All right, our next speaker will be covering a leg and ankle, and that's Corey Edgar from the University of Connecticut. Thank you. All right, so we got a, I have no disclosures that have anything to do with this. I want to give props to the people that have done this before me, Dr. Beals and Dean Taylor. I've been doing this since 2015. So we have a lot of things to cover today. We're going to go through some basic anatomy. Remember, this is all review. Go through a lot of questions that I pulled from self-assessment exams, the AOSSM fellowship exams, and intermittently a few, like, OIT questions that may be pertinent to a topic. We're going to go through traumatic bone and ligament injuries, leg, chronic ankle injuries, tendon problems, and then miscellaneous stuff with fractures and tumors. Now again, typically I talk much faster than I can roll through things, so just hang tight and all the stuff's in your handout. So basic anatomy. The first thing we have to remember with the ankle mortis, it is a mortis joint with the tibia plafa and medial lateral malleolus. Very constrained articulation with the talar dome, which comes into the particular aspect of alignment of the ankle. It's very sensitive to articular cartilage malalignment with ankle arthrosis. The other thing about the tibia mortis is its shape. It's trapezoidal. Therefore with dorsiflexion, you'll get an external rotation effect with the fibula as the ankle dorsiflex. The lateral ankle anatomy is obviously the things that come up most commonly. The fibular collateral ligaments, the more superficial ones and more distal ones, the anterior talofibular ligament, most commonly injured with ankle sprains, is the weakest. The posterior talofibular ligament is the strongest, and then the calcaneofibular ligament centrally is the second one to be injured during ankle sprains. Lateral ankle ligaments in general, you'll have the more proximal anterior aspect of the syndesmosis, which is the anterior tib-fib ligament. Just anterior to that, that can be a problem intermittently with some ankle impingement is this hypertrophies with chronic ankle instability. The posterior talofibular accessory ligament, also known as Bassett's ligament. In terms of the drawer test and testing of the ATFL integrity, you want to test this in plantar flexion. Calcaneofibular ligament is typically tested in neutral or even dorsiflexion, and you can look at tailored mobility to the medial side of the ankle. The medial ankle anatomy, obviously we're talking about the deltoid ligament. It has some complex anatomy. The superficial contributes really little to stability. It really has to do with rotation. The tibial navicular ligament, tibial calcaneo ligament, and superficial tibial tailor ligament. The deep is the primary stabilizer to medial translation. It's interarticular and deep tibial tailor ligament is the most important. So the superficial really controls rotary instability. As an ankle injury progresses, you get more rotary instability. You get an increase in deltoid injury. This oftentimes does not play out in x-rays, as there is on the medial side. The anterior colliculus and posterior colliculus, which has been well described. The anatomy, typically the superficial fibers are more anterior. The deep fibers are more central and posterior. So a lot of times we can see stable ankles with some tailored tilt, with just injury to the superficial deltoid ligaments, but no lateral translational laxity or quote unquote instability that needs to be addressed from a surgical standpoint. So again, the superficial deltoid controls the rotation and the deep deltoid controls coronal plane or translational motion, meaning clear space widening. So medial anatomy, so Tom, Dick, and Harry is the old adage. So we go from basically anterior to posterior, posterior tibialis, flexor digitorum, Tom, Dick, and so artery, nerve, and then Harry, the neurovascular bundle is obviously located between the digitorum and flexor hallus. Lateral view of the tendons, the superficial perineal retinaculum is the primary stabilizers to the perineal tendons. At the level of the base of the fifth metatarsal, we can often see avulsion injuries that have to do with injury to the lateral band of the plantar fascia, as well as the brevis tendon attachment. Typically the Jones fractures are in this area between the tertius and the brevis. Typically Jones region is more central at the joint line, and the stress fractures are more proximal along, or more distal rather, along the base of the fifth metatarsal. So the testable facts around this area and regarding to anatomy is the blood supply of the talus. The main blood supply of the talus is the artery of the tarsal canal, which is a branch off the deltoid. This is a circumferential branch that can come both from the lateral and the medial side. The medial side, it comes off the posterior tibial artery. On the lateral side, it's the extension of the perforating arteries around the perineal, as well as the dorsalis pedis. The gait is complex, and you have to remember it's a hinged joint. This will be covered in