Justin and I are really happy to be moderating the trauma session next, and we've got a great group of speakers, and we're excited to bring up Dr. Stewart to talk about some blast injuries in the foot and ankle. Good morning, everyone. I'm Major Sarah Stewart. I'm a military trauma and orthopedic resident based in London, United Kingdom, and I had the pleasure of having our esteemed President, Dr. Chris DiGiovanni, examine my PhD viva last October, and it must have gone okay because not only did he pass me, but he invited me to come and present some of my PhD work today. We have no disclosures, but I do have to issue a warning that there is some basic sciences in my presentation, so I will take it slow. I know it's pretty early still. The Iraq and Afghanistan wars that dominated the first decade of this century saw the advent of what we know as blast warfare, whereas in previous wars, the weaponry that we saw was predominantly ballistic in nature, affecting the chest and abdomen, causing death by that. For the first time in the Iraq and Afghanistan wars, we saw people being maimed and killed from the ground upwards through the use of improvised explosive devices, and I'm sure you're all familiar with the photograph on the right of the lone soldier out ahead of his pack tracking the ground for these IEDs. Because of this new nature of warfare that we saw, it's unsurprising that the number of foot and ankle injuries that came in went up exponentially, with a study showing that almost a quarter of all battlefield trauma cases being related to foot and ankle injuries. Blast trauma can injure and maim and kill through two mechanisms, the dismounting mechanism, where the soldier is on foot, he steps on an IED, and the blast wave propagates up through the foot and ankle and into his body, and these typically are fatal, and if they're not fatal, then the soldier's lucky to get away with a couple of traumatic above-knee amputations. What's more likely to maim and give horrendous injuries to the foot and ankle is the mounted mechanism where the soldier is in a vehicle, the vehicle drives over an IED, detonating a blast wave, which then comes up through the vehicle floor, which then comes up through the vehicle floor, propagating through the foot and ankle, and leading to these type of devastating injuries that we see here on the screen. Horrendous comminuted calcaneal fractures, and a new term was coined for them called the new deck-slap injury, and on the right you see the photograph of the typical type of soft injuries we saw during the conflicts, with large zones of injury, high rates of contamination, and massive chunks of bone missing, and if the soldier was lucky to save his foot and have it salvaged, then many went on to develop nonunium because of the high energy nature of these type of injuries that we saw. So my PhD was looking at whether we can try and mitigate this problem and try and promote healing in these devastating injuries that were coming in thick and fast through the trauma hospitals in Bastion, primarily. So what exactly are blast waves? Blast waves are a subtype of shock wave with a very unique waveform called the Friedlander wave, and the Friedlander wave is illustrated there, and what causes the damage is this initial up flexion of the peak overpressure here, that does the most damage on the battlefield, and that's what's characteristic about a blast wave, and it's typically emitted from explosions such as IED detonations, but also from mines and vehicle explosions. I'm going to deviate slightly and talk briefly about heterotopic ossification, or HO, because it plays in quite importantly into my presentation. So we all know HO is the pathological formation of de novo bone and soft tissue, and as the Iraq and Afghanistan wars progressed, we saw a huge increase in the incidence of soldiers coming in with HO formation, and the one thing they all had in common was they'd been exposed to this massive hit of energy from the blast wave in the battlefield's environment, and a study by Potter et al. actually showed that 64%, up to 64% of blast amputees developed HO, and you can see in that radiograph a soldier with a traumatic above knee amputation a year down the line having developed pretty uncomfortable HO in his stump. So it got us thinking at Imperial College, if HO is a formation of mineralized calcium in soft tissues, osteoblasts lay down mineralized calcium, and osteoblasts are derived from mesenchymal stem cells, is it the blast wave that's driving osteogenic differentiation in the stem cells in the soft tissue? Ultimately, is it the blast wave that's causing this formation of new bone? Therefore, the aim of my work was to basically test that hypothesis and test whether blast waves do indeed possess osteogenic properties, and if they do, could these osteogenic properties be harnessed and used in a therapeutic modality to try and promote healing in these devastating foot and ankle injuries that we were seeing? To test our theory, we took some bone marrow-derived MSCs, which we commercially sourced, and we developed and built a novel tabletop blast tube shown here in the schematic, and it's about yay high. It's fully compact, compact and autoclavable, can be used in an OR theoretically, and it basically produces that Friedlander wave that I described in the earlier slide. The upper section has compressed air driven into it, which is then separated from the lower section by a thin diaphragm sheet, which then ruptures at a given pressure, driving a blast wave down into the MSC cells at the bottom. We exposed the bone marrow MSCs to four blast wave pressures, from 15 psi to 60 psi, and that represents the pressure of that peak overpressure, the front wave of the blast wave. Just to give you context as to how strong we're talking, if you were to put your hand under the blast tube at the 60 psi setting, then it would probably blow your hand off. We also took some control samples, which weren't exposed to the blast wave. Two outcome measures were tested, osteogenic gene expression in the MSCs at 24 hours after blast exposure, testing three genes which correlate with osteoblastic differentiation of MSCs, and also we looked at calcium mineralization in the MSCs at day seven and day 14 post blast. If the MSCs were differentiating into osteoblasts as a result of the blast wave, then they'd lay down new calcium, which we'd be able to test for using a quantum chrome kit. Here are our results. On day... At 24 hours, day one post blast, we saw up-regulation of two of the three genes in the 45 psi test group, which was really encouraging. Interestingly, we didn't see any osteogenic change in the third gene, and these results were reproduced in the calcium mineralization studies at day seven, both in the 45 and 60 psi test group, which was statistically significant with an ANOVA test. Then at day 14, again, this was reproduced, but