All right, I think we're ready to start our afternoon session. I think that was a great lunch. So our next speaker is Eileen Crawford from the University of Michigan, and she'll speak to us about leg and ankle. Thank you. All right, thank you. Good afternoon. It's great to be here, part of this course here. So these are my disclosures also, President, and your binders. So as part of this review course, my objective will be to cover the breadth of topics for the leg and ankle, relevant both to taking the exam and to your normal practice. And then we'll divide it up into these five sections, going through some questions at the end of each section. So for time's sake, the slides are intended to have kind of all the information you need so that you can go back, use it as a separate set of slides that you can review or even closer to the test. So as you're resting and digesting after lunch now and you find your attention waning, don't worry at all, be in there, but I'll go through what we can to get through in the time allotted. If there are any topics that I don't cover, please provide that in the feedback since this will be my first year going through it all. All right, so we'll start with fractures. Tibial shaft fractures are often athletic injuries. About 25% of them occur during sports participation and they have the longest return to sport time for the sports-related fractures. Non-operative treatments appropriate for non-displaced fractures, but that's rarely going to be the case, usually in your pediatric patients. If you do have one that's appropriate for non-operative treatment, you're going to be looking at a long leg cast, but you can convert to a patellar tendon bearing brace like the one shown in this picture here once some early healing is established. Treatment, if you do it non-operative, requires frequent monitoring, so that means weekly x-rays to make sure that you don't lose any displacement or develop any displacement in the first few weeks. Operative treatment is going to be most often intramedullary nailing, but don't forget you do have alternative options here, especially plating, which avoids trauma of going through the knee joint with the intramedullary nail. And then if you have any open fractures, you're going to be looking at external fixation for definitive treatment or for provisional treatment more likely. So here's a look at some of the return of sport rates for tibial shaft fractures. This is a systematic review by Robertson and Wood that was in sports health in 2016. The return to sports rates were much higher with surgery than non-operative treatment as expected, with more than 90% returning to sport and 75% to the pre-injury level of sport, but it takes a long time. It's still 40 weeks. That's like nine months before you can get back to full sports participation. ORF with plate and screws did have a higher return to sport rate than intramedullary nail in this study, but the overall return to sport rate was longer. So there's some pros and cons. The open fractures and fractures with higher soft tissue injury, as indicated by the higher surety grade, was associated with a decreased return to sport. So some testable points related to tibial shaft fractures. Always you need to be thinking about compartment syndrome before, during, and after surgical treatment for these. If you see a spiral distal third tibial shaft fracture, that warrants getting a CT because there's a high chance that that spiral can go all the way down to the plafond and create a posterior malleolar fracture that may not show up very well on the x-rays. The evidence for reamed versus unreamed nails suggest that reaming may be better for closed tibial shaft fractures in terms of decreasing the need for a future bone grafting or exchange nailing. And then if you're thinking about thermal necrosis or see any questions on this, the risk of thermal necrosis is related to the size of the reamer you're using compared to the size of the isthmus. It's not related to reaming with the tourniquet up. Chronic anterior knee pain is common after intramedullary nailing, something that should be discussed with your preoperative complication discussion. And then if you get any questions about BMP, it may be useful in open fractures, and that's BMP2, that's the helpful one, and in non-unions, it would be BMP7. All right, tibial plafond fractures are high-energy fractures. You're not going to see them very often with sports, but you may see them some more in the extreme sports. An X-fix is usually needed to stabilize the fracture until that soft tissue subsides before you can move on to definitive treatment. Arthroscopic-assisted fixation has been described, which can be very nice for seeing the articular surface, making sure you get an anatomic reduction. But you still have to do all this hardware here, so you're not getting very far with the arthroscopic portion of it. All right, now moving on to ankle fractures. So starting just with a little biomechanics, the ankle is a modified hinge joint, it has motion in all three planes. The tibial tailor joint is inherently stable given its bony morphology. And then the lateral malleolus and the syndesmotic ligaments contribute to that stability, but also they allow a widening of the intramalleolar distance through gait. So if you have problems like heterotopic ossification of the syndesmosis that can come with trauma, that can cause problems with that normal dynamic motion of the joint through your gait, and it can lead to problems with pain and limited range of motion. So here's a review of the most commonly used classification systems we see for ankle fractures. The Deni-Weber classification is for lateral malleolar fractures. Just to remind you, Deni-Weber A is a fractured distal to the tibial tailor joint line, B is at the level of the tibial tailor joint line, and C is proximal to the joint. More proximal injuries associated with higher risk of syndesmotic injury and resulting ankle instability. The Lowy-Hanson classification covers all the muni, bi, and trimalleolar fractures. This, what I have here, is a simplification of the overall classification. It doesn't have all the ligamentous injuries that are part of it as well. But this part can be useful when you're looking at x-rays and trying to decide what type of fracture it is. The full description includes all those ligaments and things like, if you have a deltoid ligament as opposed to a medial malleolar fracture, which would be the equivalent. So we've got supination external rotation, which is typically a transverse medial malleolus fracture, short oblique fibula. And it may have a posterior malleolus fracture. Your pronation external rotation, this one here. Transverse medial malleolus, high short oblique or spiral fibula fracture, and it may have posterior malleolar fracture as well. The pronation abduction is a transverse medial malleolus fracture, and then a transverse recombinant fibular fracture. And then your supination adduction injuries, which that's that classic vertical medial malleolus fracture, and more commonly, a distal fibular avulsion. So for your lateral malleolus fractures, RAF is indicated when you have displacement more than two to four millimeters, shortening, or rotational malalignment. You have to restore that normal fibular length in order to get normal symptomatic function. You can measure that length with the talocrural angle, this measurement seen over here. Normal is about 83 plus or minus four degrees