much more detail in the next lecture. A lot of times in questions, the patient history comes up. So it's important to think about location, direction, mechanics. Remember, these are in here during testable situations for very specific reasons. Responses to medications, for example, cholesterol drugs, can cause and lead to heel pain with deposition. So information is given in the history of the question for a reason. So physical exam, obviously inspection, palpation, range of motion, the ability to reproduce pain, and the stability exam is all important aspects as you're relating this clinical information to answering your question. So assessment of Aquinas. So testing ankle dorsiflexion needs to be done in both knee extension as well as knee flexion. This lengthens distal as well as proximal. Remember, the gastroc goes across the posterior aspect of the knee joint. So if you flex the knee, you're taking sort of the gastroc and relaxing it out of this. This can also be used potentially to address neurovascular issues, especially popatial entrapment. So lower extremity alignment, we'll see a lot of this in this talk and the next talk. Hindfoot valgus, or varus, rather, or cavovarus foot. Two-thirds of these patients will have a neurologic disorder, so if it comes up at a testing, think about this. The most common neurologic disorder that comes up in these testing situations is Charcot-Marie-Tooth disease. X-ray standards really are AP, mortis, and lateral X-ray of the ankle. On the AP, we're really looking at the tibiofibular clear space overlap as well as medial side of the ankle clear space, which is more typically seen and appreciated on the mortis view in terms of the alignments and distance on this side as well as the alignment at the insura. Lateral ankle X-ray, you can visualize the centralization of the fibula, the dome of the talus, any avulsion fractures, anterior, posterior. You can look at the osteogonum. There's a lot of things that can be identified on this. For calcaneal fractures, things that come up, Bowler's angle needs to be evaluated and assessed. The critical angle of Gossain comes up. And on a Broden's view, you can look at the articulation alignment of the posterior facet. MRI, typically used for stress fractures, evaluation of anatomy, abnormality, synovitis, and certainly infections, especially when you're talking about the usage of contrasts. So this is a common thing that comes up. You can visualize accessory musculature. So this is an example of a patient of mine actually that had accessory soleus muscle belly. It is present in approximately 3% of the patient. It's a distant belly medial to the Achilles tendon. Accessory soleus is associated with pain, edema, long periods of prolonged exercises. Jumping athletes, volleyball and basketball players will often get fullness and pain, almost like a compartment-like syndrome back there with that. CT scan is best used for evaluating bony detail and anatomy, whether it's tumor, cystic changes or fracture. These are examples of the questions which we'll go through very quickly. Primary restraint to inversion, the ankle position and plantar flexion is anterior tail fibula ligament. This is an actual example. This is the MRI image. The arrow identifies which of the following structures. We just went over this accessory soleus. High school football player has been treated by PCP two months. Chronic ankle pain and swelling. So chronicity is important here. Been treated with NSAIDs, activity modification, the usuals. Exam is normal except for swelling. What's the next appropriate step? MRI is failed conservative treatment. 35-year-old woman presents for evaluation of foot pain. This has been described for five-month history. Worsening plantar pain, numbness, tingling, first three toes. Web space shows tenderness, decreased sensation along the plantar medial foot border. Positive to tennels along the medial ankle, so already you're thinking this is probably something neurologic. They give you this MRI that shows the cystic changes along the posterior medial aspect. So at this point, exploratory surgery with excision of cystic mass for alleviation of symptoms. So we're going to move forward to the next section. Traumatic bone and ligament injuries. We're going to try to touch base on all of these. Tibia shaft fracture. So no significant difference in thresholds for treatments with athletes versus regular trauma patients that come in. IM nail is still standard for mid-shaft fractures. However casting does still work. Normal and distal plating is needed for plateaus. Still two millimeters displacement is our threshold. And be aware of concomitant injury and the risk of compartment syndrome. So this is an example of two patients of mine that were treated differently and do well. So you could take a really nondisplaced tibia shaft fracture and treat this conservatively with long leg cast, short leg cast, and then conversion to functional bracing and they do well versus a Division I athlete that you could probably argue to treat this in a cast but getting them early mobility with good alignment and