to a lesser extent. This was very exciting. We all patted each other on the back. We said, fantastic, we've proved our theory that blast waves do possess osteogenic properties and can stimulate MSCs to differentiate into osteoblasts, but that's all well and good, but MSCs are very expensive to buy. Commercially, they can have immunogenic reactions with the recipient. If you want to use them autologously, they're time-consuming to culture, and they're difficult to purify, so not ideal to use in a surgical environment. What can we do instead? So we turned to bone marrow aspirate concentrate, or BMAC, which we've all heard of plenty of in the past day or so. It's easy to obtain, it's autologous, and can be taken at the time of surgery and implanted at that moment, and it's also licensed for use, so it saves a lot of paperwork on our behalf, so we decided to blow that up instead. We took BMAC from three healthy males of a median age of 23, so not that dissimilar to the demographic of patient that we see in the battlefield, and exposed it to a blast wave with a peak overpressure of 50 psi, so in that sweet spot between 45 and 60 that we saw the maximal osteogenic upregulation in the stem cells in the previous in vitro experiment. Our experimental setup was an in vitro, fairly rudimentary setup, but essentially a culture of MSCs, which represent the MSCs in the fracture site, and within that was placed an additional dish of BMAC, and the BMAC dish has a porous base, which allows diffusion of growth factors and cytokines to act on the MSCs, but prevents complete intermixing of the two substances, so it allows us to test the MSCs, knowing that there hasn't been any contamination from the BMAC or interplay. That was our first test group. Our second test group was the addition of BMAC to the MSC culture, but with it having first been blasted in the shock tube, and that BW stands for blast wave, our final test group was the MSCs by themselves without the addition of BMAC, so this represents a fracture where there is no addition of BMAC, blasted or not. And again, we tested calcium immunization in the MSCs at day seven and day 14. Here are our results. Day seven, on the x-axis, you have those three test groups I've just described. The one on the far right is the blasted BMAC. The one on the far left is the control group, just the MSCs alone, and on the y-axis is the calcium immunization assays from the MSCs, normalized as a percentage change to the controls, and we performed a student t-test between each of the groups, and really excitingly, we showed a statistically significant increase in the amount of calcium immunization that was formed, not only from the addition of BMAC to the MSCs, which we were expecting because we know that BMAC does have osteogenic properties, but having blasted BMAC and then putting it into the MSC cultures, that again increases the amount of calcium immunization that we see in the MSCs. Interestingly, we didn't see these results reproduced in day 14, suggesting that whatever effect the blast wave and the BMAC is having on the MSCs occurs in the immediate period following addition to the MSCs. So, in conclusion, foot and ankle injuries represent a major component of blast trauma and the trauma we see in the battlefield, and as long as IEDs are used in conflict, that is likely to continue to be the case, and we need to develop novel strategies to deal with these horrendous injuries that we see amongst our service persons if we want them to salvage their, if we want to salvage their foot and ankle, and this work represents what we think is a really novel and exciting new, potentially interoperative technique we can use to promote healing at the time of definitive surgery through the use of potentially blasting BMAC in this shock tube that we could use in an OR, and potentially promoting union and improving the outcomes in these soldiers. And just to give you an update on where we are at the moment, we're doing larger scale in vitro trials, and we just got funding to convert this to an in vivo model next year. Thank you for listening, and I'd like to acknowledge my co-authors and Professor Calder for his supply of the BMAC in the studies. Thank you very much. Historically, the war of the 20th century has brought us some orthopedic advances, and it's good to see, Dr. Seward, thank you for showing us that maybe the military frustrations of the 21st century can bring us some positive things too, so that was really nice to see. Next up, we have Dr. Kelly Hines on Jones fractures. Good morning, everyone. My name's Kelly Hines. I'm here from the University of Chicago. Really excited to be here as well, though, because I'm also a proud Canadian. Presenting on a very challenging topic, as I'm sure everybody in this room knows, Jones fractures, do they heal without steel? And these are my disclosures. None of them have any direct conflict with what I'll be presenting here. We all know that Jones fractures were described by Robert Jones way back in 1902 when he had a fracture himself. That's not particularly relevant to how we practice medicine right now with the patient in front of us. So what is the problem with these fractures, and why do we keep talking about them? Well, they're actually really common. So fifth metatarsal fractures make up about 50% of all foot fractures, and these happen in really high-performing athletes quite often. And the main challenges that we're often dealing with are the high rate of nonunion as well as refracture. And this is kind of the concept as to why perhaps these don't heal as well as we would like with that watershed area at the metaphyseal aspect of the fifth metatarsal. And the question that seems to keep coming up as I review the literature and try to stay on top of this issue is, is this an athlete versus a non-athlete debate? Much of the literature on Jones fractures does look at professional athletes with much less literature looking at these injuries in the non-athletic population. So maybe it's a question of who should be healed without steel. If the benefit is earlier return to sports, then perhaps we should be thinking more about the operative treatment of athletes. But what about this risk of nonunion, and doesn't every patient want to avoid a nonunion? And that's, I think, where the conflict comes up. Going way back in time to how this problem has been framed, I just wanted to highlight a few of the kind of original work on Jones fractures. Dameron in 1975 described these three zones and found that zones two and three really have more trouble healing. Zone one does seem to heal, so that's really where it all started. And they found that they had a 25% nonunion rate in athletes who were treated nonoperatively. Then in 93, Lawrence and Bodie described these three zones, which are pretty familiar to us. And these really describe zone three as a stress fracture pattern. So our focus