there. Another measurement that people often use will be the dime sign where you're looking more, it's a little hard to see here, but looking for the normal round articulation there of the distal fibula with the lateral talus. The Weber A fractures usually can be treated, they're usually minimally displaced and can be treated non-operatively. If you do need to treat it surgically, something like this four or five screw over here up the fibula is one option. The Weber B fractures are often best treated with an anti-glide plate because of their obliquity and where they're located. And then for Weber C, you're usually gonna do a lag screw and a lateral plate or a bridging plate if you have a lot of comminution. One third tubular plate is fine, you can use the LC, 3-5-LCADCP as well. When you have the bimalleolar or trimalleolar fractures, lateral malleolus will be treated just as we discussed. The transverse medial malleolus fracture can be treated with two lag screws or a tension band technique. Vertical malleolus fracture works well with an anti-glide plate. If you have a deep deltoid ligament rupture, which as I mentioned, is an equivalent of a medial malleolus fracture, that's usually treated with a suture repair. But there is controversy as to when you actually need to treat that. So if it's blocking a reduction and you have to make an incision over there, go in and remove the deltoid ligament from where it's sitting between the bones, then it's definitely reasonable to do a repair right there. But otherwise, it's not always necessary, cuz you can still have stability of the joint even without that repair. Posterior malleolus fractures warrant screws or with or without a plate if you have more than 25% of the articular surface involved or more than two millimeters displacements present. So the deltoid ligament is made up of the superficial and the deep components. The superficial is dominant in controlling the tailor external rotation, whereas the deep deltoid's more dominant in controlling hindfoot eversion. The deep deltoid ligament is really transverse in its fibers in relation to the superficial. So you can get isolated rupture of the superficial deltoid where you lose some of your stability of the tailor external rotation, but eversion is still well controlled by the deep fibers. And you may have a functionally stable ankle in that case. So a syndesmotic injury can be signified by any of these signs. Widening of the medial clear space on the AP view or on the stress external rotation view. Decreased tibiofibular overlap or increased tibiofibular clear space. And this figure all the way on the right is the one that shows the normal tibiofibular clear space, both with the AP and the mortis views. We're gonna discuss the treatment for syndesmotic injuries a little more when we get to the high ankle sprains. So recent research supports early range of motion and early protected weight bearing as long as you've established a stable construct. So that's an important thing if you have those questions. It is pretty clear that getting these patients moving and allowing weight bearing is good for their overall recovery. If you get any questions on breaking time. So it takes a full nine weeks for that normal breaking response to restore following an ankle fracture. And there should be some restriction of patient's driving abilities up until that point. So with pediatric ankle fractures, injury to the physis can have a major impact on their overall outcomes. And the problem won't manifest immediately. Premature physiol rest and physio bar formation can result in angular deformities that have a major detrimental effect on their ability to ambulate and the joint voices that occur with ambulation. The sulter hairs three and four fractures that go through the epiphysis are the ones that are most likely to cause a physio injury. Tends to be less of an issue with the transitional fractures. The ones we call the tallow and the triplane fractures. Because by the time those types of fractures occur, the growth plate is almost closed. And so if you do have some damage to it, it's usually not going to cause any major abnormalities. The top image right here shows the normal progression of physio closure. So it starts centrally, then goes intramedially, then posteriorly, and finally closes laterally. So tallow and triplane fractures occur in the young adolescents. As much as we try to avoid CTs in young patients, this is one case when you're often going to use it because it's important in determining the degree of displacement. If you have two millimeters or more of displacement with these types of fractures, then it does warrant open reduction internal fixation. With triplane fractures, usually your fracture lines are sagittal plane for the epithelial fragment, the axial plane for the physio component, and then the metaphyseal fracture goes through the coronal plane. So you end up with this posterior spike, which you can see a little bit on the back of that CT reconstruction. Triplane fractures usually occur in younger patients than to low fractures. Because more of the physis is still open at that point. And then in addition to needing to do surgery when you have more than two millimeters displacement, remember that you don't want to do repeat reduction attempts on these patients because each reduction attempt can potentially damage the physis more. Seeing these Parkeris growth lines several months or even years after the surgery, if you see a nice linear signal that's parallel to the physis, that's a good sign. That's what you want to see to know that the entire physis is growing properly. If you see physio bar formation, like shown in the pictures on the right here, that'll cause progressive deformity that's going to get worse and worse as long as the rest of the physis continues to grow. All right, so for Taylor fractures, most common fracture you're going to see is a Taylor neck. These Taylor fractures require emergent close reduction. If you have any significant displacement or dislocation, because that will minimize the chances of AVN. But sub-Taylor arthritis is your most common complication that you see after Taylor neck fractures. Even though we worry a lot about AVN, that's not the most common one. The Hawkins sign is the subchondral lucency that you see where those errors are just at the very top of the Taylor dome. Lucency is a good sign in this case. It means that the talus is getting revascularized. So if in contrast you see sclerosis of the Taylor dome, that's a bad sign and indicates that you do have a vascular necrosis of the talus. Lateral process fractures like seen in these x-rays and in the CT scan at the bottom here, these are common in snowboarders. So that's the, if you see a snowboard fracture with this ankle injury that's often not commonly seen on x-ray, you have to look at getting a CT to look for that lateral process fracture. And then finally, you can get stress fractures of the talus that won't show up well on x-ray and may need to be visualized with MRI. Okay, so stress fractures are categorized by their risk of complications, such as failed healing, progression of complete fracture. The high risk fractures that we see are those in the anterior tibia, the Taylor neck, proximal fifth metatarsal, and the navicular. The malleolar stress fractures, calcaneal stress fractures, and those in the first through fourth metatarsals tend to be lower risks. Most of the risk factors that are related to developing a stress