muscular reactivation in a Division I soccer goalie probably works out a little bit better in this situation. Pylon fractures. Remember these are high energy injuries. The principles of treatment here are control soft tissue windows. So external fixation for swelling control and then further surgical management for fracture reduction and articular alignment reduction is sort of the mainstay. A lot of times we have to graft but really external fixation is a lot of times what's going to come up with these just because the soft tissue window is not appropriate. When evaluating ankle fractures there's two common classification systems that are brought up. The Weber classification looks at the level of the fibula fracture as it relates to the joint line whereas A below B kind of add in just above and then C is a lot more proximal. Loggie Hansen. This is sort of the mainstay in the world that I grew up in which is a mechanistic foot position and then rotational mechanism injury classification system which there's data now that says that maybe this is not as true as we thought but it does come up often on examinations. So arthroscopy. This has become an emerging issue in terms of an expanding role during the treatment of fractures. Ankle fracture, talus fracture, calcaneal fractures. This may be a way for us to reduce the likelihood of unrecognized interarticular fragment or osteochondral injury and also to appreciate articular reduction if necessary. Syndesmotic injuries are real and fairly common. They can actually happen without a fracture at all but most of the time they'll happen with no fracture at the level of the ankle joint and they'll have a proximal fracture. It usually can be viewed as a high ankle sprain. It's usually a rotational injury. They oftentimes have a prolonged recovery above the normal for a quote-unquote ankle sprain. So nonoperative, you can get serial x-rays that can demonstrate the subluxation as they start to weight bear or they have poor tolerance to weight bear and usually you have to do something across the syndesmosis for fixation, screws or cortical buttons or whatever the case may be. Talus fractures or the aviator astragalus, this can be body or neck. Usually it happens with a dorsiflexed foot position and axial load. Most common complication is actually subtalar arthrosis, not AVN. So subtalar arthritis is not AVN. The classification in terms of likelihood of going on to AVN, so you can have a nondisplaced, about 13% reported, subtalar dislocation or subluxation, 20-50%. And then ankle subtalar dislocation with extrusions can be up to 40-100%. So Hawkins sign is actually a good sign. You want to see this. What this is is an area of subchondral osteopenia or decreased radial density at about 6-8 weeks post-injury. It implies that blood can get to the subchondral surface to remove the mineralization, which is part of the second stage of fracture healing, where you've got a mineral resorption and then a redeposition as it remodels. Acute lateral ankle ligament injuries, inversion injuries, oftentimes they have prior sprains, tenderness over the ATFL or CFL, and even PTFL. Oftentimes they have cable varus foot. Early return to sports play is recommended, but oftentimes they can have persistent symptoms. There's a general time of a return to sports play with residual symptoms noted. So even though they return, they often have some residual symptoms. The gradations are kind of classic, 1, 2, and 3, in terms of ligament disruptions. As this happens, it's almost typical that the ATFL happens first, CFL happens second, then the posterior, which is a rotational component, the PTFL. This can again just be detected with anterior drawer versus lateral tilt, or medial tilt of the ankle. Acute management, proper diagnosis, we're going to quickly go through the auto rules, which are whether or not you need to get an X-ray on presentation of ankle injuries. Obviously RICE therapy, so rest, ice, compression, and elevation. Propreceptive training is a mainstay in peroneal strengthening. This has sort of been expanded to add P and M to the RICE, to now the PRICE-M. So this is protection and mobility. Obviously NSAIDs may help increase recovery, weight-bearing, as they'll let you tolerate them to progress with weight-bear. You could protect them with casts, boots, and lace-up ankle braces, but early range of motion is the most important in terms of physical therapy. Trying to maintain a strength in proprioceptive exercises as soon as their muscle coordination and activation re-engages. So the auto rules basically is a good study that looked at when do we actually have to get X-rays. So if they present with any of the five positives that it's suggested to get X-rays, inability to bear weight, tenderness of palpation over the posterior medial malleolus, tenderness of palpation of the posterior lateral malleolus, tenderness of palpation of the base of the fifth, or over the navicular. So these are basically where the auto rules have come from. And again, these are the areas in which there are tenderness of palpation that it's recommended that you get X-rays