CME OnDemand: 2023 Advanced Foot and Ankle Course-Symposium 2 – Complex Sports Injuries to the Foot and Ankle: He/She Is Going Division 1

Symposium 2 – Complex Sports Injuries to the Foot and Ankle: He/She Is Going Division 1 – What Do I Do?

Video Transcription

For those who just joined us, my name is Glen Chu, one of the orthopedic surgeons here in Jacksonville. Symposium 2 starts right now, actually.  We're talking about complex sports injuries of the foot and ankle. So basically, this is a case-based webinar. So you have an athlete who's going to Division I, what should you do?  So these are all injuries that we have seen and have probably treated previously. It's kind of a difficult patient population.  So we're going to hear from our panelists to see how they treat each of the individual injuries. The first panelist is Dr. Fernando Redwan.  He's going to present on synesthematic ankle injuries. And should I operate on that ever? Dr. Redwan? Thank you, Glen. Can you guys see on my screen here?  Yeah, it looks good, Fernando. Okay, thank you. So first of all, thanks for the invitation. Let me do just... Yeah.  So thanks for the invitation, for the scientific committee, and for Miller for bringing me to talk about synesthomas. I have nothing to disclose.  I'm going to present two cases in the beginning. I'm going to talk about the subject, then I'm going to finish my presentation showing how I manage these cases.  So this is a D1 hockey player. She is 20 years old. She had a fall ski in New Hampshire. She was seen in a local emergency room. She had x-rays done.  They told her to be in a boot for about six weeks because she had no fractures, but that's how they offered her treatment in New Hampshire.  She came to see me six days later with medial mal pain, basically over the deltoid.  She also had pain over the anterolateral synesthosis, over the synesthosis, like four to five centimeters, approximately, to the joint line. She had no pain on the proximal fibula.  Posterior translation exam of the fibula was painful, too. And her ankle was very swollen and with a lot of bruises. So these were her initial x-rays in New Hampshire.  She just had a trauma.  So I assume that that's why they did not do a weight-bearing x-ray for her over there. This is what I did on her in our hospital in Beth Israel in Boston six days later.  These are weight-bearing x-rays. I got to say that I could not see any fractures in these x-rays. I really zoomed in in our electronic system. I could not find any fractures.  I was convinced that she didn't have anything because of her physical exam. So I decided to order a CT scan. And this was a CT scan. So this is a non-weight-bearing CT scan.  But that's what I appreciated. She had a posterior mal fracture that was going to the incisor. These are coronal plane views. You can see here the posterolateral mal fracture.  These are sagittal plane views. Same thing, like minimally to non-displaced posterolateral mal fracture. And now what, right?  So medial pain, pain of the stenosis, and this almost non-displaced fracture on the posterior mal. So this is case number two. This is a case from my fellowship in Minnesota.  I did this case with Dr. Seibel, 24-year-old female. She was a skateboarder and actress. She was a professional skateboarder.  Actually, she lived in L.A., just living the dream, Malibu, blah, blah, blah. She fell skateboarding. She had a lot of pain on her foot.  She was diagnosed with a foot and with an ankle fracture in L.A. And then her parents lived in Minnesota. So she decided to go to Minnesota to have her treatment there.  These are the X-rays. Here we can clearly see the posterior mal fracture. She also had a least frank injury that we would have to deal with. These are the CT scans, coronal planes.  You can see, like, comminution, the base of the second, metatarsal base. The fracture here. Then sagittal views.  You can see the posterior mal fracture, the lateral mal fracture as well. Some injuries on the base of the second.  The lateral views, again, posterior mal, fibula, and also the sacrum TMT joint. So I'm going to talk about syndesmosis. When should I operate ever?  So we've got to remember the anatomy. So we have the AITFL that has two fascicles, the paroxysmal and the distal one.  Then we have the interosseous membrane and the interosseous ligaments, and also the PITFL.  That is more like a delta shape with a wider insertion of the posterior tibia and a narrow insertion of the fibula.  We've got to remember some normal numbers from the anatomy and the biomechanics of the syndesmosis. We have four degrees of rotation.  We have two to three millimeters of diastasis when we're moving our ankle up and down, and five millimeters of anterior and posterior translation syndesmosis.  So these are normal numbers. We've got to remember this when we are treating this patient, especially when we are analyzing whether they have or not syndesmosis instability.  The AITFL is responsible for the external rotation of the fibula and also to prevent the translation on the sagittal plane. The PITFL is responsible to prevent internal rotation.  Both of them are responsible for about 75 to 80 percent of the stability of the syndesmosis overall, and the rest, 25 to 30 percent, is from the interosseous ligament.  Some papers show that just loading the specimens with instability did not change these numbers very much.  And we know that the deep deltoid prevents the lateral translation of the talus.  So to me, this is my personal opinion, I consider the deltoid an indirect ligament of the syndesmosis because it does prevent the lateral shifting of the talus.  So this is my personal opinion. What's going on here? Yeah. So we've got to remember still in the anatomy that the chronoplane instability occurred.  This is a paper published from MGH. They were studying the stability of the syndesmosis.  So they noticed that the chronoplane instability happened only after you sectioned all the three ligaments of the syndesmosis.  And you have full instability only after you sectioned all the three ligaments of the syndesmosis and the deltoid as well.  But this patient was, they only used the cotton test to test this, the syndesmosis.  This was under arthroscopic visualization. And they used the balls, the guiding balls to test syndesmosis.  But this is a test that only checks if the syndesmosis is stable or not in one single plane. So this is usually how the syndesmosis injuries happen.  So this is the King James, like 2020 at the bubble in Disney, like in the playoffs of NBA. And then a player falls over his ankle.  So there is a lateral rotation with valgus movement of the ankle. And that's the high ankle sprain happening right there.  So we've got to examine this patient appropriately. I am very detailed on the physical exam for these patients. The squeeze test is one of the most specific tests that we can do.  So we've got to do the squeeze test and the transition from the middle to the distal third of the leg.  The test that I do in all my patients, the lateral rotational test, I can do them non-weight-bearing. But several times I do them weight-bearing as well.  Pain over the syndesmosis, there's some research showing that if you have pain more than four centimeters  proximal to the joint line, this means that the amount of danger of the syndesmosis is higher  and would be, these patients would have poor outcomes and they very likely need a surgery done. Cross-leg test, functional stabilization test is also a test that I do all the time,  not on acute cases, but several times in chronic cases I do it. Besides aeroplane instability is also a good one to do. So we have many, many different maneuvers.  I used to do two, three, maybe four sometimes to be sure whether I'm not missing syndesmosis instability. Harper and Keller in 1989, they came with their radiographic parameters  that you have to measure about one centimeter proximal to the joint line. So the medial clear space, the anterior clear space, the overposition of the tibia and the fibula.  But we know that these are only 2D exams. You may miss a lot of cases if you only base your practice on these parameters.  So then came the MRI that we can check the ligaments that are torn and we can assume whether the syndesmosis is unstable or not according to the number  and according to which ligaments are torn. So here we can see the AITFL is torn. The rest of the syndesmosis can be intact.  You can also see liquid going in the syndesmosis. This is the ring of fire sign. This was published by James Scalder three, four years ago.  And when you have liquid going all around the tibia or the talus like this, you can assume that you have a complete tear of the syndesmosis  and that's why the liquid is going all around the ankle joint. Then the weight-bearing CT came and the MGH guys, they jumped on it right away.  So they proved that better than the two-view x-rays and even better than the MRI. Since these patients are weight-bearing,  if you compare the area between the syndesmosis on both ankles, this is a more sensitive way to understand whether the syndesmosis is unstable or not.  Later they just stepped forward and instead of only measuring the area, you can measure also the volume of the syndesmosis and compare to the contralateral side.  And then we know that the better way to do this is dynamically touching the syndesmosis  since only weight-bearing may not show clearly whether the syndesmosis is really unstable or not.  And we know also that arthroscopically the best way for you to test the syndesmosis is testing on the sagittal plane as opposed to only a coronal plane.  So you can actively test the syndesmosis with arthroscopy and check if the space on the anterior syndesmosis, on the posterior syndesmosis,  and when you translate the fibula, there is abnormal movement or not. So apparently this is one of the best ways for you to test the syndesmosis.  There's a lot of research out there saying that ultrasound is a way for you to diagnose syndesmosis but I am 47 now and I've been doing foot and ankle surgery for like 20 years.  