Hello, my name is Eileen Crawford, and I'm an orthopedic sports medicine surgeon at the University of Michigan. I appreciate the opportunity to be a part of this review course, and today I'll be discussing the leg and ankle. These are my disclosures, which are also listed in your binder. As part of a review course, my objective is to cover the breadth of topics on the leg and ankle relevant to sports medicine while highlighting important details for board exams and practice. I've divided it up into these five categories, and we'll run through some questions at the end of each section. The slides which you received with your course materials are meant to serve as a study guide for you. For time's sake, I won't touch on every point on the slides, but it's there for your reference. So if you find your attention fading, don't worry, you can always go back to the slides before the test. If there are topics I don't cover that you think are important, please give that feedback so we can help improve the course for the future. First up is fractures. Tibial shaft fractures are often athletic injuries with about 25% of them occurring during sports participation. They have the longest return to sport timing among sport-related fractures. A non-operative treatment is appropriate for non-displaced fractures, but they are a rarity seen more in the pediatric population. In that case, a long leg cast is used, which can be converted into a patellar tendon bearing brace, which is seen in this photo. Once early bone healing is established. The treatment requires frequent monitoring with weekly x-rays initially to check for displacement. Operative treatment for displaced fractures most often consists of intramedullary kneeling, but don't forget the alternative options listed here, such as plating, which avoids trauma to the knee, and external fixator for provisional or definitive treatment in open fractures. Here's a look at the return to sports rates from a systematic review in Sports Health 2016. A return to sports rates were much higher with surgery than with non-operative treatment. More than 90% returned to sport and 75% to their pre-injury level of sports, but it still takes 40 weeks, nine months. ORF with plate and screws has a higher return to sport rate than I am now in this study, but the time to return to sport was longer. Open fractures and more severe soft tissue injury as indicated by a higher surety grade were associated with a decreased return to sport. Some testable points on tibial shaft fractures. You always have to think about compartment syndrome when you have a tibial shaft fracture, both before, during, and even after surgery. If you see a distal third tibial shaft fracture, get a CT, because that fracture can extend to the plafon with a posterior malleolus fracture that's not always clear on x-ray. Evidence on reamed versus un-reamed nails suggests that reaming may be better for closed fractures in terms of decreasing the incidence of future bone grafting and exchange nailing. Thermal necrosis is related to the size of the isthmus, with the size of the reamer with respect to the isthmus, not reaming with the tourniquet out. And chronic anterior knee pain is common after IM nailing should be part of that pre-op discussion. BMP has supportive evidence in open fractures with BMP-2 and in non-reamings with BMP-7. Tibial plafon fractures are high-energy fractures that aren't seen in most sports, but you may encounter it with extreme sports. An X-fix is usually necessary until soft tissue swelling subsides. Arthroscopic assisted fixation has been described. It does help with visualization of the articular surfaces for anatomic reduction, but you still have to put in all this hardware, semen and photum. And next on to ankle fracture, starting with a little bit of biomechanics review. So the ankle is a modified hinge joint with motion in all three planes. The tibial-tailor joint is inherently stable given the bony morphology, and the lateral malleolus and the syndesmotic ligaments contribute to this stability, while also allowing a widening of the intramalleolar distance with the heterotopic ossification of the syndesmosis from injury inhibits that motion. And so that can cause pain and limited range of motion. Here's a brief review of the most commonly used classification systems for ankle fractures. The Dene Weber classification is just for lateral malleolus fractures. Dene Weber A fractures distal to the tibial-tailor joint line B is at the level of the joint and C is at proximal to the level of the joint. Most are certain more proximal injuries have a higher risk of syndesmotic injury and result in ankle instability. The Laugie Hansen classification covers unibi and trimalleolar fractures. This is a simplification of the classification that I have on the slide here. The full description also includes the ligamentous injuries as well, but this version is helpful for looking through x-rays. And medial malleolus fracture may be a deltoid ligament instead. So that's why you have to think about the soft tissues as well. So supination external rotations your transverse medial malleolus with a short oblique fibula may have a posterior malleolus fracture. Your pronation external rotation has a transverse medial malleolus, high short oblique or spiral fibula fracture and also possibly a posterior malleolus fracture. Pronation e-reduction has a transverse medial malleolus fracture and a transverse recombinant fibular fracture. And supination adduction injury has a vertical medial malleolus fracture and distal fibular abortion. For lateral malleolus fractures, ORF is indicated for displacement more than two to four millimeters, shortening or rotation. Restoration of the fibular length and rotation is needed for normal syndesmotic function. And the talocrural angle, which is shown in the upper right here is your measurement to assess full restoration. A normal talocrural angle is about 83 degrees. The dime sign can also be used. Weber A fractures are often minimally displaced, but if reduction and fixation is warranted, a four or five millimeter screw can be used. A lag screw with an anti-glide plate works well for oblique Weber B fractures. And for Weber C fractures, a lag screw and a lateral plate can be used or a bridging plate if there's significant convolution. A one-third tubular plate is usually sufficient, but you can use a more robust 3-5 LCDC plate. With bimalleolar and trimalleolar fractures, the