fracture have to do with compromised nutrition and endocrine or autoimmune disorders. So that's always gonna be an important part of your treatment when you're evaluating any of these or answering questions about it. The x-ray appearance can give a clue to its chronicity. So the chronic stress fractures are gonna have more cortical thickening, periosteal reaction, and sclerosis. Whereas the acute stress fractures, you're gonna see a lucency, or you may see nothing at all if it's too early. If you see a stress fracture in a cancellous bone, so like in this x-ray here, we see this linear signal that's perpendicular to the trabeculae, and that's characteristic of the cancellous bone stress fractures like we see in the calcaneus. In acute findings, the x-ray appearance will often lag behind the symptom appearance. So if you have a question and it sounds like a stress fracture, but the x-rays look totally normal, one option is to just repeat the x-ray in two weeks. That's always a good option. Often we end up getting MRIs because we don't wanna wait that long. So the first line treatment for stress fractures is typically rest and immobilization. Surgery is reserved for the high risk fractures that show signs of being complete or near complete, or if you have delayed union or non-union. Don't forget to check bone labs, nutrition labs, ask about amenorrhea, ask about diet, and then refer to your colleagues in endocrinology and nutrition. That's a part they like to stress on questions as well on your test. Right here at the bottom I have the daily recommended allowance for calcium and vitamin D. They'll often supplement more than that in athletes just because of the high physical demands. For anterior tibial stress fractures, the constant tension caused by the posterior musculature and the poor vascularity that you have at this site make it more likely to develop a delayed union or a non-union or transition onto a complete fracture. So early surgical interventions often advocate it for these types of fractures. It usually allows a faster return to sport too. Intramedullary nailing and anterior plating are both reasonable options for this. And as I mentioned, the anterior plating does have that benefit that you can avoid going through the knee, but the return to play rate is sooner with the intramedullary nail. Medial tibial stress, or sorry, medial malleolar stress fractures are uncommon, but you may see them as well, especially with repetitive impingement type lesions. And just a diagnosis to keep in mind if you have any more chronic overuse type patients or histories on your test. So medial tibial stress syndrome, or shin splints, is defined as exercise related pain along the posterior medial tibia when you don't have other signs like a vascular etiology for that pain or you don't have a stress fracture present. The etiology is not fully elucidated. One of the common theories is that it's a traction phenomenon on the periosteum from the muscular attachments that creates this periosteal inflammation. But where we most commonly see this in the distal third of the tibia, there aren't many muscular attachments. So there's more and more thinking that it's maybe coming from inside the bone itself, where you just have the normal bending and bowing of the tibia with weight bearing and the force of the calf muscles that can create just a stress reaction inside the bone. May also be related to just the increased activity that these patients are engaging in and their inability to keep up with it in terms of repairing any microtrauma there. So the risk factors for medial tibial stress syndrome involve abnormalities in foot posture, alignment, flexibility, and strength. These top five risk factors up here, female sex, the increased navicular drop test, which is what we're seeing in this picture here, going from unloaded to loaded position. Increased hip rotation, higher weight or BMI, a BMI of 20. Keep in mind this was done in cross country athletes, so that's why that's considered high. And a history of medial tibial stress syndrome or other running injuries. So those were the ones that were found to be positive in a pool of results of all the big systematic review. The ones in the second group here, the increased foot pronation, high foot, forefoot varus, increased ankle inversion, eversion, and plantar flexion. Decreased muscular endurance in inexperienced runners are also out there in the literature, but they weren't part of this big systematic review that brought up the most common ones. A lot of times we look at long distance running, sudden increases in training, running on harder surfaces, or running in worn out shoes as targets for treatment. But there is not a lot of literature to support that these are actually part of the real problem with medial tibial stress syndrome. With stress fractures, the pain is typically more localized and more anterior, whereas your medial tibial stress syndrome pain is gonna be more diffuse, so you'll have several centimeters of tenderness to palpation, and it tends to be more posterior. X-ray is usually negative in medial tibial stress syndrome, as it's rare to get a periosteal reaction. The MRI bone scan and high resolution CT will be good in confirming your diagnosis, but it's usually not needed as your first step. So if you have a history, and it sounds like medial tibial stress syndrome, you can start with treatment at your conservative options before going on and choosing the answer that shows moving on to some advanced imaging. MRI does have the best accuracy of the choices there. MRI and CT, and compared to stress fracture, if you do get a bone scan, it's gonna be positive in phase three for medial tibial stress syndrome, but it's gonna be normal in appearance in phases one and two. So rest is really the most important treatment, because this is an overuse injury. It's doing too much, too fast, too soon. There isn't really a lot of strong evidence to support bracing, heel pads, padded insoles, even physical therapy. So it's really just your rice with rest and inflammatory control. And then you want a gradual return to activity. A lot of people will suggest running on softer surfaces, avoiding hills, changing your running shoes every 250 to 500 miles. Mostly to limit recurrence when you're getting them back, but there isn't good evidence to say that that's absolutely necessary. Low energy extracorporeal shock wave therapy has been beneficial for calcitrant cases, I doubt that's gonna be the option on your test. And then surgery is really very rarely indicated, because not only does it not usually get to the point where that it's bad, but the chances of returning to pre-injury activity level are low. All right, so we'll run through some questions now in this first group. The most common complication of tailor neck fractures is osteonecrosis of the talus, nonunion of the talus, arthritis of the ankle, arthritis of the subtalar joint, or infection. And this is arthritis of the subtalar joint. So although we are often worried about the blood supply and osteonecrosis, that's your distractor here. And then just keep in mind, it's the subtalar joint that becomes arthritic more commonly than the tibiotalar joint. A 28-year-old male fell and twisted his left ankle while playing ice hockey. He describes pain over the proximal aspect of his left leg and tenderness on the lateral side of his knee. Radiographs were obtained, and which of the following structures is most important to be addressed in surgical