I've worked in many, many different hospitals in many towns in Brazil, in the United States,  and I did not see one single radiologist in my whole career that was willing to do ultrasound and stress these guys to say, listen, this is unstable, look at the ultrasound here.  So it does exist, but I don't know where these radiologists are. Hopefully I'll find them someday. There are many classifications.  One of them is the West Point is one of the most used ones. This is kind of like grades 1, 2, and 3. The grades 1 and 3 are easier for us to deal with. Grades 1 are usually stable.  You can treat them in an operating room. Grades 3 are like grossly unstable. It's like a no-brainer. Take them to the operating room and fix them.  But the grades 2 are the problematic ones because we are not sure exactly if they are unstable enough to a point where we should do a fixation.  So this is where other tests might kick in the game. So we can divide the grade 2 in A and B, and the deltoid will play an important role here.  So if the patient has a lot of pain and has injury on the deltoid, very likely his syndesmosis will be more unstable.  If the deltoid is intact and pain-free, more likely the patient will have a stable syndesmosis even though the patient has the pain.  I do this test all the time, the functional stabilization test. So I usually do a co-band based layer to avoid skin damage or just taking the hair of the patients off.  And then I do like one or two layers of canvas tape, the two-inch canvas tape. I make this really tight.  And then I not only test the syndesmosis in, but I also do the weight-bearing lateral rotational test.  So the patient here is in 10 degree of extension and doing the internal rotation of the leg to stress the syndesmosis.  And if the pain gets better, the discomfort gets better, very, very likely this patient has an unstable syndesmosis, and this patient will be taken to the operating room.  So that's how I test my patients. I do sometimes the weight-bearing CT scans if I have access to it, nanoscoping, arthroscopy,  and also can also be a very good tool to test these patients before you fix them. But that's how I test my patients in the clinic.  Then if I decide that the patient is really unstable, I have to take them to the operating room. So there's like mainly two big algorithms for this.  One of them was published by Ned and Mendola and Ken Hunt. But basically when the syndesmosis is unstable, we've got to take these patients to the operating room.  James Schouder, same thing.  He also showed his algorithm in 2A and 2B with the division that he made before.  But again, if the syndesmosis is unstable, you've got to send these patients to the operating room and stabilize their syndesmosis.  There's many ways for you to test the syndesmosis intraoperative. This is the drive-through test.  When you put the shaver, that has to be like 3.5 or 4.0, not only on the lateral side, but also in the syndesmosis itself.  And if the shaver goes in, you can assume that the syndesmosis is unstable. And then how to fix the syndesmosis. There's many, many different ways. You can use 3.5, 4.5 screws.  They can be solid, cannulated. Three, four cortices.  The position that we should fix the syndesmosis, blah, blah, blah. So we know that there's no difference between the size of the screws, if they're cannulated or not.  And if there are three or four cortices, there's no really difference between these three items here. Have the ankle positioned with the fixation?  This is a little bit more controversial.  We know that some papers show that you cannot overtight the syndesmosis, even though some papers show that after you remove the screw fixation for the syndesmosis, you can gain range of motion.  So you could assume that if you gain range of motion after you take the syndesmosis screw off, you are, like, un-overtighting the syndesmosis that was possibly overtight before.  But I think that the most important thing here is remember that according to the foot position, the fibula will be anterior or posterior in the syndesmosis incisura.  So personally, what I do, I keep the ankle in 90 degree when I do the fixation, but not to prevent overtightening.  Just to put the fibula in a proper position before I put my fixation system.  Because in 90 degree, that's where the fibula is supposed to be incisura without the five millimeter anterior to posterior translation, without the four degree of lateral or internal rotation.  So that's how I fix my syndesmosis. Regarding the open or closed reduction, I mean, actually, it doesn't really matter. If you put the fibula in the proper position, it's fine.  When I did my first fellowship in the U.S. in Minnesota with Brian Denhardt, he showed to me the Mercedes sign. So there's a kind of three-point star.  One of them goes up to the tip-fib joint. Another one is the joint line of the tibia. And the third one is going down on the fibular and talus joint.  If you have that star formed, it means that for sure your syndesmosis is well reduced. And you can see that star also arthroscopically.  So that's the way that I use to be sure whether my fixation is appropriate and whether my syndesmosis is well reduced. So that's what I do. Screw removal, I mean, who knows?  Some authors remove them all the time. Some don't. It's not really clear. Sometimes when they break, the patient gets better.  And we have a lot of support and literature to say that to our patients. I personally take them off after 8 to 12 weeks.  And I let the patient know right away just because I don't feel comfortable on convincing my patient that they have to root for their screws to break.  Because if they break, oh, it's awesome. Now it's broken. So your fibula can move again. So that's what I do. Sometimes they screw, they may break in a bad position.  And then removing screws from the syndesmosis itself can be a nightmare. So how to fix them? There's many ways. So the dynamic fixation has some advantages.  Same or maybe even superior coronal plane stability.  There's no need for removal, even though sometimes you can have some problems with the tight ropes and you have to remove them in the medial side or in the lateral side.  There's no visual failure, so you kind of misposition the tight rope. You cannot really see the ropes.  It's supposed to be a low-profile fixation, even though the knots can be pretty prominent. It is a flexible fixation, which is good and is more forgiving.  So if you malreduce your syndesmosis just a little bit and you fix it with a screw, that malreduction will stay there.  If you do it with a tight rope, likely the fibula will fall into its anatomic place, and the problem that you might be causing will be solved by the fixation.  But there are some disadvantages as well. So there's no sagittal or axial plane stability with the dynamic fixation, only coronal plane stability. You should open medially.  There's many papers from Japan, initially from Japan, showing that if you put the medial button on the perfect position to stabilize the syndesmosis, it will be right over the siphonous vein or over the siphonous nerve.  So I always open medially to be sure that the medial button is in the perfect position and is flush  on the bone. Sometimes, if you have a really poor bone quality, the button may subside,  especially if you're not using the button through the plate on the lateral side, it may subside.  The knots can be bothersome to some patients. You've got to remember you cannot mix stainless  steel plate with titanium buttons and vice versa, so these are problems. These are patients that I  did a couple months ago. If you look at here on the lateral side, the skin is problematic. The  patient has pain on the skin because the knot of the end of the button is bothering her right there  and now she has a small scar over here and I have to remove the knots in the end of the button  just because of the knots was boring or bothering the patient. This patient here, after I did the  first tightrope, this end of button, the medial button, just subsided in the tibia, so I had to  put other two ones over there, but I could not take this guy out, so you can have complications after syndesmosis fixation, and this patient here, this is a patient from Seibold in  Minnesota. After we did the fixation of the syndesmosis with the tightrope, we could still see  there was clearly like lateral rotation of the fibula and also posterior translation of the fibula.  Look at this. So you got to keep testing your syndesmosis throughout the whole procedure  because even after fixing the syndesmosis with the tightrope, you still can have some instability. So what we did in that case, we just put the tails of the tightrope  anterior to the tibia and fixed another anchor, like kind of doing an AI TFL reconstruction in that case. By the way, solution for rotational instability after  fixation of the syndesmosis that's not completely stable, it was published first in 2004 by Olin, where he publishes a technique to repair the AI TFL. You can either use  a graft or a suture button, so you put two screws on the anterior tibia and fibula and also on the telosha process, and then you do these loops with either the graft or  with a suture, and then you can prevent the lateral rotational. Another solution for this is do a hybrid fixation. So you can also do a fixational syndesmosis with an endo button  with a tightrope, and then you can add to that a screw that is proximal to the fibula. This is a technique that is used by Dr. Bob Anderson all the time. So you can have the  three-plane stability from the screw here and also the dynamic fixation from the endo button,  and then when you take the screw off in the future, the endo button stays. So that's another technique that you can prevent the three-plane instability and also give the patient the  micro-movement syndesmosis once you take the screw off, but you keep the syndesmosis together with a tightrope. This is a patient from Miller. He gently sent this case to me.  We are doing now at PI the arthroscopic reconstruction of the AITFL. So you go there, you put one anchor arthroscopically on the fibula, and then you put another one proximal to the  tibia, and then you tie it, and then with the fiber tape, you can have a reconstruction of the AITFL, and you can stabilize the AITFL arthroscopically as well. So what about...  