here is on the zone two and maybe also zone three fractures. And Max Mahalsky and his group this year really surveyed our population of AOFAS members and found that many of us, 70%, really treat zone two and zone three injuries in a similar fashion. The zones are not to be confused with the types which were described by Torgue in 1984, which are really a chronicity-based classification and mostly in stress fractures of only 34 patients. But we do hear a lot about Torgue's work, and I just wanted to make sure that was clarified. Type two is a delayed union. Type three were nonunion, which were all treated surgically. With type one, or acute injuries, with 90% of those healing. So perhaps there are some of these that can be healed without steel. In 1978, Kavanaugh published a group of patients who had really high rate of delayed union in athletes, 67%, but then 100% union rate with screws. So this was showing some promise. And this is the early work that really frames the problem of Jones fractures that we deal with today. I just put a couple of quotes in of more recent literature of kind of where the consensus seems to be in terms of treatment of Jones fractures in the athletic population. And Dr. Porter, who's here, I'm directly quoting, so please forgive me, but operative treatment with intramedullary screw fixation has become the standard treatment of the Jones fifth metatarsal fracture in the competitive athlete. And then a systematic review from 2015 by Yates, their conclusion was that surgical intervention is recommended for patients presenting with a Jones fracture, as it's found to result in a lesser nonunion rate and improved time to union. So that's kind of where we are in the literature, looking at Jones fractures specifically in athletes. Then we have to consider patient factors. The patients in front of you, they're not all the same, and so all Jones fractures don't behave the same as well. And there are some anatomic risk factors that have been found in multiple studies trying to understand this problem, that averus hind foot, metatarsus adductus, pes cavus, and even some characteristics of the shape of the fifth metatarsal itself can be risk factors for having a Jones fracture. And Dr. Raken looked at their group of patients with Jones fractures in 2008 and found that a vast majority of them had averus hind foot. So just further highlighting that aspect of the patient's anatomy that may be putting them at higher risk. And then when you're evaluating the patient, you want to think about not just the fracture pattern, but who is the patient and what is their activity level, and basically what shoe wear they're wearing as well. So narrow, flexible shoes can be a higher risk for developing these fractures, especially when they're wearing these types of shoes for sport. And then considering vitamin D deficiency. So up to 50% of Division I athletes, especially higher in African American population, have vitamin D deficiency, and it's important to consider this. Our literature on Jones fractures, though, doesn't talk very much about optimizing patients non-operatively. And so if non-operative treatment's chosen, how do we do it? And that's even a topic of debate. There's been several studies, mostly retrospective, looking at non-weight bearing versus weight bearing, non-operative treatment of Jones fractures. And really, the outcomes are pretty similar, although the traditional treatment is this kind of protocol of four to six weeks of non-weight bearing, followed by an additional four to six weeks in a boot, taking three to five months to get back to sports. The results in the literature are very, very mixed of non-operative treatment of Jones fractures, and I think that's why this question is very difficult to answer. The non-union rates range from 11% to 50% with a very variable group of protocols. The most optimistic research on non-operative treatment of non-athletes is a 82.4% union with non-weight bearing, and up to 100% union with weight bearing. But again, very variable, so hard to make conclusions. The results of non-operative treatment, if you take all the literature that's been published on this in average, most of it being retrospective, the average rate of primary healing is 75%. It possibly has an increased risk of poor outcomes if you treat these patients with non-weight bearing, with one study by Borlat. And then another group, Bigsby and their group, looked at all the patients with fifth metatarsal fractures of all types, and found that many of these patients are still symptomatic at one year. The surgical anatomy, about 52 millimeters or 68% of fifth metatarsal is straight, and the average diameter's five millimeters. If you're going to do surgery, the goal is to increase the rate of union and minimize the risk of refracture. You want to accelerate the patient's rehabilitation and treat chronic or stress fractures if they're presenting that way. And the goal is also to place the largest diameter screw that will fit. Strength selection can also be a challenge, so there are many anatomic variations, and you want to also avoid cortical perforation, which may cause, a longer screw may also cause fracture gapping. Breadths need to be across the fracture, and there's still many techniques being worked on to improve the fixation methods for these fractures. Because surgery is not a perfect solution, there are risk of complications, and some revisions will be required. A broken fifth metatarsal screw can be a challenging problem to deal with, and then most literature on looking at the outcomes of screw fixation has been in professional athletes with relatively high union rates, but also not an insignificant number of re-fractures. The goal of faster return to sport does seem to have been achieved though by treating these fractures operatively. Plates have been looked at, but implant prominence and stress fractures at the end of the plate are a concern. These can be considered for atypical fractures, revisions, or displaced zone 1 fractures. And then getting to the end here, but if you're going to revise the surgical treatment of a Jones fracture, there are many considerations. Patient's foot shapes, are you treating a cavus foot and trying to get it to heal in a poor mechanical situation? Is the screw bending, breaking, or backing out? Do you need to consider some biological adjunct to help with healing or bone grafting? And is there an optimizing of the screw size or diameter that may be done? Some advocate for a CT before a return to play in elite athletes after revision, and there are some discussions around bone stimulators or even further delaying weight bearing. In summary, athletes in general have a faster return to play and a lower non-union rate with surgical treatment, although revision is sometimes necessary and recurrent fractures are a reality. I'm not sure what to say about non-athletes. I wish I