management? So here are your radiographs here with a little helpful arrow in case that doesn't show up too well, but he's got a fracture of that proximal fibula there. And on the ankle x-ray, we can see some widening of his medial clear space. So the choices for what's most important to be addressed, the proximal tibiofibular joint, the tailor, osteochondral defect, ankle syndesmosis, lateral ankle ligaments, or the fibula. And our answer here is the ankle syndesmosis. We don't have any indication that there is an osteochondral defect there. And it's the syndesmosis that's really gonna have the biggest impact on restoring the normal joint biomechanics and making sure that you don't have abnormal forces with the ambulation. Here's a 19-year-old male motocross racer presented to the ER after sustaining an injury shown in figures one and two. So I'll show you those to start. So here we have a pretty bad pilon fracture. Physical exam shows a grossly deformed lower extremity with significant swelling. No lacerations are noted, sensations intact throughout, and the patient has palpable pulses. Able to flex and extend his toes with minimal pain. What's the most important, appropriate step in treatment of this patient? And here we need to do close reduction application of an ankle-spanning max fixator. So that's why when we need to give this type of fracture time for the swelling to calm down. Otherwise, you're gonna run into some major issues with wound healing and soft tissue complications. So that takes out open reduction internal fixation with your plate or with your nail. It is certainly important to keep compartment syndrome in mind for a history like this. But in the story here, they're telling you that, trying to give you a clue that he doesn't have high signs of compartment syndrome. That he can bend and extend his toes without much pain. And then we definitely don't wanna cast. Not only is that not gonna do anything for a bad fracture like this, but you won't be able to monitor compartments. You won't be able to check the wound. All right, now moving on to ligament injuries. So ankle sprains are considered the most common athletic injury. 85% of them are lateral ankle sprains. The ATFL is the weakest and the most commonly injured. That's running from the anterior inferior fibula to the interlateral talus. Your CFL is also involved in a majority of cases, and that runs from your inferior fibula to the lateral process, the calcaneus. And then your posterior talofibular ligament is rarely involved. That runs from your posterior inferior fibula to the posterior lateral talus. Most common mechanism is inversion and internal rotation of the hind foot. With the leg in external rotation, and your foot in plantar flexion. To test your ATFL, you're going to use your anterior door test, and you want your hind foot in neutral, and ankle in plantar flexion to best test that ligament. Your CFL, you can test with your tail or tilt test. And for that test, you wanna have the hind foot inverted and the tibial tail or joint in dorsiflexion. Always remember, you wanna compare side to side, because that can be a gauge for normal laxity for that patient. With increasing tear grade, you're gonna see more ligaments involved, more difficulty with weight bearing, more swelling, and more limited range of motion, and more laxity. The laxity tests aren't actually very useful in the acute setting, unless you have a really low grade injury, because there's gonna be too much swelling and guarding after you get a good exam. Grade three sprains can then be further divided into 3A, which has a normal stress x-ray, and 3B, which has an abnormal stress x-ray. Based on the auto-ankle rules, you wanna get an x-ray if you have either tenderness to palpation at the posterior edge, or tip of the medial or lateral malleolus, or with inability to weight bear. Tarsal coalition does have an association with lateral ankle sprains, and that can sometimes pop up on your test. Stress x-ray can be done also, not just when we're looking at syndesmotic injuries, but for looking at anterior translation or tail or tilt. Although the usefulness is questionable, because you're often not going to see this positive anterior drawer. You're only gonna see that in cases where you have a posterior talofibular ligament that's been injured as well. The tilt test is really important to compare to the contralateral side, because especially in young patients and in females, you may get quite a significant tilt there. It can be most helpful to use those when you're either comparing side to side, or when you're in surgery and trying to gauge if you adequately restored the stability. An MRI tends to be reserved just for chronic cases. So management starts with rest, ice compression, elevation. You can do a mobilization and a short leg cast or a boot, but usually for no longer than three weeks. Early mobilization and functional rehab have all good signs there, associated with earlier return to play, higher return to play rate, better range of motion, better laxity, and better patient satisfaction. So early mobilization and functional rehab are gonna be your choice for low ankle sprains. Propreceptive training is a really key part of physical therapy for these low ankle sprains. Taping or bracing can decrease ankle injury when they've had a previous low ankle sprain, but it doesn't work well for prophylaxis in somebody who hasn't had an ankle sprain before. While there are some studies that suggest superiority of surgical treatment for acute severe ankle sprains, it's generally not indicated and is not gonna be your first line treatment for acute low ankle sprains for testing purposes. So high ankle sprains are the ligamentous injuries to the syndesmosis. Much less common than low ankle sprains, but they still make up about 25% of ankle sprains in collision sports like football and rugby. You can see them in other sports like ice hockey, soccer, skiing, basketball. Syndesmosis is made up of these five parts, the anterior inferior tib-fib ligament, posterior inferior tib-fib ligament, the interosseous ligament, which is the distal continuation of the interosseous membrane, and the inferior transverse ligament seen at the back down at the bottom there. The interosseous ligament and the interosseous membrane make up the strongest part of the syndesmosis. The deltoid does contribute to stability of the syndesmosis, although it's not actually considered part of the syndesmosis cuz it doesn't connect the tibia and the fibula. And as mentioned before, the syndesmotic injuries will really alter the joint mechanics and contribute to progressive arthritis if they're not corrected. High ankle sprains are classically caused by an external rotation force on an everted and dorsiflexed foot. Compared to low ankle sprains, they've got longer recovery time, longer return to play time, and they're more likely to cause long-term joint dysfunction. The length in centimeters of tenderness above the level of the joint line has been shown to correlate pretty well with the severity of the injury and missed days of practice and competition so that can be used as a prognostic indicator of how soon you can get an athlete back to sports. There's several different physical exam tests that can be used to assess for a high ankle sprain. No one individual test is diagnostic and the inter-rater reliability is really not that good. So usually you want to do multiple tests to get a good sense of the diagnosis for