You have a couple cases coming up. I like to save those for the case discussions, if that's okay. Yeah, so I'm going to show the cases right now.  Okay. Let's save that so we can get some of the other speakers a chance to take a look at it,  and then we'll come back to this, okay? Thank you. That was excellent. So in addition to  syndesmotic injuries, we also have athletes with a very difficult problem of navicular stress injuries. So the next speaker is actually a professor of orthopedic surgery now. He's a  very well-known and a good friend of mine, my colleague as co-fellows at Duke in 2014 and 2015.  This is Dr. Christopher Gross. He has been pretty well published on navicular stress injuries.  He's going to discuss this with us and how to treat and address this problem. Dr. Gross?  Glenn, thank you so much for the kind introductions. I'm sorry for the dog barking behind me. Can you see my screen okay? Glenn?  Yes. Perfect. Thank you.  All right. Let's start. Okay. Here are my disclosures. Let's briefly talk about the anatomy because that's going to be important to consider for the biomechanical considerations.  We know it's a boat-shaped bone wedge between a lot of bones. When a singular bone is wedged between  a lot of other important things, bad things can happen. The incidence of navicular stress  fractures accounts for about a third of everything that we're going to see in our foot and ankle  world. It's interesting because since the 80s, the incidence has risen really from pretty tiny,  like 2.5%, all the way to like 35% of all stress fractures now. Are we better at diagnosing it?  Sure. We have better ability to order MRIs, CT scans, and things like that. We have better vigilance. It could be really shoewear and participating in sports that really is leading  to these changes of diagnosing these navicular stress fractures. Now, interestingly enough,  you want to keep this in mind for any of your track and field athletes that happen to  come into your office because they really account for almost two-thirds of all navicular stress fractures. The high forces that they're putting their bodies through with sprinting,  jumping, and running is going to be important to take into consideration. We know most patients are  going to be male. It's going to be unilateral. Rarely will they have any bilateral navicular  stress fractures. Their age is rather young. We'll revisit this in a few more slides, but  the important thing to consider is that lag time between symptoms and diagnosis is seven months,  which is quite a long time. Now, is that a matter of us diagnosing too slowly? I really hope not. I  hope our vigilance is a little bit better than that. Really, it could just be nagging, nagging  pain. They go to their primary care doctor and someone else, and really show up at your doorstep  expecting relief. As with any stress fracture, we know it's excessive repetitive impact loading  that over time, our bone breakdown is outmatched by our ability to regenerate bone.  So, there's continued loading conditions that can coalesce into stress fractures.  Now, one thing that we have to take into account with the navicular itself is our vascular anatomy,  and there are actually a couple of contradicting studies regarding this.  So, just in general, we know that the blood supply comes from numerous small vessels arriving from  the anterior and posterior tibial artery. Now, we do know that the navicular is covered with a lot  of articular cartilage. So, there's a lot of small areas of bone that blood supply is going  to be able to get into. In a very early study, we thought that the one-third area of the navicular  was rather avascular, and this is honestly where we see most of our stress fractures anyways.  But in 2012, we really kind of turned that on end when there is really a robust vascular supply  in 60 percent of cadaveric specimens. So, you know, the dearth of blood supply in this area  really is contradicted by this study there. So, you know, maybe this is really, we're seeing our  navicular stress fractures in these 40 percent of people that do not have a reasonable intraosseous  vascular supply. So, we know that forces are mostly exerted where this blood supply could  potentially be diminished. There are shear forces from the second metatarsal head or the middle  cuneiform. We have the posterior tibial tendon contracting, increasing medial stress on the  navicular, and there is impingement between the cuneiforms and the talus. So, this contact stress  puts the, you know, the area, the zone of maximum shear stress is placed right in this area of  relative avascularity. And so, for those patients that do have this lack of intraosseous blood  supply, that is a huge concern. We have to consider a lot of different factors when taking care of  our general patient with a navicular stress fracture and our lead athlete with a navicular  stress fracture. And it has to do with time to diagnosis, age, really activity level, and fracture  characteristics. And really, for me, it's activity level and fracture characteristics that kind of  dictate what I'm doing. So, in a casual person, you know, I place them in a cam boot or below the  knee cast, and they're really not to be walking for a good four to six weeks. And I really try  to stress that to them. I mean, again, every time they will take a step, they're essentially  nutcrackering their navicular between all the other bones in their foot. We know the navicular  is the kind of the link between the hind foot, forefoot, midfoot. So, you really want to make  sure that they keep off of it. The way they present, you know, a complaint of an insidious  onset of pain, when they're doing their activities, they have a pain really on the top of their foot.  So, they can't run anymore, but you're not going to find any like traditional forefoot stress  fracture signs like discoloration or swelling. So, what I like to do is really take my thumb and  really plan it on the dorsal aspect of the navicular, and that's the N spot. So, it's tender  in 81% of patients with a navicular stress fracture. And these patients are going to have normal strength range of motion in a neuroneurovascular exam, but they really have pain  with activity. They have pain with palpation, and you really just need to be observant. So, there are delays in diagnoses. We know that. And why is that? The symptoms are vague.  So, a lot of times, just by via what they're innervated by, their pain can radiate along their medial arch. Their radiographs are often normal, and their symptoms can go away after  a couple days of rest. So, again, look at your radiographs. They're about 33% sensitive.  If you're really concerned, I really get an MRI first, and then a CT scan later if I'm deciding to operate. So, you want to make sure that you're getting 1.5 millimeter cuts in the  plane of the tail and navicular joint to really capture the true essence of the fracture that  we're dealing with. And you want to, you know, what's important to look for on the CT scan is  a dense cortical rim because that's going to tell me really how old it is. And here's just some representative CT scan images showing our navicular stress fracture.  Maxine et al. had a really nice CT classification of these stress fractures. So, there's a dorsal  cortical fracture on a coronal image. Then there can be a fracture propagation into the navicular body. And then really you ought to be concerned when there's complete  propagation of fracture through and to the second cortex. So, here's our half in A1, B2. You can see  that navicular stress fracture spreading. And then there's complete cortical disruption.  Again, my first go-to one is a diagnostic study is an MRI. It'll tell us the extent of our bony  edema. And as soon as I see this light up in an MRI, a CT scan is gathered in order to determine  what I'm going to do for surgery if that's really the option. So, if I diagnose a navicular stress  fracture and, you know, I love this group of slides that, you know, we trained with. Six  weeks of strict non-weight bearing, take it off, take off the cast, clinically assess them. If they  still had end spot tenderness, you know, I will put them back into a cast. However, if there's no pain,  I'll let them gradually get back to supervised activity. Any pain, you have to shut them down  again. So, that's the kind of thing. It's a very touch and go issue. After the cast is placed and  taken off, you really need to listen to them. Have them send you, you know, every two weeks or four  weeks a MyChart message or a message, however you prefer, just to kind of monitor their symptoms.  A lot of times, limitation of activity and weight bearing rest can lead to fracture healing.  There are earlier studies that non-weight bearing cast immobilization in certain patients will have complete healing and return to sports. But, you know, we have to consider  what the fracture characteristics are. Is this displaced, non-displaced, complete or partial?  