could have answered this question better. A high number of patients will heal, but I think having a very patient-centered discussion about the risk of non-union and refracture is important. And based on the literature, it does not seem wrong to operate on non-athletes with a Jones fracture as long as they are understanding and willing to accept the risks of surgery. In summary, the robust literature on non-athletes is just lacking. The rate of non-union is likely higher in athletes due to the activities they participate in, and the rates of union are higher with surgery. And if the patient's goal is to return to sport sooner, it's worthwhile discussing surgical management. Thank you so much. All right. Thank you, Dr. Einz. That was fantastic. So we'll switch gears here to another controversial topic and discuss syndesmosis with Dr. Lin. Thank you so much. I want to thank Dr. Humberg and Dr. Gauss for allowing me the opportunity. Let's see. And basically, we all fix ankle fractures. And the question really is, for the syndesmotic injury, how can we reliably fix it if you don't have an intra-op CT machine? Here's my financial disclosures. There's none. We all know the clinical importance of the syndesmosis. Basically, we've learned that, of course, one millimeter lateral displacement of the talus will decrease the tibial-talar contact forces and increase surface area by 42 percent. And therefore, when you look at this X-ray and you look at the tib-fib clear space, the tib-fib overlap, and, of course, symmetry of the superior medial and lateral joint space, these are classic findings. And when you look at this picture, you go, oh, it's obvious. You know, the clear space is wide. There's no overlap. The talocrural angle is malaligned. This, you know, you know it's disrupted. And yet, this, you don't need a CT. But sometimes, it's useful. If you look at this X-ray, like, that looks reasonable. But then you get this CAT scan, axial view, you realize that, yes, the syndesmosis is malaligned and is disrupted. And therefore, it's very useful for a CT scanner to be used preoperatively for these subtle ligamentous injuries. One can also get an MRI. An MRI can really show you very nicely, let's say, the AITFL and the PITFL in a non-invasive matter. A little expensive, but, again, non-invasive matter. Now, one of the other great tools you can do before and think about is an arthroscopic stress test. I mean, basically, doing the drive-through, you can see here how it shows you the ability to detect these syndesmotic injuries. But to me, the real question is, I'm in the OR, and we're all fixing ankle fractures, and we ask ourselves, I don't have that intra-op CT machine. How can I avoid the problem? And here's the example. You look at this, you realize there's something wrong. There's asymmetry of the anterior measurement and the posterior measurement. And basically, I look at this X-ray, one of mine, I go, that looks great. And then I got a CAT scan. I go, maybe not so great. What did I do wrong? And this is the key question we're trying to learn. You know, Frankie talked to us and told us back in 2012 how the role of the intra-op 3D imaging machine, and in his series, 32.7% altered the surgical outcomes in 82 ankles. And basically, the major problem was, of course, this anterior subluxation or malalignment. Well, how do we fix it? You know, I'll be honest with you. My hospital, we're not that rich. We don't have an intra-op CT, and nor do I want to spend the time and waste the time. Well, folks, this is what we're trying to avoid. We're trying to avoid this malreduction of the fibula sitting in the incisor fibularis. And we know the anatomy does play a major role. So with this in mind, let's look at some of the tricks. One thing we know, time placement is a critical issue. And you could place it so it gives internal rotation and posterior translation, or the opposite, external rotation with anterior translation. The secret, this article that came out back in 2017, placed the medial tine in the anterior one-third. Cosgrove told us and taught us that by placing the medial tine in the anterior one-third of the tibia, there was 0% of malreduction. And this is what he showed in his picture. By placing that medial tine, you can put the lateral tine into the fibular plate. By placing that medial tine in the anterior one-third, their data showed the various parameters of really minimal malreduction. So here's a good example. Again, I believe in mud and chicken wire. If you place that medial tine interop, you can avoid a lot of the headaches. And here's an example. You basically place the medial tine, you're on the lateral side, and then you can make posterior to your vebraclamp the subsequent placement of the syndesmotic, whether it be suture or screw fixation. The other method, of course, we were taught, I was taught to really look at the incisor fibularis, look at how the fibular fits, that anterior view. Well, recently, Tornetta came out this concept of doing direct visualization through the articular method. This article in JLT 2019 taught us the critical role of looking at the joint itself. You can see from the red lines here how you have the malreduction. By then dorsiflexion and looking at how the fibula aligns with that anterior lateral tibia, you will get subsequent anatomic reduction. They looked at various parameters, compared this technique versus the traditional anterior incisor visualization, as shown here. The malalignment distance was minimal by doing that direct visualization articular technique compared to the anterior incisor technique. So again, yes, you have to peel the soft tissue, yes, you have to look at the front, but by doing that, you can minimize the malalignment. And they showed by these two parameters how there is minimal malalignment by doing the direct articular visualization technique. So again, I'd like to show it one more time. If you look at the red lines, by dorsiflexing and aligning the fibula, you can see how it anatomically fits and keys in, instead of doing that anterior. Now, I was sitting and having dinner with Dr. Lyndon Mason, and I realized, talking to him, there is one more trick, and that is consideration of fixation of the posterior malleolus. From their article of Mason Malloy, they talk about types 1, types 2A, types 2B, and types 3 of posterior malleolus. And basically, in their article, they describe different methods of fixation. When you think about it, the posterior mal is attached to the PITFL, and they talked about the guiding the treatment. But the one thing I want to point out, and for those who really love fixing the posterior mal, be careful of the 2B, because the 2B is when you have to fix that posterior medial fragment before you do the P to A posterior mal, otherwise you'll get a malalignment. But regardless, the whole point is this. In my question, in my mind, does fixation of the