lateral malleolus is treated as described in the last slide. And then the transverse medial malleolus fracture is treated with two lag screws or a tension band technique. A vertical medial malleolus fracture, which usually occurs with a supination adduction injury, can be treated with an anti-glide plate. A deep deltoid ligament rupture, which is a medial malleolus equivalent, is treated with suture repair, although there's controversy about when that needs to be repaired. If it is blocking reduction and needs to be accessed on repair, it's certainly reasonable. Posterior malleolus fractures warrant screws with or without a plate if more than 25% of the articular surface is involved, or more than two millimeters of displacement is present. The deltoid ligament is made up of the superficial and deep components. The superficial deltoid is dominant in controlling tailored external rotation, whereas the deep deltoid is dominant in controlling hindfoot eversion. The deep deltoid fibers are relatively transverse, as you can see in this MRI. Isolated rupture of the superficial deltoid causes increased tailored external rotation, but eversion is still restrained, so the medial ankle can remain functionally stable if the deep deltoid only is intact. A syndesmotic injury is signified by any of these signs. Widening of the medial clear space on your AP x-ray or with external stress views, as seen in these first two images on the left. It can be seen with a decreased tibiofibular overlap or increased tibiofibular clear space. So this photo on the right shows the normal tibiofibular clear space on more or less in AP views. And we'll discuss the treatment for syndesmotic injury more when we get to the high ankle sprains discussion. Recent research supports early range of motion and early protected weight bearing postoperatively as long as you have established a stable construct. And breaking time does not return to baseline until about nine weeks post-op. With pediatric ankle fractures, injury to the physis can have a major impact on outcomes and the problem won't manifest immediately. Premature physio arrest and physio bar formation can result in angular deformities that have a major detrimental impact on joint forces with ambulation. Salter-Hare's three and four fractures that cross into the epiphysis are the highest risk fractures for physio injury. It's less of an issue with the transitional fractures which are the triplane and to low fractures because the physis has already started to close with these fracture types. The image on the top here shows the order of physio closure, central, intermedial, posterior, and then low. To low and triplane fractures occur in young adolescents as the physis is closing. As much as we try to avoid CT in young patients due to the radiation, this is one exception where CT can be very helpful with assessing the degree of displacement and the orientation of the fracture lines. With triplane fractures, usually the fracture is in the sagittal plane in the epiphysis, the axial plane in the physis, and the coronal plane in the metaphysis. And that results in this posterior spike that we often see with these fractures. Triplane fractures occur in younger patients than to low fractures when more of the physis is open. Surgery is warranted for an articular step-off of more than two millimeters. And another point is that you want to avoid repeated manipulation or repeated reduction attempts as this can further damage the physis. Park-Harris growth lines that are parallel to the physis are good, indicating normal growth following fracture healing. In contrast, a physiobar will cause progressive deformity for as long as the rest of the physis continues to grow. Fractures of the talus most commonly occur at the neck. These require an emergent closed reduction for displacement or dislocation to minimize the chances of AVN. However, subtalar arthritis is the most common complication seen with this fracture type, not AVN. Hawkins sign is a subchondral lucency of the talus that indicates that vascularity is intact. So it's a sign you want to see. Lack of the Hawkins sign, which shows up as sclerosis of the talar dome is a bad sign. Lateral process fractures are usually seen in snowboarders. You can also get stress fractures of the talus that can be missed on x-ray. Stress fractures are categorized by their risk for complications, such as failed healing or progression to a complete fracture. High-risk stress fractures include those of the anterior tibia, the talar neck, the proximal fifth metatarsal, and the navicular. Stress fractures of the malleoli, calcaneus, and the first or fourth metatarsals are lower risk. Most risk fractures for developing, most risk factors for developing a stress fracture are related to compromised nutrition and endocrine or autoimmune disorders. The x-ray appearance of a stress fracture can give a clue to its chronicity, with chronic stress fractures showing more cortical thickening, sclerosis, and periosteal reaction rather than lucency. Stress fractures in cancellous bones, such as the calcaneus, will show a linear sclerosis that's perpendicular to the normal trabeculae, as shown in this image. In acute cases, x-ray findings often lag behind symptoms. So you can get an MRI or repeat the x-ray in two weeks if the x-ray looks normal, but you have a high clinical suspicion for a stress fracture. MRI is at least as sensitive and more specific than bone scan for detection. CT is generally not used unless MRI is equivocal because it's lower sensitivity and radiation is a issue. First-line treatment of stress fractures is typically rest and immobilization. Surgery is reserved for complete or high-risk fractures, delayed union, or non-union. Don't forget to check bone and nutrition labs, ask about amenorrhea and diet, and check bone density, and refer to your colleagues in endocrinology or nutrition. Here is the recommended daily allowance for calcium and vitamin D, though many providers will supplement more than the RDA, especially in athletes due to the high physical demand. Diphosphonates and teriparatide, which is Forteo, has been used to speed up healing, but there's not strong enough evidence that this would be the right answer on the exam, especially given the risks of these medications. The results of pulse ultrasound, in other words, a bone stimulator, are mixed, and extracorporeal shockwave therapy also has inconclusive results for treating those stress fractures. For