Are there cystic changes, sclerotic changes? What are we really dealing with? And nonely and easily  in 2022 came up with an algorithm, again, like how Glenn and I trained, really breaking down  what we do for these navicular stress fractures. So, first, any acute fracture, obviously you have  to fix it. This is not an insidious issue. If they have a chronic fracture that you see on CT  scan and they have symptoms for a long time, we're going to open that up, graft it, and you can use  proximal tibia, distal tibia, calcaneus or iliac crest. If there is any chronic fractures with  evidence of sclerosis or AVN, you really have to consider something else. Acute fractures,  there's a million different types of plating systems, if you so choose. I typically am able  to, I'm okay getting these by with just some furrow cannulated screws. But there are, again,  dedicated plates. If the fracture is way too comminuted, and thanks, Craig, for this case,  you know, if it is dislocated and fractured, you know, consider really bridging these patients  with the expectation that you can take out that bridge later. Chronic fractures, you really have  to be aggressive about cleaning out the sclerotic area and bone grafting this. And again, we talked  about our bone grafting options. The way that we manage this operatively is you're approaching it  via dorsal incision, and you really have to pry open the fracture, and it's not going to be too  hard. You put a Hennerman distractor in there, give it a little wiggle, and it'll show you where  your fracture line is. And you really have to be aggressive about getting rid of these sclerotic  margins, whether you're using a curette or a drill. And then you have to bone graft and compress  away. So here are just some representative images. Again, we got a little carried away with this  navicular fracture, but it does show you what you have to do in order to really fully prepare the  joint. I'm sorry, the navicular. And here's just some post-operative x-rays. So there are  complicated chronic fractures if you have sclerosis, avian, and prior surgery. You know, our solutions  are revision, open reduction, internal fixation, or bone autograft. You know, there is the option  for vascularized bone grafting. I don't know how to do that. You want to talk to your microvascular surgery colleagues in order to do that, but that is certainly an option.  Again, in order to monitor fracture healing, I use the EndSpot Tenderness.  Using Dr. Nunley's algorithmic treatment, they had about an 80% union rate for acute stress  fractures, ORIF, 75% with subacute fractures, and they had an incredible union rate with these  vascularized bone graft via the cuboid. So, you know, the operative management is pretty broad.  Patients generally tend to do very well. The average return to activity is about three months  in patients operatively treated versus 4.5 months. In a really reasonable meta-analysis  in 2010, which is interesting, is that they found no advantage in surgical intervention when  compared with casual mobilization and complete non-weight bearing. So, again, you always want to  try in your casual athlete or patient, you know, strict non-weight bearing in a cast. So, if they  fail that, then you really have to go to the operating room. Now, Glenn, I can stop at this point because this is just one case, or we can keep on going.  I think I previewed this case. It's pretty short. I think you can present it now, and then we'll move on.  Okay. So, this is a young gentleman, 17 years old. He has signed a plan in college. I think he's going  to a D2 school. Really large BMI, 38.5, of course. What would you expect from a South Carolina guy  going into D2 sports? So, x-rays are not terribly remarkable pretty early on, and I just saw this  patient. So, you can see that between June and August, you can see some sclerosis at the margins  of the fracture in the navicular, and that's getting me a little bit concerned. By January,  there's a complete line here, and, you know, what I'm not really telling you is that he was shut  down for six weeks in a non-weight-bearing cast. They tried getting him back to sport. It just,  I mean, every time he'd play or, you know, practice, he'd flare back up again. So, that's  kind of concomitantly what's going on with these radiographs. He had an MRI prior to seeing me  where there was a lot of edema within the bone itself, and here's our CT scan, and again, here's that view that we want to see in the middle right here looking at our fracture  line, and, you know, I'll put the, I'll have the radiology tech sometimes isolate the navicular  just for me so I can better understand the anatomy and where I'm going to have to put my screws.  So, we did this over one weekend because he really needed to get back for football, and  this is how he's doing. He's now six weeks, I'm sorry, he's now 10 weeks from surgery. We've let  him start weight-bearing in around six weeks in a boot with some strengthening and proprioception  program. So, in summary, these are our young athletes. We have to be vigilant. Any vague  pain in these athletes really have a low threshold if you're considering a navicular stress fracture  to get an MRI. Monitor their clinical healing constantly, you know, push on the end spot,  find out how they're doing, find out how they're feeling. Primary treatment for these patients is  cast immobilization for six weeks, even though the parents may stress out about, you know, the length  of treatment. You know, in earlier studies, it does show very reasonable healing rates in athletic  and non-athletic patients combined, and then operative intervention is really indicated for displaced fractures, non-unions, high-level athletes, or, you know, sclerosis that you're  seeing on CT scan. Thank you so much. Thank you, Chris. Very nice talk. The next speaker is  Dr. Itur Volcano. He is going to be speaking about Hagelin's deformity, Achilles tendinosis in the  athlete, and what he does with it. Dr. Volcano is an orthopedic surgeon, and I believe the chair at Mount Sinai in Miami, he's going to be speaking next.  All right. Can you hear me? Yes. Yes. All right. Thanks to the organizers for having me today. I'll try to be succinct. These are my disclosures.  So, this is a case of a patient I operated on a couple of years ago 23 year old male professional soccer player with a two year history of pain at the Achilles tendon at the back of the ankle as he described it.  He was in the morning and after prolonged periods of immobility. He tried physical therapy, low energy shockwave therapy PRP injections amniotic fluid injections, and just came almost sobbing and in the office saying I can barely walk, let  alone play. So, you know, what do you do in this cases. First of all, sorry. First of all, what is the diagnosis.  The answer is an insertional tendinopathy the two images here do not belong to the same person.  I find that oftentimes, these two conditions are these, these two terms are used interchangeably, and this is completely wrong, because the Hagglunds deformity and the pain from the Hagglund syndrome is a completely different animal than the insertional  tendinopathy.  Yet, I have a feeling that the Hagglunds is oftentimes over diagnosed when the true problem is in fact the insertional tendinopathy, you know, from a clinical standpoint, patients typically with the Hagglunds deformity tend to present with more of a poster  medial lateral bump, whereas with the insertional tendinopathy. It's more of a poster medial bump, and then obviously you can have some red flags if you want on the x rays patients with insertional tendinopathy, almost always have some form of  calcific metoplasia at the level of the Achilles tendon, but that is not always the case, obviously.  So, you know, in this patient's case, the, the, the patient's symptoms were consistent with insertional tendinopathy though the x ray which is actually the one you see here on the left hand side wasn't very suggestive of that so this is one of the  cases where I do obtain an MRI to help me with the diagnosis, and it indeed show that it was an insertional tendinopathy. So what do you know about it.  I think we've all been taught that once the search non operative treatments have failed then the surgical treatment is next.  So what is the problem with the open the treatment, obviously the extended recovery we all know that for full recovery patients have to expect about eight to 12 months.  There's always this big question mark on how much tendon do you take and then if you take this completely arbitrary 50%.  You augmented with FHL.  And when I say arbitrary it's because there really is no important literature that supports this, who, who said and why you have to augment with the FHL, if you remove more than 50% of the tendon, the return to sports is long especially high impact sports  and this can be very frustrating to young athletes.  So this is where we started on the wound issues, and the sort of nerve issues even though they're not as frequent as the wound issues are certainly very problematic.  And this is my problem with the open the agreement, not granted. This doesn't happen in everyone, but when it happens, it is bad for for you and for the patient.  This is what has brought me to shift to the zetac osteotomy which I know there's a lot more talk, and the last few years but this is a fairly old procedure this has been around for several decades, described by zetac described by Kevin Kelly,  basically it removes a dorsal closing wedge from the calcaneus. And then you close down that osteotomy to interior rise, the insertion of the Achilles tendon and remove some of the tension from that Achilles tendon.  And if you think about it, when, when I talk about the interior rising the tendon. That's exactly what we do with the open the breed meant when we are removing that posterior bomb and reinserting the tendon, what we're doing is we advancing it more interior.  So this is probably why the zetac osteotomy works.  The other thing is that it can be done minimally invasive. When I started my practice in in 2016, the percutaneous instrumentation was still not FDA approved in the, in the United States and so I was doing these open, but with some of the frustration  with doing them open so some irritation of the, of the surreal nerve and the painful scar and just, you know, overall increased recovery, but doing it minimally invasive has really been a game changer for me.  So what I do is I place the patient in either a sloppy lateral or lateral position with the foot at the very edge of the bed, or if you want, you can even be with a foot off the bed.  The CRM comes from the very bottom of the patient, and you can rest the foot directly on it.  So what you do is under fluoroscopy mark your osteotomy site. Now, when I first started doing this I used to mark two limbs of the osteotomy, make the osteotomy cut at both of those limbs and then with a wedge for remove the interposed bone.  So I changed my technique to what I currently do, and that is I make a single osteotomy line, and then with the birth, I start shaving down the, the bone, I feel I can tighter in the correction.  Better. Sometimes when you make the two limbs of the osteotomy, you might end up over resecting bone.  