or inability to bear weight. So there is good studies. The original one showed 100% sensitivity with a 40% specificity for detecting malleolar fractures with this. Recent studies have not been as good. However, that said, it's still a good tool. Other indications, if the patient can't communicate, alternate status, alcohol intoxication, pain that seems out of proportion, or any time you're just not confident in your physical exam or their history, it's safe to get. So questions. A 36-year-old speed skater slips, injures ankle, no effusion, tender over the ATFL radiograph show a medial osteochondral defect, which they give you same as two years ago. These are typically more chronic. So you're just going to treat them for the ankle sprain. College athlete with lower extremity injury that is being evaluated in the training room, which allows you to defer the radiographic imaging. This again, referring to the Ottawa rules. So they have distal and anterior fibular tenderness only. No X-ray is indicated. 13-year-old male, six-month history, medial hind foot pain, increase with sports activity. The pain allows, the patient enjoys running, playing soccer, but is unable to because of this pain. Parents deny any trauma. He has increasing complaint of foot pain after walking from school. Exam shows tenderness over the hind foot, mid foot, and forefoot. On exam, the most important, he has decreased in subtalar motion with no obvious instability or swelling. Those are your MRI images. He obviously has a coalition, so the indication is surgical treatment. Open reduction internal fixation is generally advocated for bimalleolar fractures. This is recommendation is primarily based on biomechanical data that implies the abnormal pressure distribution of talus shift. So even one or two millimeters of lateral directed talus shift, the tibial talus mortis does not line up appropriately and changes the articular cartilage pressures and therefore potentially progresses arthritis. Most common complication of talus neck fracture is arthritis of subtalar joint. 53-year-old obese male, painless deformity of the ankle, denies significant trauma, but notes progressive loss of sensation over his feet. So you see where the question is leading you. Radiographs show displaced bimalleolar fracture. Ankle has disorganized callus, chronic process. So he obviously has diabetic neuropathy on top of this, so we need to check fasting sugar. 29-year-old male, sustained talus neck fracture with an associated dislocation of the body from the talus, of the talus from the subtalar joint and tibial talus joints. He was treated with immediate open reduction and internal fixation. 12 weeks later, there's a lucency observed in the subcognitive bone. So again, this is a good thing, so you want to continue your observation of protected weight bearing. 27-year-old female, twisted her ankle, sustained a trimal fracture. Determined to be a supination external rotation type four. So this is a Loggie Hansen classification that says it's a full rotational, medial and lateral sided injury. She had surgery for open reduction and internal fixation. One year later, she complains of ankle pain with ankle range of motion, radiographs reveal degenerative joint disease. What's the most likely etiology for this outcome? That we missed something in terms of an intra-articular occult chondral injury at the time of initial trauma. 16-year-old male, sustains ankle injury practice, is inverted, with ankle is inverted, excuse me, everted. Visible swelling around the ankle, ecchymosis is medial. He has tender, distal, medial malleolus, anterior lateral between the tibia and fibula, about four centimeters. Physical exam with external rotation stress pain is positive. He is able to bear weight with minimal issues, but lateral movements cause discomfort. He has radiographs that are negative for fracture. Stressed and non-stressed radiographs are normal. You still want to treat him, even though he has the components of a high ankle sprain with rest, ice, compression, elevation. 28-year-old male, twisted left ankle, playing hockey. This is pretty typical in a hockey player. Describes pain over proximal aspect of his left leg, tightness over the lateral side of his knee. Radiographs show, not unexpectedly, a proximal fibula fracture with still some medial clear space widening. So he obviously has a mesoneum type injury with the ankle syndesmosis injury that needs to be addressed because it is an unstable ankle fracture. 26-year-old male tennis player presents in the clinic for evaluation of a sprain of the right ankle. Reports catching an ankle when he walks. Examination reveals tenderness over the anterior medial joint line of the ankle with an effusion. Radiographs and MRI demonstrate a displaced osteochondral lesion of the medial talar dome with a loose body. You got to get that loose body out of there, so the answer is remove loose body and address the defect. Functional bracing's not gonna work. Orthoplasty's not gonna work. And all the rest are pretty much conservative management. 