anterior tibial stress fractures, the constant tension caused by the posterior musculature and the poor vascularity make it more likely to develop delayed or non-union and return into a complete fracture, so early surgical intervention is commonly advocated and usually allows a faster return to sport. IM nail and anterior plating are both options. Medial moleular stress fractures are not seen very often, but it is a diagnosis to keep in mind for an overuse-type medial ankle injury. Medial tibial stress syndrome, or shin splints, is defined as exercise-related pain along the posterior medial tibia without a vascular cause of stress fracture. The etiology is not fully elucidated. One theory implicates traction on the periosteum from muscular attachments leading to inflammation. However, muscular attachments are not present in the most common site of MTSS. It may be more likely generated within the bone as a stress reaction from bending in the tibial plate bearing, or simply the strain from the causative activity exceeding that individual's repair capacity. Risk factors for medial tibial stress syndrome involve abnormalities of foot posture, alignment, flexibility, and strength. The first five risk factors here at the top were found to be positive and appalled. Results of the 27 risk factors examined in a systematic review. Female sex, increased navicular drop test, increased hip rotation, higher weight, or VMI, which was classified as greater than 20 because these were all cross-country athletes and a history of medial tibial stress syndrome or running injury. The picture here is the navicular drop test and offloaded versus the full weight bearing positions. The other five risk factors below them are, they have been associated with medial tibial stress syndrome as well, but long distance running, sudden increase in training, running on harder surfaces, and running in worn out shoes are often targeted in treatment principles, but they're not well supported as important risk factors in the literature. Stress fracture pain typically is more localized in the anterior, whereas MTSS, tenderness to palpation, often spans several centimeters and is more posterior. X-rays usually negative in MTSS as the periosteal reaction is relatively rare. MRI, bone scan, and high resolution CT can all be used to confirm the diagnosis, but they're not needed for initial treatment if you're asked what to do first. MRI has the best accuracy in symptomatic patients. Bone scan will be positive in phase three, but normal in phases one and two, unlike stress fractures. Rest is really the most important treatment because it's an overuse injury thought to result from doing too much, too fast, and too soon. There's not really strong evidence to support bracing, heel pads, padded insoles, or even physical therapy. Along with gradual returned activity, some suggest running on softer surfaces like tracks, avoiding hills, and changing running shoes every 250 to 500 miles to limit recurrence, be it without good supporting evidence for these changes as mentioned. Low energy extracorporeal shockwave therapy has been shown to be beneficial in recalcitrant cases. Surgery is rarely indicated, and the return to pre-injury level of support is low if surgery is performed. All right, first question. The most common complication of talar neck fractures is arthritis of the subtalar joints, as mentioned. It's not osteonecrosis of the talus, even though that's something that's always a high concern with these types of fractures. 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 over the lateral side of the knee. Radiographs were obtained, which of the following structures is most important to be addressed in surgical management of this patient? So here, that arrow is pointing out for you this spiral proximal fibula fracture. And on the ankle x-ray, you can also see widening of the medial clear space. So this is a nascent fracture, and the most important part to address is the ankle syndesmosis. A 19-year-old male motocross racer presents to the ER after sustaining the injury shown in figures one and two. Physical exam shows a grossly deformed lower extremity with significant swelling. No lacerations are noted. Sensation is intact, and the patient has palpable pulses. He is able to actively flex and extend his toes with minimal pain. What is the next most appropriate step in treatment of this patient? So here are his x-rays showing a severe tibial plafond and pilon fracture. The answer here is closed reduction and application of an ankle-spanning external fixator. So that's her provisional treatment so that the swelling can go down prior to definitive treatment with internal fixation. Next we'll move on to ligament injuries. Ankle sprains are considered the most common athletic injury. 85% of them are lateral ankle sprains. The ATFL which runs from the antero-inferior fibula to the neck of the talus is the weakest and most commonly injured. The CFL runs from the inferior tip of the fibula to the lateral tubercle of the calcaneus and is also commonly injured. The PTFL runs from the posterior border of the lateral malleolus to the posterior lateral talus and is involved in less than 10% of cases. The most common mechanism is inversion and internal rotation of the hind foot with the leg in external rotation and the foot in plane reflection. With the hind foot in neutral, the ATFL is the primary restraint to anterior tail and motion. The CFL is tested with tailored tilt with the hind foot inverted in the tibial tail joint in dorsiflexion. Always remember to compare ligamentous tests to the contralateral side to gauge for normal laxity in that individual patient. With increasing tear grade, you see more ligaments involved, more difficulty with weight bearing, more swelling, more limited range of motion, and more laxity. Laxity tests are not very useful in the acute setting except for low-grade injuries because there's too much swelling and pain to get a good exam. Grade 3 sprains can be further divided into 3A which has a normal stress x-ray and 3B with an abnormal stress x-ray. Based on the Ottawa ankle rules, an x-ray should be ordered if there's tenderness to palpation at the posterior edge or tip of the lateral medial malleolus or inability to weight bear. Tarsal coalition has been associated with lateral ankle sprains. Stress x-rays can demonstrate instability with anterior drawer and tailored tilt as seen in these x-rays here. However, some