these. Workup also includes x-ray to assess for any fracture or syndesmotic widening. You really want to get weight-bearing x-rays once they're tolerable and don't forget that if there's any tenderness to palpation more proximally in the calf you need to get a full tib-fib x-ray to check for a mesonear fracture. MRI does have high sensitivity, specificity, and accuracy for diagnosing these injuries, but it's usually not needed early on because you can make the diagnosis clinically. So while grade one injuries are clearly stable, grade three are unstable. There is some controversy about grade two lesions where some experts will say they're all unstable and others will say they can be stable or unstable. But essentially stability can be confirmed by one of three ways, stress x-ray, MRI, or arthroscopy. These images here, the one on the left shows what a stable syndesmosis looks like. The middle one, or sorry, what an uninjured syndesmosis looks like. The middle one gives you an injured but stable view and the one all the way on the far right is an unstable syndesmotic injury. So the stable injuries can be treated with rest, inflammatory control, a brief period of immobilization, usually in a boot, and then PT for work and getting your mobility, strength, and ambulation back, and then finally a gradual reintegration into sports. The unstable injuries, whether or not they have a fracture, usually warrant surgical stabilization of the syndesmosis. When you have an ankle fracture present with a syndesmotic injury, you fix the fracture first, reassess the syndesmosis intraoperatively, and then you only have to stabilize the syndesmosis beyond that if it remains unstable after fracture fixation. Despite a large body of literature looking at this, there's no clear evidence to reach a consensus on the number of screws needed for syndesmotic fixation, the size of the screws, 3-5 or 4-5, the number of cortices, 3 or 4 for a screw, or the need for screw removal. If screws are removed, it's best done around 12 weeks, although sometimes you can push it as early as 8 weeks to get an athlete back. If they're left in, they will break, but there's no evidence to show that that causes problems. So you don't usually have to plan on taking them out if you decide you're just going to let them break in and let the athlete play with that. The other option is a suture button construct shown here on the right. One benefit of the suture button construct is you don't have to worry about screw breakage and what that's going to mean for the athlete or just even the counseling about it. But it is a newer technique. There's less long-term data compared to the screws. One of the benefits that has been discussed with the suture buttons is that malreduction may be less common and it may allow a little more physiologic motion. Some of the complications that you can see with suture button construct though are osteolysis, implant failure, or entrapment of the tibialis anterior. Chronic ankle instability is characterized by recurrent sprains or instability episodes or just persistent pain long after an acute ankle injury should have resolved. It's often related to inadequate initial rehabilitation. So physical therapy is a good choice even for chronic ankle injuries, chronic ankle instability. If you see any signs in the vignette that it hasn't been well rehabbed. If you are looking at doing any surgical treatment, MRI should be performed first because it can demonstrate associated sources of pain beyond the ligament injury. So that can be chondral injuries, occult fractures that if you treat just the ligament injury and forget that, they're not going to have any resolution of their symptoms. Surgery is warranted when there's residual mechanical impairment after it's been fully rehabilitated. And if you do have, if you do go on to surgery, one thing you have to keep in mind is cavovarious deformity. That's something that is a risk factor for failure of your repair or reconstruction. So that has to be addressed at the same surgery if it is present. So the surgical options include repair and imbrication of the ligaments or reconstructive techniques. The modified Brostrom-Gould techniques, the most commonly used one today. Reconstruction techniques can be anatomic or non-anatomic tenodesis. And the peroneus brevis and longus are dynamic ankle stabilizers that resist inversion. So you don't want to do a technique typically that will totally sacrifice that, but you can do split type techniques where you just take part of the peroneus brevis and use it for the reconstruction. So arthroscopy sometimes performed at the time of ankle instability surgery. The benefit is that you can address and treat any of these additional problems like a chondral injury, osteochondral injury if you have any loose bodies in there, or adhesions from the chronic injury. All right, proximal tibiofibular joint instability. This is a commonly misdiagnosed. It can range anywhere from just subluxation of that joint to complete dislocation and fracture. It's usually seen in sports where you have a forceful twisting motion while the knee is flexed. The proximal tibiofibular joint is stabilized by the posterolateral coronal structures of the knee. So when the knee bends to 90 degrees and those structures become lax, that's when that joint is at risk. Injury is more common when there's an oblique orientation of the tibiofibular joint like shown in this picture where the arrow is there. Atraumatic subluxation is seen with ligamentous laxity. If you have a true dislocation that can occur in any of these directions with antralateral direction being the most common. If you have just atraumatic subluxation, that should be treated conservatively. It usually gets better with age. But if you have an acute dislocation, that should be treated with a closed reduction. You flex the knee up to 90 degrees to reduce it. And if you can't get it reduced in that manner, then open reduction and internal fixation is warranted. Always check the knee ligaments after the reduction because that will determine if you have to do any additional states, repair, reconstruction of your LCL or posterolateral corner structures. All right, next set of questions. So a college athlete has a lower extremity injury that's being evaluated in the training room which allows deferred radiographic imaging. Proximal fibular tenderness, navicular tenderness, distal and anterior fibular tenderness, fifth metatarsal base tenderness, or distal and posterior fibular tenderness. So this is getting at both the otto ankle rules and the high risk stress fracture. So distal and anterior is not one of the rules for having to get an ankle x-ray, whereas the distal and posterior fibular tenderness is. And then your metatarsal and navicular or high risk stress fractures, your proximal fibula could indicate a major nerve fracture with a syndesmotic injury. So a 16-year-old lacrosse player sustains an ankle injury during practice when his ankle is everted. It's visible swelling around the ankle and echemosis medially. He's tender distal to the medial malleolus and anterolaterally between the tibia and fibula for about 4 centimeters. Physical external rotation stress test is painful. He's able to bear weight, but lateral movements cause discomfort. His radiographs are negative for fracture and stress and non-stress radiographs are normal. What's the best initial treatment to suggest to this athlete? And here it's rest, ice compression, elevation. This is a