Another important thing is to mark the plantar hinge of the osteotomy, you want to leave five to 10 millimeters of that plantar hinge intact to avoid violation of the cortex because violation, especially if you then don't fix it will increase your  risk of non union. Now, there was recently a bit of a debate on LinkedIn, though with a colleague who sustained that the zetac osteotomy is only valid in patients with a canvas alignment, because doing the osteotomy will inevitably change the  calcaneus pitch. This is really not true. If you orient your osteo osteotomy accordingly, you can play around with that pitch. So with patients and with a canvas alignment, I tend to make the osteotomy a little bit more vertical, so as to reduce the calcaneus  pitch. In patients with more of a flat foot and make the osteotomy more oblique to reduce the impact on the calcaneus pitch when I close the osteotomy down.  So I make the incision at the apex of the osteotomy and then I advanced, typically a three by 30 cutting burr, and I started making the osteotomy in in quadrants, I usually do the near cancellous first, the far can sell us next.  And then I make a poke hole, the far cortex. And lastly, I connect the dots along the far cortex. And then with the same burr I start shaving down bone from either sides of the calcaneus, and I want to remove about eight to 10 millimeters of  dorsal bone.  It doesn't necessarily have to be a wedge, it can be, as you see in this case here, even a sort of uniform removal of bone, it doesn't matter when it closes down and closes down  very well and they ultimately heal very well like most calcaneus osteotomies to close down the osteotomy I hyper dorsal flex the ankle.  And this is really a very sexy video that you see on your on your fluoroscopy.  As the, as the osteotomy closes, it's it's oddly gratifying. And then I stabilize it now routinely really with two screws. I put one screw really at the level of the plant or hinge, and then one screw more dorsal to close down the osteotomy and  I put that second screw at the hinge is because the one complication I've had.  That was a non union was a patient where not only had I violated that plantar cortex. I had only stabilized with one screw, and because I let the patients walk immediately after surgery.  That led to a displacement of the of the tuberosity that required a revision. So, this is how it looks after surgery you've got a little single stitch there.  I typically allow patients to wait they're tolerated in a cam boot. I don't tell them to to wear at night, I don't believe it's necessary, but they do have to start ankle range of motion, immediately, physical therapy for strengthening and stretching  at least starts two weeks after surgery, and then by six weeks I let them back into sneakers running jumping pounding activities are allowed anytime, anytime after eight weeks from from surgery.  I've had patients who complain of discomfort at the medial and lateral sides of the osteotomy for four months and then I don't know why it's four months, but almost magically tends to disappear.  At that time, whereas the pain that they had at the insertion of the Achilles that seems to disappear already by the first post of visit so it's an incredibly powerful and fascinating procedure.  As far as the outcomes are concerned.  A recent review, published by black on the zetac osteotomy essentially put together the overall 247 zetacs that were done, and these were a combination of both open and and percutaneous.  And as you can see the complication rate was overall pretty low. It was under 3% of symptomatic hardware. The sterile neuritis, 2%, and the non union rate with 1.2%.  One of those non unions is mine.  This other paper was specifically done on 52 athletes that had a open zetac osteotomy.  To be honest, I have some doubts as to whether or not these patients actually had insurgents and anopathy or true Hagglunds because my experience is while a true Hagglunds is definitely more common in a young athlete and insertional tendinopathy  in a young individual is quite rare. I usually see it, either in women in their 40s, or in men in their late 50s, so I'm not sure how these people got 52 athletes for this but in any case, let's assume that it really did have a truly  I'm sorry these 52 athletes, their outcomes with the open zetac were also excellent in 38 of the 52 patients good in 12 of the 52 patients and fair in two of the patients with with one patient requiring a revision.  Based on my personal experience which I'm in the process of publishing. I reviewed patients that had at least two years of follow up for that underwent surgery for with a percutaneous zetac and overall identified 82 patients with a mean age of 51, and I mean  of close to four years, their foot function index improved from 55 to 11 and their bass from 7.7 to 0.5 with a satisfaction rate which was very high 97.5% including the satisfaction of some patients that say you know what, I'm not 100%, but I'm glad I did  and I would do it again because I really did not want to do the open procedure.  The complications. I had one non union to painful hardwares, and surprisingly no astral neuritis and no wound assistance.  So this is the same patient I presented before, and this is what I ended up doing the percutaneous zetac. These are his x rays at eight weeks. And this is the patient at eight weeks in my office.  That was during that visit.  In this particular case 28, I'm sorry a 20 year old professional hockey player with a history of a Davis foot reconstruction done several years prior came to my office with more than one year of pain at the Achilles tendon the pain was worse when walking  sports he tried a PT someone had done a cortisone shot.  And he walked. So, I got an MRI in this case, essentially to confirm that there was no involvement of the Achilles tendon and in fact there was not. And this is someone I did a percutaneous Haglund's exostectomy.  The way I do it is also completely percutaneous I make an incision where you see the x here on the right side on the right image.  And you don't want to stay on top of the apex of this Haglund's deformity otherwise you're going to have trouble shaving it down with a with a bird I use a three millimeter which were, and then you just shave everything down and I flush with a 60 cc syringe,  and an 18 gauge blunt needle.  It's an incredibly quick procedure takes really under five minutes. And to those that say well why don't you do arthroscopically at least you can remove the bursa which is a source of pain.  I reviewed also my cases and identified 31 patients with at least a two year follow up as well.  years of age, and the satisfaction was 100% so I think the bursa really stops meaning anything wants to remove the really the culprit which is that bump rubbing against the Achilles tendon. And again,  in this case, I was very lucky not to have any wound dehiscence and unknown erratus. So this is a procedure that I love doing because the patient satisfaction is excellent, the  surgical time is minimal, and both the patient and myself are very happy. Thank you. Thank you, Dr. Boccano. That was excellent talk. The next speaker is Dr. Eric Tan. And  I remember Eric from back in the day when we were interviewing for fellowships and also taking our boards. So Dr. Tan is from University of Southern California. He's an associate  professor speaking to us about Jones fracture in the athletic population. He didn't heal and why and now what? Dr. Tan? Awesome. Thank you, Glenn. Can you hear me okay? Am I coming  through okay? Yes. Perfect. All right. So thanks a lot, Glenn, at the other USC from on the way on the West Coast. So again, an interesting topic, definitely Jones fracture  stuff. We're going to kind of review some of the basics and get into kind of how it goes wrong. And so disclosure wise, just nothing really specifically for this talk. The other  stuff's kind of uploaded. When we talk about first metatarsal fractures, you know, really location kind of matters, right? It's the most often fractured metatarsal that we have  in the general population, females more than males. In the sports realm, it's really males more than females. And the incidence does peak in kind of the third decade. When we  say location, location matters. We always talk about the zone of injury of the fifth metatarsal, right? The proximal zone kind of being that zone one area that we typically  believe is kind of more non-operative. And then you have zone two and kind of that metadiophysial  Jones area, and then zone three and that kind of proximal diaphysial area. And so what's the big deal, right? Well, we know that it's a blood supply issue, right? Proximally and  distally the blood supply tends to be a bit better, especially distal in the metatarsal and really proximal in there. But then in the central kind of metadiophysial proximal  diaphysial area, we know that the blood supply tends to be poor. And that leads to our belief  that it's going to have a higher risk of not healing well, or a higher risk of a non-union. And so the Jones fracture itself, again, I think in this setting, we're talking about  Jones being a metadiophysial fracture, but also kind of in that proximal diaphysial area that represents about 14% of all fractures that occur. So it's not, you know, it's not  the most common one, but it can be the more debilitating one in terms of long-term stuff. So it's that watershed area leading to the risk of having a non-union. The prevailing  thought, you know, in that we've always been taught as residents and basic things is that, you know, if they're an athletic patient, you kind of need to fix it in order to reduce  that risk of problems. Well, is that always the case? I mean, the data out there suggests that you can treat this without doing surgery, right? You know, this is a study out of our,  you know, our university with just small number of patients, 27 patients saying, you know, about not, you know, 89, 90% of them achieved clinical union and they were able to move  forward. But that being said, also one patient developed a non-union. So, I mean, even in  these settings, you never get 100%, you know, activeness or 100% healing. And so other papers  that have come out that looked into this is basically, you know, again, looking at whether you need to put people in a cast or put people in a boot. And again, the short story with  that is essentially even these patients, a majority of them do heal, but you do get, you know, three of their patients in each of the groups don't heal or have a non-union.  