experts argue against routine use because anterior tibial translation is typically only seen if the PTFL is disrupted, which we know is occurs in less than 10% of patients, and tailored tilt can be affected by age and gender. They're most useful when there's asymmetry with the uninjured side or for assessing restoration of stability intraoperatively. MRI tends to be reserved for cases of chronic instability. Management starts with rest, ice, compression, and elevation. Immobilization and a short leg cast or boot can be done for a short period, no longer than three weeks. Early mobilization with functional rehab has been associated with earlier return to play, higher return to play rate, increased range of motion, decreased laxity, and increased patient satisfaction when compared to casting. Propreceptive training is a key component of rehab for ankle sprains. Taping or bracing can decrease the risk of repeat ankle injuries, but they're not preventable in the absence of prior injury. So without a history of ankle sprains, you don't use taping or bracing as a prevention. While there are some studies that suggest superiority of surgical treatment for acute severe ankle sprains, it's generally not indicated unless it develops into chronic instability, which we'll discuss a little later. High ankle sprains are ligamentous injuries to the syndesmosis. They're much less common than low ankle sprains, but still make up about 25% of ankle injuries in collision sports such as football and rugby. They're also common in contact sports such as ice hockey, soccer, basketball, as well as in skiing. Syndesmosis is composed of these parts, the AITFL, PITFL, intraosseous ligament, intraosseous membrane, and inferior transverse ligament. The intraosseous ligament is the thick and distal continuation of the intraosseous membrane. The intraosseous membrane and ligament make up the strongest part of the syndesmosis. The deltoid contributes to syndesmotic stability as a strong restraint to lateral tailored motion, though it's not considered part of the syndesmosis since it doesn't connect the tibia and fibula. Syndesmotic injuries alter joint mechanics and contribute to progressive arthritis if 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 have a longer recovery and return to play time and are more likely to cause long-term joint dysfunction. The length in centimeters of tenderness proximal to the joint line has been shown to correlate with the severity of the injury and missed days of practice and competition. There are several different physical exam tests that can be used to assess for high ankle sprains. No individual test is diagnostic and inter-rater reliability isn't great, so typically it's a good idea to do more than one of these. Workup also includes x-ray to assess for any fracture and syndesmotic widening. Don't forget to do a tib-fib x-ray as the patient, if the patient has any pain proximally, as this could represent a masonry fracture. MRI has high sensitivity, specificity, and accuracy for diagnosing these injuries, but it's usually not needed for diagnosis. So while grade one injuries are stable and grade three injuries are unstable, there is some controversy about grade two injuries. Some experts believe that they're all unstable while others believe that they can be unstable or stable. Stability is confirmed with stress x-ray, MRI, or ankle arthroscopy. And this image shows a normal syndesmosis in figure A, a stable syndesmotic injury in figure B, and unstable syndesmotic injury in figure C. Stable injuries are treated with rest and inflammatory control, including a brief period of immobilization, usually in a boot, then PT for gaining mobility, strength, and normal gait, and finally a graduated return into sports. Unstable injuries with or without fracture warrant surgical stabilization of the syndesmosis. When an ankle fracture is present, the fracture is fixed first, then the syndesmosis is re-evaluated and fixed only if it remains unstable. A high fibular fracture or a masonry fracture can typically be indirectly reduced with the syndesmotic fixation, but it may require an ORF if the fibular fragment is shortened or rotated. Despite a large body of literature, there's no clear evidence to reach a consensus on the number of screws, the screw size, 3-5 or 4-5, the number of cortices, 3 or 4, or the need for screw removal. If screws are removed, it's best done about 12 weeks post-op, though sometimes it's done at eight weeks in athletes. Though they will break if they're left in, there doesn't seem to be a difference in outcome, so they can be removed only if symptomatic. One benefit of the suture button construct is that it avoids the consideration of implant removal. In general, the outcomes have been equivalent to screw fixation, with some evidence that malreduction is less common with the suture button construct. However, it's a newer technique and there's less long-term data, and it carries its own complication risks, including osteolysis, implant failure, and entrapment of the tibialis anterior. Chronic ankle instability is characterized by recurrent sprains or instability episodes or persistent pain. It's often related to inadequate initial rehabilitation, so physical therapy is beneficial if there is any residual functional impairment present that can be addressed. An MRI should be performed before any surgical intervention occurs, as it may demonstrate additional sources of pain, including chondral injuries and occult fractures. Surgery is warranted when there's residual mechanical impairment related to the ligamentous laxity. Cable varus alignment can contribute to failure of the repair or reconstruction surgery, so that should be addressed at the same time as the soft tissue procedure present. Surgical options include repair and invocation of the injured ligaments or reconstructive techniques. The modified Brostrom gold technique is most commonly used today. Reconstruction techniques can be anatomic or non-anatomic tenodesis. Proneus longus and brevis are dynamic ankle stabilizers that resist immersion, so they're less ideal to harvest. Splitting the proneus brevis and just using part of it is one technique that can be used to avoid this, and this picture here on the bottom right shows the number of the different reconstruction options. Arthroscopy is sometimes performed at the time of the ankle instability surgery. The benefit is that you can identify and then treat any co-existing