posterior mal improve the syndesmotic alignment, and therefore, its overall correct appearance? And basically, the articles by Gardner have given some insight. They've shown how by doing the posterior mal fixation, the stiffness of the ankle restored to 70%, in contrast to only 40% with just simple screw fixation. And another article, again by Mason Malloy, they looked at patients improving their outcomes. By fixation of the posterior mal, they were able to show a better functional outcome score. Now, it didn't become statistically significant, but the trend was there. So what I'm trying to say is this, folks. You're in the OR, you're trying to fix it, you don't have an intra-op CT machine, what are the methods? Well, we talked about placing the medial tine in the anterior one-third. Number two, using that technique espoused by Tornetta, looking at the direct articular articulation between the tib and the fib. And thirdly, consider fixing the posterior mal. By the PITFL, it's going to pull the fibula into a more anatomic alignment, and therefore, these are the tricks for synesthematic fixation. And thank you. At the start of the 20th century, Dr. Cotton said, the man with a calcaneus fracture is ruined, or something like that. So let's see what happens in the 21st century. Dr. Kwan, please. So I'd like to thank the organizers of this meeting for the opportunity to speak this morning. Dr. Christy Giovanni for his mentorship, and Dr. Greisberg for encouraging me to give a little bit of a different talk than we normally hear at these meetings about calcaneus fractures. All right, so these are my disclosures. So our treatment of calcaneus fractures has certainly been an evolution. Plato said that necessity is the mother of innovation, and we've certainly had to innovate over the years to better take care of these patients with these really tough injuries. Now, we started with initial just cast immunization, and then over time, there were different treatments such as closed manipulation, traction, and percutaneous techniques were really the start of surgical treatment, and then we went on to open reduction internal fixation. Now, over the past two decades, we certainly have developed safer and smaller incisions. We've had advances in not only our preoperative imaging, but our intraoperative imaging. We've developed ways to better obtain reduction using arthroscopes and different types of percutaneous techniques, and our plates and screws have certainly gotten better. But where do we go from here? So I think some of you see a sunrise, and some of you see a sunset, and it's really hard to tell what we're looking at. And so are we approaching the twilight of our innovation for calcaneus fractures, or are we approaching the dawn of a new day? So what about implants? You know, there certainly have been advances in materials, anatomic contouring, polyaxial locking instrumentation. There have been some developments of some interesting intramedullary locking nails. But really, our implants today are derivative of rudimentary lateral plating from decades ago. So I'll make the argument that I don't think implants are going to change how we treat calcaneus fractures moving forward. What about approaches? Many of us have adopted the sinus tarsae approach. Many still use the extensolateral approach, and I'll make an argument that we have to use both. But our approaches are really dictated by the fracture patterns, the surrounding anatomy, and our understanding of the angiosomes. So I don't think that there's going to be an innovative new incision that we use to treat calcaneus fractures. We did a survey study of 50 foot and ankle surgeons, and these were high-volume surgeons who treated, on average, two or three calcaneus fractures a month. And we asked them, from the start of their practice, what was the single aspect of their surgical management that changed the most, and it was incisions. So I do think many of us are going to smaller and safer incisions. What about timing of surgery? Dr. Gus and I did a multicenter study looking at timing as it regards to time from injury to time to surgery. And what we found is that if you do the sinus tarsae approach, if you operate earlier, it's probably safer for the patients. And there's some cooperative studies in other journals that have looked at this. Again, when we polled our surgeons and we asked them, from the start of your practice to now, what have you done? And the large majority have started to operate earlier, and we know that this is, depending on the incision, safer. What about super subspecializing? Is this where we go into the 21st century? There are studies that show that the more you do, or the more your institution does, the lower your complication rate. But this is true across orthopedics and any complex injuries, but this isn't practical. It's not practical to have just a handful of surgeons treating these difficult injuries, as we all have to take care of these patients in our community. So where do we go in the 21st century? I think that where we go is we start letting go of some of the traditional beliefs that we have, and I'm going to focus on the reliance on level one evidence and the dogma of our learning curve. And so this is a really silly slide. I showed this to my six-year-old, but I think it's really intuitive that if you bend your rim on your mountain bike, if you're able to straighten it out and not damage your bike further by repairing it, it's going to function better than if you leave the rim bent. And so this is intuitively true, but then the question becomes, why are our level one studies not showing what we know to be intuitively true? So you can draw two conclusions. One is logical, and one isn't. But you can draw a conclusion that the calcaneal morphology doesn't matter. So this beautiful structure with multiple sets angulated tangentially, it doesn't matter if it looks like that or if it's malunited, wide, and invarious. And that doesn't make a lot of sense. So the second conclusion is that our studies are flawed. We're all familiar with Buckley's study from 2002, where they looked at 500 calcaneus fractures and found no difference with the VAS and the SF36. And of course, when we looked at subgroup analysis, there were a population of patients that did do better with ORAF. But you can make an argument that maybe the pendulum swung back a little bit to non-operative treatment in 2002. Well, we know the devils are in the details, and the non-operatively treated group developed arthritis requiring a subtalar arthrodesis five and a half times the operatively treated group. And this was taken out of the analysis. This wasn't just mildly symptomatic or radiographic arthritis. These patients were doing so poorly that they required a fusion. There was a lot of bivariate analysis, which could lead to significance by chance. And even though a 25% loss to follow-up isn't terrible