19-year-old male motocross racer presents the emergency room after sustaining injury. Here, pylon again. So what's the next appropriate street? In most of these situations, it's going to be address the soft tissue and address the alignment. It's not really gonna be about sort of fracture reduction or treatment. All right, moving on to the leg area. We're gonna talk about some general topics here. So the basic science. So we have to remember that collagen type one is related to bone and ligaments. Type two, related to and found in articular cartilage. And type three is a healing ligament and early scar tissue. Cross-linking within the collagen adds to strength. Elastin, typically 1% by volume, allows for length maintenance of a tendon or a ligament. Ligament is really unmineralized fiber cartilage. Once it becomes mineralized fiber cartilage, now we're really talking about bone. Ligament avulsion injury typically happens between fiber cartilage layers. Strength of healed ligament diminishes due to less cross-linking as we age. Normal and disorganization of the collagen orientation in terms of a scar formation and repeat injury like a hamstring tear. Muscle force created by myosin and actin interface. Type one muscle fiber distinctions. Type one is slow twitch, red, aerobic metabolism, more mitochondria, endurance athletes, i.e. marathon runners. Type two, fast twitch, white, shorter contractions, more lactic acid, power weightlifters and sprinters, explosive. So this is on here, which is actually pretty easy. So toaster. So type one, aerobic, slow, twitch, endurance, red. So again, just looking visually at a graph, type two, fast, powerful, short timeline, big tension, slow duration, type one, over the length of time. So sprinter, marathon runner. Muscle function. Force proportional to the cross-sectional area of a muscle. Velocity is related to displacement over time. So it's proportional to a muscle fiber length. Leg or thigh contusions. This happens quite often. So contusions are typically related to direct blows. Most of the time we try to institute a quote-unquote West Point protocol, which is immobilized in a flexed or a flexed knee position to extend the muscle length. You can do this with a dorsiflexed ankle, early motion, better than casting. Muscular strains can be done by an indirect force. Obviously prevention with strengthening, stretching. No consensus on treatment with NSAID steroids or various protocols. This is happening more and more often as people are getting into these combative sports where we see this quite a bit. This is an example of a guy that, especially with certain fighting, like Muay Thai styles, they actually intentionally click this and develop, well this always flips, literally develop acute compartment syndromes. They're not emergent, but they develop it and they often lead to this, myositis ossificans. So the distinction of this on an X-ray is the cortex is not involved on the plain film, not to be confused with, if it is, the osteocartilaginous lesions like osteochondromas. The cortex is part of the lesion and malignancies osteosarcoma, the lesion is attached to the cortices. So myositis ossificans has a mature ossification of the periphery, whereas in osteosarcoma, it's mature centrally as it causes a peripheral ossification effect. Classically in the thigh, the football players, hockey, lacrosse, you can get it in the forearm as they get hit with the lacrosse sticks quite often. Certainly in martial arts, they'll do it in the thigh and in the anterior lateral compartment of the leg. 40% are just idiopathic, without known trauma. Most of them happen in the thighs. They're typically asymptomatic, but when they are symptomatic, you can remove them after they have metabotically matured, and most of the time, we recommend bone scans, you can get CT scans to look at maturation of the process. Stress fractures, insidious onset of pain, increases with duration and intensity of activity. Tibia is one of the more common places. Fracture localization, commonly associated with jumpers, distance runners, or people that have really changed their activity levels dramatically in a short period of time. They often have focal tenderness. Images can show periosteal reaction, sclerosis. They can even show the quote-unquote dreaded black line. MRIs can show diffuse changes, intramedullary, as well as along the cortices, and there's a good classification system, and then obviously, bone scan can be done as well. Once they progress to a true fracture along the anterior cortices, i.e. the dreaded black line, they really, we gotta be a little bit more aggressive with our management. Risks, marketed increase in training, distance or intensity, initial poor condition, excuse me, change in surface for runners, beware of metabolic stressors, the amenorrhea in patients, the female triad, changes in medication use, vitamin D deficiency, thyroid issues, and celiac disease. Anterior tibial cortices is one of the more common. It's a tension side of the bone, it has poor vascularity. There is no consensus on treatment, which means there'll probably be very few questions on surgical management outside