pathologies such as chondral injury, osteochondral injury, impingement, adhesions, and loose bodies. Proximal tibiofibular joint instabilities are commonly misdiagnosed and can range from subluxation to complete dislocation and fracture. That's most commonly seen in sports with four twisting motions that occur when the knee is flexed. The proximal tibiofibular joint is stabilized by the posterolateral corner structures of the knee, so when the knee is flexed and these structures become more lax, the joint is more likely to be injured. Injury to this joint is more common when there's an oblique orientation of the tibiofibular articulation as we see in this x-ray. A traumatic subluxation seen with ligamentous laxity and true dislocation can occur in the interlateral, posterior medial, or rarely in the superior direction. A traumatic subluxation can be treated conservatively and typically improves with age. Acute dislocation should be treated with closed reduction with the knee flexed to 90 degrees where open reduction and internal fixation of closed reduction attempts are unsuccessful. Always check the knee ligaments post-reduction as the LCL and posterolateral corner structures may need to be repaired or reconstructed if injured. Next question, a collegiate athlete has a lower extremity injury that is being evaluated in the training room which allows deferred radiographic imaging. This is getting at those Ottawa ankle rules, so distal and posterior fibular tenderness warrants x-rays but not distal and anterior fibular tenderness. So this can be deferred, this can allow deferred radiographic imaging whereas the others are all concerns for high risk fractures. 16 year old male lacrosse player sustains an ankle injury during practice when his ankle is everted. He has visible swelling around the ankle and ecchymosis medially. He's tender distal to medial malleolus and anterolaterally between the tibia and fibular for about four centimeters. Physical external rotation stress test is painful. He is able to bear weight with minimal issues but lateral movements cause some discomfort. His radiographs are negative for fracture and stress and non-stress radiographs are normal. What is the best initial treatment to suggest to this athlete? And this is a high ankle sprain but since stress x-rays are normal, it's confirmed as a stable injury so therefore rest studies compression and elevation is best for the initial treatment. The next topic is tendon disorders. We refer to the group of chronic overuse pathology affecting the Achilles tendon as chronic Achilles tendon disorders. Achilles tendonitis is really a misnomer as there are no inflammatory cells found in the tendon itself. The first three disorders listed here are part of the same process that's often referred to as Achilles tendonitis. Peritoneitis is stage one with inflammation of the peritoneum septum. This progresses to peritoneitis with tendinosis stage two and then just tendinosis stage three. The other two disorders here are separate entities so insertional tendinosis is an inflammatory condition that occurs at the tendon insertion into the calcaneus and retrocalcaneal bursitis is a mechanical irritation of the retrocalcaneal bursa that can be caused by Haglund-DeVoyne for example. The Achilles peritoneum is highly vascular and thus susceptible to inflammation. On physical exam, the site of focal tenderness to palpation does not move with ankle dorsiflexion and plantar flexion. The MRI appearance is high signal and thickening of the peritoneum as seen in this axial slice. The majority of cases will resolve with non-invasive treatments. Brismon is an intervention in which saline or a local anesthetic is injected into the sheath to break up adhesions. Surgical treatment is rarely needed and if excision of the peritoneum is needed you should leave the anterior peritoneum intact as that's where the majority of the blood supply to the tendon is located. Achilles tendinosis seen in the later stages is often asymptomatic once the peritoneitis resolves so the rupture can seemingly come out of nowhere. You may be able to elicit tenderness or palpate swelling and in contrast to the peritoneitis, a site of pain or swelling will move with ankle dorsiflexion and plantar flexion. Ultrasound image shows tendon thickening and calcifications and MRI will show tendon thickening and focal signal change. In the absence of rupture, the mainstay of treatment is still non-operative but for those who fail surgery but for those who fail non-operative treatment, surgery to debride the tendinotic portion of the tendon can be performed. Do not use corticosteroids for treatment of Achilles tendinosis as it can cause tendon rupture. The pathology for retrocalcaneal bursitis is located anterior to the Achilles tendon. It's often associated with the Haglund deformity, the bony prominence seen in the posterior superior calcaneus in this x-ray. The repetitive hyperdorsiflexion seen with running uphill commonly provokes this type of pain. Surgery is usually not necessary but removing the bony prominence can be performed for refractory cases. Insertional tendonitis can also be seen with a Haglund deformity and retrocalcaneal bursitis as seen in the MRI image here where you have all three findings. An exam tenderness to palpation will be located right at the tendon bone interface. As with chronic Achilles tendon disorder, stretching and mobilization and physical therapy can alleviate symptoms in surgery to debride the involved tissue and remove any bony prominence as reserved for refractory cases. An acute Achilles tendon rupture typically occurs in the vascular watershed area two to six centimeters proximal to its insertion. It can result from a forced plane reflection action or a sudden dorsiflexion on a planar flex foot. Fluoroquinolone use and corticosteroid injections are risk factors for rupture. Physical exam will demonstrate a palpable gap, a positive or otherwise non-reactive Thompson test which is shown in this drawing here. It also shows increased passive dorsiflexion and decreased planar flexion strength. This diagnosis comes from the history of physical so imaging isn't necessary but it can be helpful in determining the degree of retraction. Historically, non-operative treatment was associated with a higher re-rupture rate. However, it involved casting for six to eight weeks with delayed mobilization in those studies. More recently, functional bracing and early range of motion