogi, Dr. Locker, and Dr. Atwater for your time this evening. Everyone have a wonderful evening. Great, good night. Thank you, Sarah. Thanks, good night.

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