in these large trauma series, you can make an argument that this was a single-surgeon series, where many surgeons contributed to just one or two cases. And some of these things that we always juggle in our minds on rounds, smoking, diabetes, substance abuse, were not critically examined in this work. Well, how about this level one study? It was done a little bit better. They had the AOFAS Heinfitz score. They used post-operative CT scan. And while they did find that operative intervention was somewhat protective for subtalar arthritis, they found no difference at one year. So aside from being underpowered and having some other problems with this study, you can make an argument that this study was comparing non-operative treatment to poorly done operative treatment. Now, we know these fractures are very difficult to treat. But 36% in this group essentially were malunited after RAF. And so this is, in fact, combining the worst of operative and non-operative treatment. Now, these studies are very hard to perform, and they're costly. And those that have pursued this are certainly saints in our field, because we know how difficult these studies can be to perform. You know, but the question really becomes, can we truly perform a level one randomized study? These two patients who have Sanders II calcaneus fractures, can we randomize that patient on the right to non-operative treatment? You know, we have an ethical and personal obligation to our patients who come into our office very well informed, even before we discuss treatment options. And so one of the things that we certainly face as we move forward is attrition bias, where patients simply refuse to be randomized to one treatment arm or another. There's different approaches, different techniques, different skills. And if you're thinking about building this level one study, how we need to do it, there's increased granularity of the methodology. And so as you do that, that creates even more of a power problem in an uncommon injury. The second thing that I think that we need to think a little bit more about is this dogma of the learning curve. And so I've had the opportunity to talk about calcaneus fractures on occasion. And one of the questions I always get asked is, well, do you need to learn how to do the extensile approach? How many do I need to do before I learn the sinus tarsie approach? And I think the argument set forward is twofold, that one, there's this thought that you have to learn fracture reduction through direct means to be able to do it indirectly. But more fundamentally, that you need to do it open to have a better conceptual understanding of the fracture pattern before you can use less invasive approaches. And I simply don't think this is true. You know, many of our trainees have never done an open rotator cuff repair, right? And it's arthroscopic, or we look at other examples in orthopedics, ACL surgery. There's percutaneous pelvic fixation surgery, that if you understand the pathoanatomy and you understand how to navigate in the OR, you can treat these injuries without quote-unquote learning the old ways. So I do think that for those of us treating calcaneus fractures, you have to know less invasive approaches. You have to know how to do an extensile lateral approach. Use all your tools that you have in the OR, and learn how to use medial and lateral combined approaches. And I think our patients will benefit from that. So moving forward in the 21st century, I think we need to release some of our past dogma. We need to capture what's beautiful in all our advancements in the present, and embrace the morning here talking about another controversial subject from the closet fuser himself, Dr. Coetzee. Thank you very much. I initially thought it's a little weird to ask me to talk about not fusing, but let's do that. First, if you think about classifications, I wish I was like Steve had that can beat you into submission with great data about polyethylene wear, but this is not polyethylene. This is complex, so you need to think a little bit more than when you do a total ankle replacement. Also, if you think about classifications for less frank injuries, I don't think there's a single classification that works because it is a very complex injury that can go over multiple joints. To use non-Lean-Vertulo or whatever Meyerson classification is helpful to some degree, but not much. My classification now only has two members in it. The one that I show you there that is not too bad and bad. It's as simple as that. The bad ones you fuse and the ones that are not too bad, you can think about other options. Specifically for this talk is how do you treat this one? It's obviously in that category that's not too bad, so you don't have to think right away about a fusion. It's also interesting with my own practice. I don't do level one trauma anymore, so for better or worse I see fewer of the really bad ones and I saw more of the not too bad ones with sports injuries. I thought I would try to do a literature example of how to deal with this, but just in the last two years there were more than 64 articles on less frank, so it's more than five a month. You can basically find in the literature whatever you believe in, instead of looking at individually and try to come up with your own plan. These are the options. You can either do a primary fusion for that one or do an open reduction fixation with a bridge plate. I think both might do okay. How do I decide? I think this is very important if you deal with less franks is to stress every single one of them. We are lucky to have a fluoroscope in the clinic, so I can take all of them and stress them and decide how unstable I think they are and that will help me. Also, you really have to think about the anatomy. Less frank ligament itself can be very complex. I don't do MRIs for the bad ones. They are dislocated. It's easy, but for the not too bad ones I do an MRI on probably all of them because I want to see what the ligament structures are and what is involved in the injury because if you think about some people have a single interosseous ligament. Some people have a dorsal muddle and a plantar one and depending upon what is torn it will tell you what the instability factor is. This is an important study also by Carr. If you just think very simple about transverse and longitudinal instabilities, you get a transverse instability with sectioning of your less frank ligament, but then also the plantar ligaments between cuneiform one and metatarsal two and three and longitudinal instability with sectioning of the less frank ligament and then the interosseous ligament between C1 and C2. This is I think one of the more important conclusions of that study that manual stress x-rays show a greater displacement compared to weight-bearing x-rays. Try to manually stress all of these and it will give you some a better idea of where you are. So when not to