So it's a problem, but you know, that being said, it's still a controversial issue, you know, whether you need to fix it, whether you don't. In the athletic population, like  I said, we typically lean on the fact that it is something that we do fix, but even when we fix it, we do run into some issues. And so again, when we talk about fixing it, there's  data out there, meta-analyses that does say that there are beneficial effects for operative  intervention. You know, what they include is just a quicker return to sport, more reliability in the healing. We also look at this kind of, I'm getting a little bit of a delay on  these slides. Here we go. So looking at the systemic review, some specifically in athletes,  right? So fixing it, whether you fix it with the plate or with the screw, the idea is that  the screw and plate fixation was more superior to non-operative intervention. What that means  is that we get a higher return to play, shorter return to getting them onto the field, quote unquote, better union and improve functional outcomes. So it's something that, again, I  think dogmatically we all kind of subscribe to, and we all do. That being said, you know, all roads can lead to healing, right? So this is an 18-year-old tennis player at our  university. About 2016, he sustained this fifth metatarsal, you know, this kind of metadiaphyseal  fracture, elected not to undergo surgery. Basically at five months, you can still see the fracture line, but he's not symptomatic. He returned to play, no problems on this side.  Then four years later, when he's kind of in his senior season, this fifth metatarsal base fracture. In this sense, we, I'm not exactly sure why he elected for the other treatment.  I think he felt that it maybe was a long time in terms of letting it heal. So we elected to fix this with a screw. This is him at two months. You can see that it's nearly healed,  maybe on that lateral cortex, not necessarily fully healed. And then at four months, it's basically completely healed. He's returned to play. So arguably from his standpoint or  his report, you know, having the surgery was more helpful in terms of just making sure that the timelines were a little bit more accurate and just a little bit more reliable,  especially in these athletes that, you know, where the schedule and things like that become more important or more imperative. And so what we do know is that healing itself, it's  the interplay between mechanical stability, right? We need to have enough fixation of the bone as well as biologic potential, right? So when we assess when these goes wrong, we  do have to assess sort of how are both of those things coming into play. And so looking at the management of, you know, fifth metatarsal fractures, we can see from a complication  standpoint. So these patients, you know, returned to play in 11.15 weeks, complications over  22%. So sometimes it doesn't work out, right? And so you can have a delayed union or a non-union  that happened about 7% of the time, a refracture that happens as well as hardware that becomes  symptomatic. So these are all the things where even though we think it fixed, you know, we fixed it, we're giving us each other high fives, it can still not really work out. And  so another kind of retrospective study looking at their population where these more athletic folks, again, a 7% risk of refracture, and that happened after people returned. So this  was eight months postoperatively. And so again, it's understanding even when we do the best surgeries, or even when we heal things, it maybe doesn't always go right. So how do  we address that? Or how do we fix that? And so in this study, the refractures did occur in patients that had small diameter or cannulated screws. So again, the dogma always shifts  that you know, you try to use the biggest screw you can in the canal, and then also a solid screw if possible, just from the standpoint of, you know, trying to get the thickest or  strongest kind of rebar in there. And so Dr. Hunt and Anderson, they both published kind of their things on refracture and how they treat them. So they looked at 21 athletes,  they revised it to a bigger screw plus also putting some level of biologic, right. So the mechanical stabilization from the bigger screw, plus using autograft or a bone marrow  aspirate concentrate plus a DBM, people return to play 12.3 weeks. And so again, that's how they kind of address this issue. But each of these issues are pretty unique. And I think  that that's kind of the point of trying to highlight in this talk, or what are the things that can occur? One of the things I did take out from this, or you know, takeaway is not  only from their data was also using a drill in reverse. So kind of using that in reverse as you make a new path for the screw can act as a reamer to kind of freshen things up and  create more additional biology to the area. So I thought that was a nice tip that that  I took from the paper as well. And so there's things I like to talk about a kind of considerations,  right? So preoperative considerations, intraoperative considerations, and postoperative considerations,  because I think those are important things to think about when we're talking about kind of the revision situation, right? So things that we got to think about, or even in primary  situations, things that we need to consider, but it's more important, obviously, to seeing  why things went wrong, or how do we fix them. And so in smokers and diabetics, we obviously they're going to be a higher risk population that they don't heal. So it's things that  we need to counsel them, things we need to address, looking at bone health evaluation, especially if it's something that they haven't healed. So getting, you know, seeing if they  have thyroid issues, seeing what their vitamin D levels are. And that may take you on a different  path in terms of saying, do they have enough setup in the situation in order to get that healed? And then when we start to go back, it's thinking about what is their alignment?  How did this happen? Or why didn't it heal? Is there an issue with their alignment such that they have a cavus foot such that they're overloading that metatarsal? And so that's  why it hasn't healed, or that's what caused the fracture, metatarsus seductus in a similar  fashion. And so this is a 35 year old athletic male. He had a fifth metatarsal base fracture treated outside with basically went on to non-union. And so when we talked to him about  surgery, we talked about not only the fact that we have to kind of address the part that hasn't healed that fifth metatarsal base, but also addressing kind of the cause. And  some of the causes basically that having a high arched foot. So the things we think about are kind of, well, are there alignment issues to consider and how are we going to fix that?  Shift the heel laterally, do a dorsal flexion osteotomy of the first ray. What are we going  to do with regards to fixation? Well, a screw or plate kind of depending on your own construct  preferences, but then also adding, augmenting it with biologics, whether that's concentrated BMAC,  allograft, autograft, any sort of synthetic. And so kind of going there, doing that dorsal  flexion osteotomy, shifting the heel. And then we can see that basically we've compressed across  there. And then hopefully he does heal because you've not only addressed that primary issue,  but you've also addressed the underlying factors that are going to affect or facilitate the healing.  When we think about intraoperative considerations, well, so, you know, we can see from this x-ray,  it looks like the screw may be a little bit in a bad place, but then you look here and you can  kind of say, oh, that they kind of totally whiffed, right? So we want to make sure when we're thinking intraop, how do we address those things? What are the fixation options, right?  We're looking at plates versus screws. And some of that is a preference. Some of that is going  to be data-driven. A lot of it is more preference saying, you know, we believe screws tend to kind  of be something that you can put inside the bone. So it's not as prominent. There can be some  impingement and things from that versus a plate where we feel like in general, it does mechanically  make sense because you can put it on the tension side of the fracture, but it does become something  that is more prominent and may need to be removed. Other fixation principles, solid versus cannulae  screws, headed versus headless screw, trying to get the maximum diameter with regards to the actual  placement of it, trying to make sure it's high and inside where, you know, we've kind of learned  that that's the best way to get into there, making sure it's not too long. So it doesn't  kind of distract your fracture and talking about the trajectory issues. And so this is a gentleman,  you know, he was a transfer wide receiver to our university. He got treated at an outside hospital.  You can see that he has a non-union there, right? And so he's about six months, seven months out  from the surgery, still having continued pain in the area. And so when I looked at this, my big  thing was that, well, I mean, on the, on certain views, it looks okay, right? Like on the lateral  view, you can kind of see that that's going down the pipe on the, uh, on the, uh, oblique view,  you can see it's maybe a little bit more medial, but then something looks really kind of off on  that, uh, straight AP view. And so in this setting, you know, we knew we had to revise him from the standpoint of, you know, biology and trying to kind of stimulate that. But I also  tried to change the direction of the screw to get better compression and to try to avoid,  uh, you know, any sort of maybe impingement on the cuboid or other things that may be happening. So in this setting, again, this is our CT showing that it hasn't healed.  