protocols show re-rupture rates and functional outcomes that are similar to surgery while also avoiding the risk of surgical complications. Recently, non-operative treatment of Achilles tendon ruptures has been on the rise. These non-operative protocols involve a short course of non-weight-bearing immobilization followed by weight-bearing in a walking boot with a progressively decreasing heel lift and starting early physical therapy. There's limited evidence to support a faster return to work and improved planar flexion strength with surgery. Some studies show no difference, however, but that's why surgery is more likely to be favored in athletes to potentially get this improved planar flexion strength. When surgical treatment is selected, options include percutaneous repair, a limited open repair, or standard open repair. The serral nerve is the main at-risk neurovascular structure and injury rates are generally found to be higher with percutaneous repair. As with non-operative treatment, early mobilization and protected weight-bearing are important in optimizing outcomes. Biologics will not be a correct treatment choice for acute Achilles tendon ruptures, as there is currently no proven clinical effectiveness. The definition of chronic varies when it comes to Achilles tendon ruptures, but it can be as short as four weeks from injury. Because contractures developed with the chronic injuries, restoration of the normal resting length is key to having an optimal outcome. The length of the gap after excisional debridement of the non-viable tendon determines your options for repair. A tendon gap of less than three centimeters after this debridement can typically be repaired directly. If you have a tendon gap of three to five centimeters, that typically warrants either a VY advancement, a local turndown flap, or a tendon transfer. For even bigger gaps, you should be prepared to use allograft or synthetic grafts. To start the review on peroneal tendon disorders, let's just touch on the anatomy. Knowing that the peroneus brevis muscle extends more distally than the peroneus longus muscle helps with identifying it on imaging or during surgery. They both pass through a fibro-osseous tunnel at the posterior tip of the fibula and the superior peroneal retinaculum access the roof of that tunnel. The SPR keeps the tendons from subluxating or dislocating, and you see subluxation of these tendons in the photo here. The peroneus brevis inserts on the fifth metatarsal. The peroneus longus continues along the planar foot and inserts into the medial cuneiform in the first metatarsal. That may contain an os peroneum that may contribute to symptoms. Accessory peroneal muscles can cause peroneal tendon disorders due to crowding of the tunnel. On exam, pain occurs with passive planar flexion and inversion as you stretch the tendons, and also with active planar flexion and eversion as the tendons contract. Peroneus longus involvement usually localizes more distally and may involve an os peroneum. Resistant eversion or active circumduction may demonstrate tendon subluxation. The x-ray image here demonstrates a fibular avulsion with the SPR attached to the avulsed fragment, allowing for tendon dislocation or subluxation. Peroneal tendon disorders fall into these three categories, tendinopathy, tears, and subluxation or dislocation. Peroneus longus sits more laterally, so it's more prone to dislocation. Peroneus brevis is more prone to tearing. The sernal nerve is most at risk with any surgical treatments. When treating the tendon pathology, the SPR must be repaired if you open it or go through it to access the tendons. Posterior tibial tendon dysfunction is not commonly seen in athletes because it usually doesn't present until the sixth decade and it's more common in obesity, but you may see it with runners and triathletes. The actions of the posterior tibial tendon include hindfoot eversion, medial arch support, and forefoot adduction and supination. So inability to perform a single leg heel rise is a sign that the condition has progressed beyond that first stage of LPTT dysfunction. With progressive disease, patients will develop Achilles tightness, failure of the medial longitudinal arch, and degenerative joint disease. Stage 1 is characterized by tenosynovitis without flat foot deformity and responds well to anti-inflammatory techniques, physical therapy, orthoses, and boot immobilization. Tenosynovectomy can be done in stage 1 if non-operative treatment fails. Stage 2 involves a flexible flat foot deformity. Ankle foot orthosis is used for non-operative treatment, but surgery is more likely with a combination of soft tissue and bony procedures utilized. In stages 3 and 4, the flat foot deformity becomes rigid and arthrosis develops. So surgical treatment involves arthrodesis with the extent of the arthrodesis depending on the location of the disease. So subtalar, subtalar, and talonovicular are triple arthrodesis. All right, next question. A 40-year-old female recreational runner develops increased pain in the Achilles tendon over the past four months that has prevented her from running. Pain is episodic but worse with starting exercise. She has tried ibuprofen with little relief. An exam reveals a palpable painful thickening in the mid-portion of the Achilles tendon. What is the best treatment recommendation to return the patient to active running? And the answer here is PT to include eccentric stretches. Oral insetches already done. We don't want to do any corticosteroid injection on the Achilles tendon, and PRP has no proven benefit, and shock wave therapy also does not show proven benefit. A 10-year-old soccer, 10-year-old male soccer player has foot pain and flat foot deformity. What is the most accurate physical exam test to differentiate a flexible flat foot from a rigid flat foot? And the answer is reconstitution of the arch on toe raise, so that single leg heel rise. The photo here is of the Coleman block test. This is not the answer, but just so you know what that is, that differentiates a flexible cavovarious deformity from a rigid cavovarious deformity. On to joint disorders. Anterior ankle impingement manifests as anterior ankle pain with terminal dorsiflexion, commonly seen in dancers in the plie position and in turf athletes. Imaging studies will show anterior kissing exostoses on the anterior talus and the dorsal navicular without involvement of the tibial-talar joint. These exostoses don't even necessarily