treat surgically, obviously people with open growth plates and then the mild grade one less frank sprains where there's no or minimal displacement on weight-bearing x-rays and stress testing or if you do an MRI and it's an incomplete injury of the less frank ligament. So you can let go and treat them non-surgically. So in my mind when not to fuse the longitudinal injuries, grade two injuries if there's mild or moderate instability and then potentially in younger people, but again that depends on the injury pattern. If it's a bad one then I still think you can fuse it even in young people and interestingly with people with significant flexible flat feet I think you should be careful in fusing because again with my patient population with a lot of ballerinas and gymnasts they have to be flexible through their midfoot. So if you fuse them it's unlikely that they will return to their sport. Well if you have somebody with a cavus foot they already essentially fused. There's no movement so those you can fuse without thinking too much about it because you just bring them back to baseline. If you leave them unstable through the midfoot then they will do worse than what they would have done with a fusion. So again I'm not going to show you a lot of literature. This will be a little bit of nuance because I think less frank is nuance, it's not dogma. So this is a 17 year old female gymnast. She injured herself at dismount and you can see looks like a longitudinal injury with widening of the less frank space, but then if you look closely there's also an avulsion of the medial cuneiform. So that should make you think that there's a first TMT joint involvement as well. So always do an MRI and that basically confirms both that there's an avulsion at the medial side of the first TMT joint, but then also a less frank ligament injury. Test them and then do a fixation of what's unstable. So stabilize the medial column followed by less frank. Question can be where do you put your hardware? I do my best not to do trans-articular screws anymore because if you decide not to fuse then you don't want to do it across the joint except the less frank screw. You can theoretically put the plate dorsal as well, but I like the medial plate because it gives me transfer stability as well as longitudinal stability and then I can use my less frank screw through the plate which just makes it easier to remove later on. So this is an NFL linebacker. He had a great one, the less frank, that was not really unstable. When I tested him he missed four weeks and then returned to play and he did okay but not great. So about four months later we tested him again and now he was more unstable even though we could play it just was not great. So even though it's four months later then you still do an MRI, less frank is torn, but if you look at the right hand slide there's a plantar ligament between the medial cuneiform and probably the third cuneiform that's intact and I think that's why this was not obviously unstable to start with. Then interoperative, that typical longitudinal less frank injury and fixed him with a medial plate and two screws and he's still playing and so far he licked it not to have it removed. So I'm a closet fuser in that case. So 16 year old with a grade 2 instability. Question is how do you mobilize? I don't think you should use screws alone. And then which joints? Again this is a combination of a transverse and a longitudinal instabilities you have to deal with both. And then first do the medial column because it was longitudinal between medial cuneiform and middle cuneiform. I used that screw to immobilize that joint as well and then finally the less frank screw. And also important if you do an open reduction you should not compress the joint. You just should reduce the joint because you do not want to cause chondrolysis by compression over the first dorsal metasal joint. Sometimes you see these combination of instabilities. In this case it's clearly a longitudinal instability but then also a transverse instability with the second metasal sliding laterally on the middle cuneiform. With this one with testing there's no instability of the first dorsal metasal joint. Again that's the nuance of less frank. You really have to test them and see what is unstable and only treat what is unstable and not just do the same thing for everybody. So in this case immobilized the second dorsal metasal joint first and then the longitudinal instability and did not need to do anything for the first dorsal metasal joint. There is however a note of caution with these not too bad ones where you decide to do an open reduction. I still think you need to remove the hardware. That's debatable but that's how I do it and I think it's correct. But this was a garden variety longitudinal instability so it might do screws for it that fine and then when we remove the hardware that screw was broken while it was not broken two weeks before when I saw for a preoperative visit. So it happens we all know it happens but what do you tell this patient? Do you say okay this is just what happens we know some of these screws will break and it's not going to be an issue. Sometimes that's true but this is two months later so that's already wide. So even in the ones that you do not fuse you have to accept that there will be a percentage of them that will be unstable afterwards and you need to relay that message to the patients that even in these longitudinal ones that I routinely do not fuse that you might have to go back later and fuse. This was another longitudinal Lisfranc. You can see dislocated in two joints. Same idea you fix what's unstable. I do not put a screw across the navicular cuneiform joint. I don't think it's necessary and that's the one joint that you really want some movement in. But the same thing there's a screw that's broken so theoretically down the road this might be an issue. So in conclusion there are hundreds of articles about Lisfranc injuries and most of them patients do well. So again you can read whatever you want and follow that. I think you have to think about Lisfranc and develop your own system for it. This was back in 2013. I don't think it's much different now. Non-displaced injuries will do well with non-cytical care. Displaced injuries warrant an open reduction. Should be anatomic. At that point the evidence supports screws. I think now it will be bridge plating and not transarticular screws. And if it's a severe injury it is a severe injury but these people can return to sports. If it's a severe injury they might do better with a primary limited fusion. Very important not all Lisfranc injuries are equal. So you need to examine everyone individually and make a plan for that individual patient. Less severe injuries open reduction. Consider extra articular fixation. Severe injuries might still need a limited fusion. Thank you. Thank you to all five of our speakers