So again, trying to revise that screw and then placed by a logic to help facilitate the healing  in this case. So we took out the screw. I placed a bigger wire to just kind of block the canal for  me. And then I wanted to change the direction of the screw. This was a little bit tricky in terms  of trying to do it in a way where I wouldn't blow out the whole metatarsal. And so I went with a  smaller wire kind of at the tip where I wanted to kind of start this. I put that as a blocking wire  to prevent me from, uh, you know, from going back into the proximal part of that, um, of that bone.  And then once I got what I was happy with, then I sequentially basically used a cannulated drill  bit in order to create a new path of the screw. I accepted the fact that distally, you know,  because there's only so much room, it's probably going to end up distally where the other screw  ended up, but proximally I could change the trajectory to be more perpendicular with the fracture site. And so went ahead and kind of changed that trajectory of that screw,  went ahead, tapped it, you know, but went to the fracture site, cleaned it out, added the biology there, and then went ahead. And so you can see, we've changed that trajectory of  that screw, I think in a better place, added the biology. This is him at three months. And so you  can basically see it's a nearly healed and then, you know, kind of able to kind of return and get  back to sport again, distally. I'm not sure I could really change that. You can make the argument  for a plate and things like that, or maybe we just got lucky that it was able to heal, uh, by  stimulation of the biology and things, uh, in that, uh, in that setting. Another case, this is  from Dr. Anderson. Uh, so this is kind of, you know, straightforward Jones, we think, right? So  you go ahead, you have this Jones fracture. You can see that on the plantar cortex there. He went  ahead and placed a, uh, you know, a screw well-placed, obviously good, you know, really  good capture into the canal, really good fit. And so he started to have pain with running. He had  this recurrent fracture. We can see through there on that CT scan, he went home and they had it  revised. And so it's unclear exactly what was done, but it looked like, I don't know exactly  how they revise it. It might've been a smaller screw, but it looks like there's that washer there  plus, you know, kind of that metal fragment. So it's not exactly sure what happened, but basically  at persistent pain, kind of a non-union of that fracture. The problem was when he got a CT scan,  you could see that this was going to be something you couldn't really revise us again to another  screw because of the fact that the, uh, the fracture line is super proximal, right? So there's a high chance that you are going to blow that out. And so in this setting,  the revision was done with a plate. So went ahead with a plate construct, cleaned it out,  bone grafted it, and then went ahead and put the plate in there. And so again, just having to be  versatile based on the situation. And so you can see here, this is the patient at 11 weeks after  that most recent surgery, you know, evidence of CT healing and, you know, continuing to, uh, on  with their career. So again, just trying to be versatile about what the situations are and how  you need to address them. This is another one of Dr. Anderson's cases, a defensive back, you know,  had a refracture here and this, in this setting, he elected, you know, sometimes the screw just  doesn't work. Sometimes you can't revise it to a bigger screw and other situations like that.  And so there's nothing wrong with plating, right? And so with plating, you can plate the plate,  place the plate more on the plantar side on the tension side. It does make a lot of sense to do  that mechanically. Um, but you do have to kind of counsel patients that may have a higher risk  of having some issues, uh, in terms of tenderness or, or some sort of symptomatic nature to that  plate, but it does work and it is something that you should have in your armamentarium there.  And again, so when we look at the intraoperative considerations, the other things we have to think  about, you know, so we talked about grafting options, whether you're going to do an autograft  from the proximal tibia or the calcaneus, whether you're going to take concentrated BMAC synthetics,  and then you also want to think about your hardware, right? Whether it's a plate or screw,  uh, in this case, again, one of his cases where he showed that basically the screw was placed  while things did heal, but the problem is there was, you know, this was impinging on the cuboid  causing pain. And so they did an injection into that area to kind of prove it and then solve that  by removing the hardware. You can also get neuritis and other symptoms from the hardware  as well. So you do have to consider taking those things out or maybe injections and other things to  address for that. And so, again, just some other situations where when you need to revise something,  it doesn't always work out, right? Sometimes it's because the screw is broken. You need to  be versatile where you can plate across that, span across that fracture site and be prepared to do  that. In addition with plates, it's not always good news too, where you may have a situation  where it actually fractures distal to the plate, right? It's a stress riser there. And so  understanding what are things that can go wrong and, you know, having to expand to a longer plate  or another situation there, because it might be a harder thing to place a screw across, because you really can't, that bowing of that bone is not going to allow you to do that.  And so, you know, this is, I kind of leave you with, this is one of my difficult cases where basically, so, you know, garden variety, this is tight end. We basically, you know,  thought this was going to be kind of a chip shot fracture, went ahead, put the screw, everything looked good. Three months, returned back to play, ready for spring ball.  Didn't see him again for about a year and a half. Came back, had this refracture here, kind of in that plantar lateral cortex there. So plan A in the operating room was to go ahead  and take that out, upsize it to a bigger screw, bone graft it, but potentially plate it if I needed to or depending what was going on.  And so intraoperatively, this was probably the case that has humbled me the most. I spent three hours and I couldn't get the screw out. So you can see that I could back it out.  I backed the screw out a little bit right here, but you can't, but I wasn't able to take this out. I don't know, I'm not sure if it has to do  with the titanium or some other aspect of the metal there, but I wasn't able to take it out. So I ended up having to kind of debris the site and impact graft it.  He ended up healing, so this is at three months, he ended up kind of healing there. As he started to return to play, six months, he fractured again. And so this time I did send,  we sent him to Dr. Anderson to see if he had any additional thoughts or things like that. He had kind of the same plan as me. He spent time trying to remove it, couldn't remove it,  and basically tried to do the same thing where he basically did a bigger debridement, impact grafted it, and we're about a month, we're about six weeks out from him doing that.  And so hopefully he heals. I mean, the problem is in that situation, what are your options? Your options are you can kind of do, you can do a metatarsal osteotomy,  but that's a pretty, that's going to be a pretty morbid procedure if you're doing that to take out the screw. And so our hope is that it heals, but those are kind of things where  it doesn't always quite work out, things you have to be consider, considerate of and things you have to explain to the patient. And then finally,  with regards to postoperative considerations, right? Immobilization, therapy, return to play. We typically keep people off of it for two to four weeks, start getting them,  increasing four to six weeks back into SHU and starting to increase their activities as they become less tender with the hope of returning back to play  in probably about three months, especially in the revision situation is going to be a lot longer than the primary situation. And finally, just some postoperative considerations  using a bone stimulator. You know, certainly there's a lot of, you know, appeal for that. Vitamin D, calcium supplementation, supplementation with things like Forteo  and then custom orthotics to kind of offload the area. And, you know, usually we typically get a CT scan to confirm full office is healing, especially in the revision situations.  And so in conclusion, you know, surgical fixation is recommended in the athletic population, but you know, complications are real.  They include the delay union, non-union and refractures. Every revision case is unique. So we need to consider the biological and mechanical factors and be prepared for that.  And obviously we would recommend full osteosis bridging before returning to play. So thank you.  Thanks, Dr. Tan. Excellent talk. There are some questions that are in the Q&A section. Please continue to type those and we'll try to get to those as best as we can.  I do wanna jump back to Dr. Radwan's case. I did preview it before this talk and I would like him to present his D1 hockey player.  Fernando?  Thank you, I'm here.  So that's her.  This is me. So just remember the case a little bit. So these are the x-rays that the patient had in the beginning.  CT scan showing the postural malfracture.  So I was like, I think this is unstable too. She has pain on the medial mal. So I decided to do arthroscopy on her and then I could check that the synos was really unstable.  I could see the fracture on the back over there. I discussed this case with Miller actually before I went in there. So under arthroscopy view,  I saw that the postural mal was in good position. I put the K-wire from the front to back. When it touched the posterior cortex, I just measured it from the front.  Then I just drove the K-wire all the way through through the back.  You can see here on the right side for us with the image that the head of the screw that is on the back is on the postural lateral side of the tibia right over the fragment.  