stable high ankle sprain. The key part here is that the stress and non-stress radiographs are normal and that's how you know this is stable and you can treat it at least with conservative measures. All right, tendon disorders. So the, we refer to the group of chronic overuse pathology involving Achilles tendon as the chronic Achilles tendon disorders. Achilles tendonitis is really a misnomer because there are no inflammatory cells found in the Achilles tendon itself. The first three disorders here are part of the same process. That's often referred to as Achilles tendonitis. Peritonitis is stage one where you get inflammation of the periton and the septum. This progresses to peritonitis with tendinosis and then in the third stage just tendinosis of the Achilles tendon. These other two disorders are separate entities. So insertional tendinosis is an inflammatory condition. That's where you do have inflammatory cells present at the tendon insertion. And retrocalcaneal bursitis is a mechanical irritation of the retrocalcaneal bursa that can be caused usually by a Hagelin's deformity. The Achilles periton is highly vascular, susceptible to inflammation. On physical exam, one key factor of this is that the site of tenderness to palpation will stay fixed. It won't move as you take the ankle through range of motion, whereas the converse is true with Achilles tendinosis. MRI, you see a high signal appearance of the periton right here where that arrow is and it can be thickened as well. Majority of the cases will resolve with non-invasive treatments. Breezemont is just something to be aware of, but usually that's not going to be your choice. That's when you inject fluid under the sheath to break up any adhesions. Surgical treatment is very rarely needed. It should not be a commonly chosen option for your test. But if you do have to do a surgical incision, it's very important to leave the anterior portion of the periton in place because that's where the majority of your blood supply to the Achilles tendon is located. Achilles tendinosis is often asymptomatic once the peritonitis resolves. So it can be late and not detected until you actually get to the rupture, which seems to come out of nowhere in those cases. You may be able to elicit tenderness or palpate swelling. And then in contrast to the peritonitis, this type of tenderness will move as you take the ankle through range of motion because it's part of the tendon, not just the tendon sheath. On ultrasound, you may see thickening of the tendon, calcifications, which we see on the arrows up there. On MRI, you're going to see that thickened tendon and some signal changes in the area of the tendinosis. In the absence of rupture, your mainstay of treatment is going to be still nonoperative. But if you do have somebody who fails nonoperative treatment, there is an option for just debriding the tendinotic portion. Don't ever use corticosteroids around the Achilles tendon for tendinosis because that has a high risk of tendon rupture. The pathology of retrocalcaneobrasitis is located anterior to the Achilles tendon, often associated with the Hagelin deformity, which is the bony prominence that we see at the posterior superior aspect of the calcaneus. The repetitive hyperdorsiflexion that you see with running uphill tends to provoke pain. Surgery is usually not necessary. If you do get to surgery, just take off that exostosis there. With insertional tendinitis, you can also see that with the Hagelin deformity and retrocalcaneobrasitis. This MRI here shows all three with the Hagelin deformity at the thick arrow, the retrocalcaneobrasitis at the thin arrow, and the insertional tendinitis at the arrowhead there. On exam, tenderness palpation will be right at that site where the tendon meets the bone. As with the other chronic Achilles tendon disorders, stretching and mobilization and PT can all alleviate symptoms. And surgery is really only indicated for refractory cases where you can take away any bony prominences and degrade the degenerative or diseased tendon there. An acute Achilles tendon rupture typically occurs in the vascular watershed, which is two to six centimeters proximal to its insertion. Can result from a forceful plantar flexion action or sudden dorsiflexion of a plantar flex foot. Fluoroquinolones and corticosteroids are the common associated things that can increase the risk for rupture. The physical exam will demonstrate the palpable gap. You can do a Thompson test, which is shown in the drawing here where you get no reaction with squeeze of the proximal tibia. You can also see increased passive dorsiflexion and decreased plantar flexion strength. It's diagnosed from the history and physical, so you don't need imaging. Usually that's just done more to assess the degree of involvement or retraction. Historically, nonoperative treatment was associated with higher risk of re-rupture, but that's when it involved casting for six to eight weeks and delayed mobilization in those studies. So more recently it's been very clear that functional bracing and early range of motion show re-rupture rates and outcomes that are stem-letter surgery and they avoid the surgical complications. So that nonoperative treatment has now been on the rise for Achilles tendon ruptures. The nonoperative protocols all involve a short course of nonweight bearing and immobilization followed by weight bearing in a walking boot that usually has a progressively decreasing heel lift and then early physical therapy. There is some limited evidence to suggest that faster return to work and improved plantar flexion strength is present with surgery and some studies show no difference, but that's, those are the two reasons where you may consider surgery for athletes. When surgery is indicated, options include percutaneous repair, a limited open repair or a standard open repair. Your sural nerve is your main at-risk structure in terms of neurovascular injury and the injury rates are generally found to be higher with the percutaneous repair. As with all nonoperative treatments, the early immobilization and protected weight bearing are important in optimizing the outcomes too. Biologics will not be a correct treatment choice when it comes to acute Achilles tendon ruptures. There's no clinically proven effectiveness currently. So with chronic Achilles rupture, the definition of chronic actually, it varies, but it can be as short as four weeks from the injury. The key with these types of injuries is that you want to restore your normal resting length of the gastroc soleus complex. So after you debride all the nonviable tissue, you have to measure your tendon gap. With less than 3 centimeters of a gap, usually a direct repair is appropriate. If you're looking at 3 to 5 centimeters, then you have to start considering things like a VY advancement. That's what's drawn out in this picture here. A local turndown flap or a tendon transfer. And if you're getting even bigger than that with greater than 5 centimeters, then you have to consider an allograft or a synthetic as well. So peritoneal tendon disorders, we'll just start with a little anatomy here. Knowing that the peroneus brevis muscle extends more distally than the peroneus longus muscle makes it easier to identify when you're looking at an MRI, like an axial image or during surgery. They both pass through the fibro-osseous tunnel at the posterior tip of the fibula. And the superior peroneal retinaculum is what makes the roof of that tunnel. It keeps the tendons from