have to touch to cause symptoms. There can be just inflammation or impingement of the surrounding soft tissues that contributes to pain. In the early stages, disorders tend to occur only with causative activity, but in later stages, they can occur with activities of daily living. This x-ray technique described by Van Dyck utilizes an oblique angle of the x-ray beam and over-penetration to better identify the exostoses. MRI and dynamic ultrasound can also be useful when there's a suspicion for anterior impingement but normal x-rays. Non-operative treatment is worth trying, although symptomatic relief may only be temporary. PT is aimed at optimizing ankle stability. Operative treatment involves arthroscopic or open excision of the exostoses and the affected soft tissues. If arthroscopic management is selected, awareness of the at-risk neurovascular structures is critical, so the superficial perineal nerve with interlateral portal, saphenous vein with intermedial portal, and the dorsal neurovascular bundle when you're resecting the spur. If lateral ankle instability coexists with the ankle impingement, a lateral ligament reconstruction should be considered at the time of the exostoses excision. Posterior ankle impingement occurs with terminal plantar inflection, also often seen with ballet dancers in the end point position. Nostrigonum is common etiology of posterior ankle impingement, and this occurs when the posterolateral process of the talus fails to fuse with the rest of the talus. FHL, tenosynovitis, is common in strong and repetitive push-off sports like running and tennis. Symptoms may be present with wearing high-heeled shoes. Note in this picture that FHL sits in the groove between the posterior medial and the posterolateral recesses. While the diagnosis of posterior ankle impingement is typically made based on history and physical exam, imaging studies are useful to determine the etiology. The standard first-line non-operative treatment options apply, as well as additional modalities such as casting if there's an acute and occult fracture or taping in relative dorsiflexion to allow sports participation. Operative treatment depends on the etiology and may involve excision of the nostrigonum, FHL tendon-sheath decompression, or treatment of an osteochondral lesion of the talus. Have a high suspicion for an osteochondral lesion of the talus when you have a history describing chronic ankle pain in the absence of trauma or a history of persistent pain after the normal amount of time for resolution of an acute injury. Ankle sprain is the most common acute ankle injury associated with these lesions. The average age at presentation is 20 to 30. They're more common in men and 10% have bilateral involvement. There are multiple classification systems, but they follow the same pattern as the Burt and Hurdy classification listed here, with higher grade becoming more unstable. This one is based on x-ray, but other classification systems will use MRI, CT, or arthroscopy to grade lesions. Medial lesions are usually atraumatic, more posterior on the talus, and larger, deeper lesions. Lateral lesions usually have a history of trauma, but more central, anterior on the talus, are superficial or smaller and less likely to heal with non-operative treatment. Non-operative treatment in the form of activity restriction, weight-bearing restriction, and immobilization may be appropriate for grade 1 and 2 lesions. However, success rates are still only about 50%. Operative treatment for more advanced lesions or those that fail non-operative treatment may involve transarticular drilling or retroarticular drilling, ORIF epifragment, osteochondral autograft or allograft, or autologous chondrocyte implantation. It has been suggested that excision alone is worse than non-operative treatment. There's not a good consensus on the use of biologics, but they have been used to augment both operative and non-operative treatments. With ORIF, an osteotomy may be needed to access the lesion. Osteochondral autograft and allograft can be done if the lesion is not salvageable, and osteochondral autograft can come from the anterior talus or the distal femur. Osteochondral lesions of the tibia are much less common than those of the talus, but they generally follow the same evaluation and management guidelines, and this is what an MRI appearance of an osteochondral lesion of the tibia. 23-year-old ballet dancers felt to have chronic pain due to osteogonim syndrome and is to undergo surgery. Relative to the FHL tendon, the osteogonim is lateral, and that's just showing this picture again of the relationship of the FHL to the osteogonim. A 26-year-old male tennis player presents to a clinic for evaluation of a sprain of his right ankle. He reports catching the ankle when he walks. Examination reveals tenderness over the intermedial joint line of the ankle with an effusion. Plane radiographs and MRI demonstrate a displaced osteochondral lesion of the medial talar dome of the loose body. What is the appropriate initial management for this patient? Remove the loose body and address the defect. So with a displaced osteochondral fragment, functional bracing and immobilization and not a weight bearing are not going to be helpful for him. The corticosteroid injection may give just very temporary relief but won't address the problem, and ankle arthroplasty is certainly more severe than what's needed for this and would be used more for severe degenerative changes. The 27-year-old female twisted her right ankle and sustained trimalleolar fracture. It was determined to be an SER type 4 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 and radiographs were revealing for development of DJD. What is the most likely etiology for this outcome? So one of the keys here is that they tell you you have anatomic reduction of the major fracture fragments. So the correct answer is occult interarticular chondral injury at the time of the initial trauma. All right, the last category to cover is neurovascular disorders. Chronic exertional compartment syndrome is exercise-induced leg pain with or without paresthesias that predictably begins at the same point of a workout and resolves with rest. In later stages, it can occur just with walking. The anterior and lateral compartments are most commonly involved and bilateral pathology is very common. Muscle volume increases 20% without a proportional expansion of the fascia. However, the theory of tissue hyperperfusion