Then I checked the medial aspect of the ankle. She had the open book description for Jodi Vega. So I put an arthroscopy, I put an ankle over there  to do a medial brostrom, to do a deltoid repair. I tested her synosmosis again. The synosmosis was stable. So that's what I did for her. She was like four months up now.  She's already, well, she's over. The season is over now, but she was able to play some of the playoff games for her team here. So that's what I did for her.  And she was pretty happy. I was happy with this too. I didn't have to fix the synosmosis because after I fixed the posterior mal, it was stable.  And also the deltoid, it was stable enough. So I didn't have to fix it. This is the other, this is the other case from Minnesota that we did a fixation.  So this is the fixation that we did. Same thing. So I fixed this, we fixed the fibula, then fixed the synosmosis. Was still unstable opening here,  especially on the anterior part of the synosmosis was still opening.  Then we did this. And these are the final x-rays on the foot and also the posterior screw on the posterior mal. So that's what was done.  So I would say that take home message for my talk  was like, remember the anatomy, be detailed on a physical exam. Remember the three planes of the stability or the instability. Test the synosmosis all the time during the surgery  and only stop testing after you are sure that it is stable, not stable, stable in all planes. And if you do it right, like the, your ankle will smile to you in the end.  So this is a patient that I did like maybe two months ago and that's it.  Thank you, Fernando. Just to follow up that case, what is your go-to examination of the synosmosis in your preference that you prefer to do?  So for acute cases, for acute injuries, I do like the squeeze test. I do- Oh no, interoperatively. After you fixed it, how do you evaluate your reduction in synosmosis?  I started doing this like a month ago. After I plate the fibula, I put the locking tower of the plate in one of the holes. Usually the hole that I leave open  if I possibly have to fix the synosmosis. And then I use that as a joystick. So then I use that to pull, to do the cognitive test. And I also do the rotational test with the fibula  with the tower of the locking plates. That's what I do.  What if there is no fracture and it appears sports a synosmotic injury, how would you evaluate that?  Then I do the arthroscopy and then I use my fingers to try to do translation of the fibula back and forth. Yeah, no, I think it's still somewhat of a challenge  even with the arthroscope. I know we have some studies to show what quote normal should be, but it's very difficult to tell. Yes. Oftentimes we see these syndesmotic injuries  are somewhat missed. They become a chronic problem and the only result is the anterior pain. When you scope them,  I'm actually gonna steal this from you for a quick second. What do you typically see on the MRI  are these lesions right here. Yeah. I think at one time it was the ring of fire while you talk about, but now it's been over a year or two. This is a 17 year,  I think this was a 17 year old cheerleader that came with this injury from two years ago. And of course you're dealing with the cheerleader and the injury and the injury  and of course you're dealing with the cheerleader who's entering national competitions and then also the dance mom getting her daughter back to work. And you see this right here  in the anterolateral corner here in the arthroscope, what you see is this tissue.  And I'm sure we've all seen it right there. And I think in 2019, there was an interesting presentation at AOFAS annual meeting from our Korean colleagues  saying that simple debridement of this tissue can actually resolve in pain. But typically after debridement, I also do what you do. I actually try to fix it, fix the synesthesmosis  to regain some stability relationship. I'm not sure if there's much out there on that. I just want to share that with you because I think it's highly relevant  to the topic you've been given. Yeah. So these cases are the ones that I, when you do this stability fixation test, like with the taping, it's can be very valuable.  I mean, the pain doesn't get completely better, but the patients say, oh, wait, this feels better. It's not perfect yet, but feels better. And then it's a matter of you decide  whether you're going to fix the,  like the tightrope and the AITFL, or maybe if the AITFL is intact,  we might be able to only fix the AITFL. I mean, you close the back door and then you close the front door. You don't have to close the door to the kitchen  to avoid wind coming through the whole house, you know? So maybe in the future, we're going to do only the AITFL reconstruction and not the tightrope itself, for example.  I don't know. Yeah. There is a anonymous attendee asking a question for Dr. Volcano, I believe. And this is the same question that I have.  I guess for patients with large insertional,  I guess a pump bump,  and there's, is there a concern for persistent pain?  I guess, Dr. Volcano, I would ask you in a different way. Is there still a use for the open option, the open partial calcitectomy,  a tenon debridement and reattachment in your hands?  In my hands exclusively, if the patient already has excellent ankle dorsiflexion, because when you do the Zadig, they will get a lot more.  The overwhelming majority of patients with insertional tendonitis have calf tightness anyway. So that's a very desired outcome of the Zadig.  But I do recall a patient that had excellent flexibility.  And in that case, I decided to go open, but otherwise I absolutely do not care about that large bone spur. I mean, I've done some cases, they were huge.  The second the biomechanics of the tendon improves, the pain is essentially gone. I don't think the spur is the cause of the pain. I think we've been obsessing over this spur  for so many years. And I think it's really time to start looking a little bit more closely at this. I don't think we have to worry about that spur.  Glenn, I'd like to step in for a second.  Ettore, can you hear me? I can. Ettore turned me on to this about four years ago because I've been around long enough that I've had open Haglund's excisions  in people who come back to see me 20, 25 years later for another problem. And I would say, hey, let me take a look at that. How are you doing? And they would be okay, but not great.  I'd x-ray them and I'd see the spur reforming, which made me think that maybe we were doing the wrong operation and that we needed to do something  that biomechanically really changed the load on the tendon. So I started doing these. I don't have 80 like Ettore does, but I have about 50. And he's right.  The first week they come back, the posterior heel pain is gone. The patient will be in the room on the bed with their heel, their posterior heel on the examining bed.  That never happens with an open Haglund's procedure.  And it really works. But my question is Ettore, I have about 20% of these people will get plantar fasciitis.  And I can't figure out why they have it. The posterior heel pain will be gone.  They'll have plantar fasciitis. And I have two of the 50 that say they feel like they're walking on a ball on the bottom of their foot. And those are the only two  that I haven't been able to satisfy. So I just wanted you to comment on plantar fasciitis and plantar pain in the Zadig.  So that's an excellent point. I think the reason they might get the plantar fasciitis is because as you move that posterior tuberosity interior, it does detent the Achilles tendon,  but it does put more tension on the plantar fascia. I'm really not seeing this because when I have patients do physical therapy at two weeks,  I have them work on the plantar fascia as well routinely. And I've always done this from the very beginning because it always was a concern of mine. I always said, okay,  if you're interiorizing the posterior tuberosity, you have to stretch the plantar fascia, which is probably gonna hurt. So I do that routinely  before the patient even develops the problem.  And the plantar spur, yes, that can happen.  If when you rotate the osteotomy, that spur ends up pointing plantar. So that's something that you have to account for when you plan the orientation of the osteotomy.  So before you even make it. So you would make that oblique or straight up and down if there's a big plantar. More oblique, it will bring the spur down less.  I do consent the patients beforehand for possible plantar exostectomy if needed. And if I notice that when I close the osteotomy, the spur points down significantly,  I will just have a low threshold to just go in and shave it down.  Thank you.  Well, it is eight o'clock here Eastern time. I'm gonna hand the show back to Dr. Bailey for final closing comments.  Well, I'd like to thank everyone for their participation and for the questions.  The questions were excellent. We're going to start tomorrow, same bat time, same bat place. And we invite the panelists to also participate tomorrow as well. Julie from AOFAS,  do you have anything you'd like to add as we close?  Everyone would like to look in the chat box. I did upload a couple of slides with CME information  and also with the chair's email addresses. If you have questions, they agreed that they can share their emails with you for any questions after the course.  Okay, thank you.  Is Chris still with us? Chris, do we have anything? Is Chris gone? Okay, I guess we're done. Great, great time tonight. I look forward to seeing you guys and gals tomorrow.  Have a great night.  Bye.

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Asset Subtitle

Moderator: Glenn G. Shi, MD

Syndesmotic Ankle Injuries: “Should I Operate on That? Ever?”
Fernando C. Raduan, MD

Navicular Stress Fracture: Cast, Fix, or Fuse?
Christopher E. Gross, MD

Haglund's/Achilles Tendinosis in the Athlete: What Do I Do With That?
Ettore Vulcano, MD

Jones Fractures: It Didn't Heal, Why? And Now What?
Eric W. Tan, MD

Cases and Discussion

Support for this session is provided by an educational grant from Medline UNITE Foot & Ankle.