subluxating or dislocating. And we see some of that subluxation in the photograph down there at the bottom. The peroneus brevis inserts on the fifth metatarsal. The peroneus longus continues under the plantar side of the foot to the medial cuneiform and first metatarsal. And contains, can contain an os peroneum. Accessory peroneal muscles can be a cause for tendon disorders because you get crowding in that narrow tunnel. On exam, you can have pain that occurs with passive plantar flexion and inversion, which stretches the tendon, or active plantar flexion and eversion as that contracts the tendons. The longus involvement usually localizes more distally than brevis involvement. If you have the patient do resistive eversion or active circumduction, that can demonstrate a subluxation of the tendon. Any x-ray image that looks like this is cluing you into an avulsion of the fibula where the superior peroneal retinaculum attaches. So a consequence of that type of fracture will be a peroneal tendon subluxation or dislocation. Usually fall into these three categories, tendinopathy, tears, and subluxation or dislocation. The peroneus longus sits more laterally, so it's more prone to dislocation. Whereas the peroneus brevis is more prone to tearing. With treatments, with surgical treatments, sterile nerve is the most at risk structure here. And if you do have to get down, open the superior peroneal retinaculum to get down to the tendons and perform any work there, it's really important to repair that. Otherwise, you'll end up with iatrogenic subluxation or dislocation. All right, posterior tibial tendon dysfunction. It's not commonly seen in athletes because it tends to occur more in the sixth decade and later and often in obese patients. But you may see it with runners and triathletes. Actions of the posterior tibial tendon include hind foot eversion, medial arch support, and forefoot adduction and supination. If the patient is unable to perform a single leg heel rise, that's a sign that it's progressed beyond that first stage. And then with progressive disease, they get Achilles tightness failure, the medial longitudinal arch, and degenerative joint disease. Stage 1 is characterized by tenosynovitis without a flat foot deformity. That responds well to conservative measures like anti-inflammatory techniques, physical therapy, orthoses, and boot immobilization. Tenosynovectomy is an option, but that's unlikely going to be the correct answer for any stage 1 disease. In stage 2, you do get a flexible flat foot deformity, so one that the arch will reconstitute when you do a single leg rise as opposed to the rigid flat foot deformity that you see in the later stages. You can use an ankle foot orthosis for non-operative treatment of stage 2, but more likely to require surgical treatment such as some combination of soft tissue and bony procedures. When you get to stage 3 and stage 4 with a rigid deformity and arthrosis, that's when you need to start considering arthrodesis. And it'll either be a subtalar, subtalar or tibiotalar, or a triple arthrodesis depending on the location of the disease. All right, questions for this section. A 40-year-old female recreational runner developed increased pain in the Achilles tendon over the past four months that has prevented her from running. Pain is episodic, but worse when starting exercises has tried ibuprofen with little relief, exam reveals a palpable painful thickening in the mid-portion of the Achilles tendon. What's the best treatment recommendation for returning the patient to active running? Correct answer here is PT to include eccentric stretches with these chronic Achilles tendon disorders. Definitely don't want to use corticosteroid injection. We know she already tried ibuprofen and that didn't help. And then the PT with eccentric stretches is really the key over shockwave therapy or PRP. A 10-year-old male soccer player has foot pain and flat foot deformity. What's the most accurate physical exam test to differentiate a flexible flat foot from a rigid flat foot? Here it's reconstitution of the arch on toe raise, the one main distractor here is the Coleman block test. That's for testing the opposite of flat foot deformity, the cavovarious deformity, and that's shown in this picture here. All right, joint disorders. So anterior ankle impingement manifests as anterior ankle pain with terminal dorsiflexion, commonly seen in dancers when they go into the plie position, also in turf athletes. On imaging you'll usually show these kissing lesions of the anterior talus and the dorsal navicular, but the tibial-talar joint will remain healthy appearance as opposed to OA. The excess doses don't even necessarily have to touch to cause impingement. They can cause just inflammation of the soft tissues all around that area, which also contributes to pain. In the early stages you'll have pain just with the causative activity, but pain can come with activities of daily living as it gets more advanced. This x-ray technique shown here by Van Dyck utilizes an oblique angle and overpenetration and that makes it a lot more likely to get proper visualization. You can also use MRI or dynamic ultrasound to diagnose the anterior impingement. Nonoperative treatments worth trying, although symptomatic relief may only be temporary. PT is aimed at optimizing ankle stability. An operative treatment will involve arthroscopic or open excision of the excess doses in any affected soft tissues. If arthroscopic management is selected, awareness of the at-risk neurovascular structures is critical, so the superficial peroneal nerve with the interlateral portal, the staphinous vein with the intermedial portal, and the dorsal neurovascular bundle with spur section. If lateral ankle instability coexists, taking care of that lateral ankle ligament reconstruction should be considered at the same time. Posterior ankle impingement occurs with terminal plantar flexion, also seen in ballet dancers, but now this is when you're in the on-point position. Ostrogonum is a common etiology of posterior ankle impingement. This occurs when the posterolateral process of the talus fails to fuse with the rest of the talus. FHL, tenosynovitis, is another common cause. It's commonly seen in sports that involve strong, repetitive push-off, like tennis or running. While the diagnosis of posterior ankle impingement is usually made based just on history and physical exam, imaging studies are useful in this case for determining the etiology and how you need to treat it. Standard, first-line, non-operative treatment options all apply, and then you may have additional modalities such as casting if it's an occult fracture that's the cause of the posterior impingement, or you can do some dorsiflexion taping where you try and prevent them from getting to that terminal dorsiflexion. Operative treatment depends on the etiology. It may involve excision of vastrigonum, FHL, tendon sheath decompression or treatment of any osteochondral lesions of the talus. You should have a high suspicion for an osteochondral lesion of the talus if you have a history describing chronic ankle pain with no trauma or persistent ankle pain long after what's normal for resolution of the acute ankle injury. Ankle sprain is the most common acute injury that's associated with these osteochondral lesions of the talus. They're more common in men. Average age at presentation is 20 to 30, and they can be bilateral in about 10% of them. Multiple classification systems, but they all follow