with ischemic pain has recently been challenged as studies haven't found that process to actually occur. So other theories include a stretch of the fascial pain receptors or inability of myocytes to meet the increased metabolic demand. Compartment pressure measurements are the gold standard for diagnosis and the one-minute post-exercise measurement is the most reliable for diagnosis. Imaging is primarily used just to rule out other diagnoses, although some experts have utilized post-exercise MRI or infrared spectroscopy. Since most athletes don't want to give up their sport, non-operative treatment is really rarely successful. Definitive treatment involves open or endoscopic fasciotomy of the involved compartments. The superficial perineal nerve is the primary structure at risk with these techniques. Recurrence may be related to incomplete release, incorrect diagnosis, or excessive scarring from the surgery. Popliteal artery entrapment syndrome is intermittent claudication caused by dynamic compression of the popliteal artery. This condition is much more common in men and is usually found in patients less than 30 years old. The compression can lead to permanent damage of the artery including aneurysm or thrombosis. Patients typically will describe leg cramping and pain with exercise and occasionally paresthesias. The ankle brachial index is typically normal with popliteal artery entrapment syndrome. Duplex ultrasound arteriography or CT or MR angiography is diagnostic. Passive dorsal flexion or active plantar flexion during the test aids in diagnosis. This MRA is of the same leg in the same patient but on the right image the patient is doing active plantar flexion and you can see the difference in that popliteal artery stenosis. Usually once the diagnosis is made, these patients are referred to vascular surgery for consultation because after a compression site is released, treatment of the aneurysm or envelope disease may be necessary. There are various nerve entrapment syndromes that can affect the lower leg and ankle. Trauma is the primary cause for all of these, although nerve entrapment may not be detected until after the acute injury has resolved. They can result from repetitive microtrauma, muscle herniation, direct compression or iatrogenic consequences of knee surgery including knee arthroscopy which is usually the saphenous nerve when it's related to arthroscopy. The image here shows the soleal sling that can cause tibial nerve entrapment. With nerve entrapment syndromes, the pain tends to get worse with continuation of that activity. The symptoms are consistent with the affected nerve distribution and the diagnosis can be confirmed with EMG and NCS. There is limited evidence to require post-exercise EMG. First-line treatment is non-operative, including the options listed here. Operative treatment usually involves decompression of the affected nerve. Finally, DVT in athletes. Virchow's triada venous stasis, endothelial damage and hypercoagulability does not immediately seem problematic in athletes compared to the patients in whom we normally worry about DVT and PE. There are some factors that can increase this risk in athletes even in the absence of surgery. These include long bus rides or flights for competition, collision during contact sports that can cause endothelial damage and oral contraceptive use that contributes to hypercoagulability. Chemoconcentration can also be a factor with altitude training, anabolic steroid use and dehydration. The standard recommendation for a provoked DVT is anticoagulation for three months with a restriction from contact sports while on that anticoagulation. 25-year-old collegiate soccer player presents to your office for popliteal artery entrapment syndrome. Which of the following statements is correct concerning diagnosis and management? The correct answer is in patients with normal popliteal artery, musculotendinous sectioning is the proper treatment. Patients with PAE will have decreased foot pulses and arterial pressure with active motion of the ankle when measured with ABI, DELFOR, ultrasound or angiography. PAE is most common in patients less than 30 years old, 15 times more common in men than women. So D is not correct. And vascular reconstruction is obviously only needed for cases when there is vascular injury or chronic arterial occlusion. A 25-year-old military officer presents your office with a 15-month history of vague right calf pain without prior injury. He describes burning in the back of his calf exacerbated by prolonged standing or running and radiating into the plantar foot. No swelling, color changes or weakness are present. PAE reveals diffused tenderness with deep palpation over the proximal calf. Positive tunnels over this area with radiation into the plantar foot. No masses or cords are palpated and reproduction of the symptoms occurs with foot dorsiflexion within the infall extension. Distal pulses are symmetric. Management has consisted of PT, NSEDs and activity modification all without resolution of symptoms. What's the most appropriate management of this patient? So this vignette describes tibial nerve entrapment as it's passing through the soleal sling. A PT with gastroc soleus stretching is a good initial treatment, but this patient's already failed PT. So the next step would be a soleal sling release. A 17-year-old female high school field hockey player complains of bilateral leg pain. This occurs shortly after she begins playing and she feels paresthesias over the dorsum of the foot when she continues playing. The pain resolves about 30 minutes after resting. Physical exam in the office is nonspecific. Plane radiographs are unremarkable. What's your next most appropriate step in evaluation? This is described in chronic exertional compartment syndrome. So the answer is post-exercise compartment pressure measurement. Really, you need both pre- and post-exercise measurements to make the diagnosis here, and one-minute post-exercise is the most reliable. MRI and bone scan would be options for evaluating stress fracture, and angiogram or Doppler can be used to test for palpital artery entrapment. And that's my final question there. Here are the references, and I want to thank you for taking the time to listen to this presentation and wish you all good luck.

Dr. Eileen Crawford

orthopedic sports medicine surgeon

University of Michigan

leg and ankle

board exams

fractures

ligament injuries

tendinopathies

joint disorders