for making really great talks and staying on time. Equally important both of them. We have a few minutes for questions if people from the audience want to make their way up to those microphones in the middle of the room. I'm going to start out while you guys are all getting ready for questions with an easy one for our whole panel including my co-moderator Tom. So Dr. Kwan raised some really good questions. How do we do surgical research? How do we know if what we're doing as surgeons is actually good or right whatever that means? With medical research one treatment arm might be giving a patient a pill and everybody in that arm gets the same pill. With surgical treatment studies my surgery might not be as good as Tom's surgery. So how do we do surgery? Should we have multi-center studies? That's kind of our gold standard. Or is a study better to be a single surgeon study which shows how surgery does the way I do it assuming I do it the same every time. It takes a lot of intrinsic confidence to publish single surgeon data. You know that study the famous one from JBS on calcaneus fractures comparing op to non-op with Dr. Buckley and his colleagues. It's mostly Dr. Buckley. So is our conclusion that calcaneus fracture surgery is not better than non-op or that surgery by Dr. Buckley is not better than non-op? That takes a big level of confidence and ego to put that question out there. So panel how do we do surgery research? Easy question guys. I can start with some of my thoughts. I think that one of the inherent problems that we have is for uncommon injuries. In order to get a study that is adequately powered you need to do it multi-center. So multi-center inherently involves more surgeons and that if you include a lot of surgeons you'll get your numbers higher but you'll have maybe less experienced surgeons so you have to try to tease through less experienced surgeons treating very difficult pathology. If you have at these different centers just a handful of very experienced surgeons treating these injuries then of course the question becomes of translatability and generalizability of the of the of the results. So I certainly didn't answer your question but just introducing some other thoughts. You know I think the key thing is folks you have to be honest with yourself and one of the key things that really has always shocked me is after we do an RA of calcaneus we get a CAT scan. Did you reduce your articular surface? Therefore did you do the job and therefore when you're gonna do these studies you can compare apples to oranges. So in our institution the trauma center you do a femur fracture you get a CT scan of graying mechanical axis and leg lengths. You're going to learn each time you do this did you achieve what you're supposed to achieve? Now be honest and therefore if it's off like that you're saying 26% of that one study was off or badly done you'll learn and that's the best way. Whether it's a single surgeon or multi-surgeon did you do what you're supposed to do? That's great guys. Let's go to some questions from the group. We have Mike one I can't see who's over there. Yep Kevin Martin Ohio State. So I had a question about calcaneus fractures. So we've been taking Sanders threes and fours and acutely fusing them. Is there a role for acute fusion? Joe Hsu had that good paper this year talking about it. Do you think there's a role for that? And then we've been doing them arthroscopically trying to reduce injury to the angiozones that you described. Is there an opinion of the panel? Are we doing this right? Yeah that's a great point. The truth is is that certainly has vexed me because we're all practiced we're all you know obligated to practice evidence-based medicine and Buckley did a level one study looking at threes and fours and there wasn't a difference in fusion versus RAF. But we all have treated individual patients where we know they do really well if we fuse them right off the bat. I was part of this panel we're discussing calcaneus fractures and it was probably the first time I thought about myself and if I had about calcaneus fracture what would I want? And I'd want to RAF with a primary subtalar fusion. Just a comment about Buckley with all due respect to Buckley and his co-workers that study has been questioned many times. So I think you have to that was 2002 whatever we're 22 now. So I think a primary fusion is a good thing and I still lean towards fixing calcaneal fractures and not treat them non-surgically. Mic number three. Hello this is Emilio Wagner from Santiago Chile. A question for Chris. Chris we do many sports injuries about the least frank joint and when you have an instability in between c1 and m1 and c2 and m2 we first start with the screw the least frank screw which goes from c1 and m2 and then magically the first ray instability goes away. So I would like to know your opinion because we first start with the least frank screw and then we don't need to do anything with c1 m1. I would like to know your opinion. Yeah Emilio thanks that's a that's interesting. I think that sometimes happens but again that's why I do an MRI on these not too bad injuries because I want to see if there's ligamentous instability around first tassel and I maybe err a little bit more towards fixing first tmt as well because I do not want them to end up with the first tmt instability. But if you do that home run screw and it's stable I suppose you can leave it there. I just don't think there's much morbidity in immobilizing first tmt at the same time. We've got time for one more question number four. For Chris Coetzee, Nick Abiti from California. Hey Chris I know you're not a closet internal brace user. Why aren't you using internal brace for the least frank with the simple construct like Eric Giza's or the fold over construct? That way you can leave it in place and nothing breaks. I got away from the plates for that reason had it go back second time and now that I switched over to that Eric Giza technique with the internal brace I don't take anything out. Again it's sometimes personal experience. I've taken a few internal braces out for less frank and we actually saw one this week again so I think if you're an internal bracer for less frank you need to know how to fix it and what you fix and make sure that you immobilize all the instabilities. I'm a big internal brace user but this is one place where I don't use it. I think maybe I'm too old. The young guys can experiment with that. I take my spot at the podium to plead that we need that's a great topic for a prospective study to look at whether suture fixation for less frank can be adequate. I think we're pretty much running out of time so thank you our panelists doing a great job and thanks everybody for coming today.

trauma

blast injuries

calcaneus fractures

surgical treatment

diagnosis

imaging techniques

treatment planning

individualized treatment

patient factors