this general progression of higher grade leading to more instability. And this Burnt and Hardy classification is based on x-ray, but there are similar ones used for MRI, CT, and arthroscopy grading. Medial lesions, usually atraumatic. They're more posterior and larger, deeper lesions. Lateral lesions usually have a history of trauma. They're more central or anterior on the talus, and they're superficial and smaller, less likely to heal well with nonoperative treatment. Nonoperative treatment in the form of activity restriction, weight bearing limitations, immobilization, can all be appropriate for grade 1 and 2 lesions, but there's still a relatively low success rate, only about 50%. Operative treatment is first line for higher level lesions, grade 3 and 4, for those that fail nonoperative treatment. It can involve retroreticular drilling, transarticular drilling, ORF, osteochondral allograft or autograft or ACI. Excision alone has been suggested to be worse than nonoperative treatment. So if you get a question where it just says excision or excision plus some intervention, it's always going to be excision plus intervention for the lesion itself. There is not a good consensus on the use of biologics, but they have been used both with nonoperative and operative treatments. That won't be your first line treatment on any questions you get. Osteochondral lesions of the tibia are much less common. Follow all the same general evaluation and management principles, but this is what it would look like if you get some MRI with this little lesion here. That's an osteochondral lesion of the talus. All right, some questions related to joint disorders. A 23-year-old ballet dancer is felt to have chronic pain due to osteogonem syndrome and is to undergo surgery. Relative to the FHL tendon, the osteogonem is lateral. And this is just an image you want to burn in your mind for any of the osteogonem or posterior impingement type questions. 26-year-old male tennis player presents to clinic for evaluation of a sprain of his right ankle. He reports catching in the ankle when he walks. Examination reveals tenderness over the anteromedial joint line of the ankle with an effusion. Plane radiographs and MRI demonstrated displaced osteochondral lesion of the medial talar dome and a loose body. What's the appropriate initial management for this patient? So the key here is that there's a displaced lesion and a loose body, so you can't do the nonoperative treatments for these. This is a high grade, grade four lesion. You need to remove the loose body and address the defect at the same time. 27-year-old female twisted her right ankle and sustained a trimalleolar fracture. It was determined to be an SCR4 injury. She has surgery for ORF with anatomic reduction of the major fragments. One year later she complains of pain with ankle range of motion, radiographs revealing development of DJD. What's the most likely etiology? Occult intraarticular chondral injury at the time of initial trauma. Well, several of these can be causes for DJD. We have to take their word that they did an anatomic reduction, so poor reduction or malposition internal fixation is unlikely. But it is really common to see these chondral injuries when there's pain long after. All right, and finally we'll go on to neurovascular disorders. So chronic exertional compartment syndrome is exercise-induced leg pain with or without paresthesias. It predictably begins at the same part of the workout and resolves with rest. In the later stages you may have it even occur with walking. Anterior and lateral compartments are most likely, most commonly involved. Bilateral involvement is very common with this process. Muscle volume increases 20% when you're exercising but you don't get that corresponding increase in the fascia, so that's one of the reasons it's thought to be a theory related to hyperperfusion, although some of the studies recently haven't really supported that. So there are some other theories like just stretch of the fascial pain receptors or inability of the myocytes to meet their increased metabolic demand. The compartment pressure measurements are the gold standard for diagnosis here and that one-minute post-exercise is the most reliable for diagnosis. Imaging is usually only used to rule out any other diagnoses. Since most athletes don't want to give up their sport, non-operative treatment is not often successful. Definitive treatment is open or endoscopic fasciotomies. Your superior perineal nerve is the main nerve vascular structure at risk. If you have recurrence it may be related to an incomplete release, an incorrect diagnosis or excessive scarring. Popliteal artery entrapment syndrome is intermittent claudication caused by dynamic compression of your popliteal artery. It's much more common in men, usually in patients less than 30 years old. The compression can cause chronic problems like aneurysm at that site or thrombosis. The ankyl-brachial index is typically normal in these patients. Ultrasound, duplex ultrasound arteriography or CTMR angiography is diagnostic and an important thing to do during those studies is have the patient do either passive dorsiflexion or active plantar flexion because that makes it more likely to be positive. So this MRI here is the same patient, same leg, but in the image on the right, the patient's actively plantar flexion, doing active plantar flexion and it causes that constriction there. Usually once the diagnosis is made you're referring these patients to vascular surgeons because beyond just the decompression you're going to need to treat any present aneurysm or thrombosis at that same time. So there are various nerve entrapment syndromes that can affect the lower leg and ankle. Trauma is the primary cause for all of them, although it may not be detected until after the acute injury has all resolved. They can come from repetitive microtrauma, from muscle herniation, direct compression, as an iatrogenic consequence of knee arthroscopy. That's usually a saphenous nerve. This image here shows your soleal sling which is a source of compression or site of compression for tibial nerve. With nerve entrapment syndromes the pain tends to get worse with continuation of that activity. Symptoms are consistent with the affected nerve distribution and the diagnosis can be confirmed with EMG or nerve conduction studies. First line treatments, nonoperative, but operative treatment will just be related to decompression of the affected nerve. And then finally DVT in athletes. So the Birchell's triad, venous stasis, endothelial damage and hypercoagulability, not something we're often thinking about with our athletes, but there are cases when that can really be a problem. So they can get venous stasis with long bus rides, plane rides, high risk for endothelial damage with the collision sports or microtrauma just with endurance sports. A lot of young female patients will be on oral contraceptives and even hemoconcentration with altitude training. If you have a provoked DVT in an athlete, the typical treatment, standard treatment is anticoagulation and most importantly no sports while they're on anticoagulation, no contact sports. I think just in the interest of time we'll wrap up with this last set. Those questions are in your handout there. And thank you very much. Thank you.

leg injuries

ankle injuries

fractures

tendon disorders

joint disorders

neurovascular disorders

DVT in athletes

tibial shaft fractures

ankle sprains

Achilles tendon disorders