of stop the activity. Medial tibial stress syndrome, also known as shin splints, more common in runners, poor condition people, surface changes, foot pronators, flat foot deformities. Periostitis is really what we're talking about at the origin of the posterior tibialis, and along the fascial periosteal interface. It is associated with pes planus. It's a non-focal, can be focal, tenderness, non-focal on imaging, time limited, typically treated conservatively. Oftentimes, we have to consider orthotics in these patients. Exertional compartment syndrome, it's relatively uncommon. I think sometimes it sees us and we don't see it. It happens oftentimes in runners, soccer players. Compartment pressures, diagnosis comes from measuring directly the compartment pressures, which are oftentimes you stimulate the patient, have them run or run on a treadmill. You can measure direct pressures at rest, after activity, and during recovery with striker needle. Oftentimes, foreleg compartments are measured. It's sometimes that the deep compartment is involved. The deep does communicate with the foot, but not all of the time involved with the anterior lateral, which is the most common. Surgical fasciotomy is the treatment, and recent studies suggest that barefoot or forefoot running may be effective in alleviating these by strengthening various muscles. Diagnostic criteria, resting pressures greater than 15 millimeters, one minute post-exercise greater than 30, five minute post-exercise recovery still greater than 20. Increased pressure within a closed fibro-osseous space leads to ischemic pain, neuritis, and motor dysfunction. They oftentimes describe numbness, a slapping foot as the anterior compartment starts to weaken and they can't elevate their foot and dorsal flexion as they run. They'll have anterior lateral pain. They can even get herniation along the superficial perineal nerve. It's the most at risk during this condition, as well as during the treatment and release. Popliteal artery entrapment presents with similar type of symptoms. It's probably a much more rare cause of exercise-induced pain in the young people, possibly due to repeated popliteal artery compression leads to, in the posterior aspect of the knee, leads to intimal fibrosis of the artery. Exercise compartment pressures may be elevated or normal, so you test them for exertional compartment pressures and everything becomes normal. This is what we were talking about, that sometimes, I suppose if you're lucky, you can find, determine a loss of pedo-pressures as the knee goes into extension with the foot placed into dorsal, or plantar, excuse me, dorsal flexion, and then resolution of the loss of pedo-pulses as the knee is flexed. Don't forget about the spontaneous DVT. This happens. Consider duplex for any leg, thigh swelling and non-traumatic cases. Tenderness along the midline, posterior leg. Most of them are distal. Some of them can be proximal after knee scopes. Duplex ultrasound is the test of choice. Ongiography is to evaluate for aneurysms and popliteal entrapment. DVT risks. Obviously, the history is the most important. First degree relatives with PE, DVT, medical causes, hypercoagulability states, which often aren't diagnosed until after they present with a DVT. Obviously, females on birth control or anybody on hormone supplementations, recent surgery or trauma, even knee scopes can lead to DVTs. So proximal tip-fib joint injury. This often happens after a violent twisting and flex of the knee, proximal lateral leg pain, stable knee exam. You can either have subluxations, which is typical with people that have loose ligaments, or dislocation, which is typically anterolateral. Treatment can be closed reduction. Leg tumors. None are common. They often present with pain at rest or at night. So this is, again, a history thing within the question. Swelling without trauma. Types are osteochondroma, which happens typically outside of the cortex. Fibrous cortical defect, or NOF, inside the cortex, UBC, ABCs. These can happen typically in younger patients. Osteosarcomas, Ewing's, multiple myeloma, chondrosarc, and osteoid osteoma, which I've actually seen myself in a patient. This is a case of a UBC in a young girl that was like 12 or 13, in her epiphysis or fibula. This was a patient of mine, 22-year-old male with a posterior knee pain, greater than two years, getting worse. No trauma. Pain at night. Did not correlate with specific activity or improvement at rest. X-rays were negative. PCP obtained an MRI out of frustration, which was otherwise benign. We just sort of got lucky on this cut that we saw something sort of back here in this edematous changes within his posterior aspect of his posterior lateral knee MRI, and a CT scan confirmed the diagnosis, which was treated with radiofrequency ablation. Chronic ankle injuries, instability, malalignment, and arthritis. Assessment of limb alignment, tibial varus, muscular atrophy, and Charcot-Marie-Tooth disease is paramount. Assess the foot shape. Is cavus or varus present? Coleman block test is what we look for in terms of flexibility or rigidity within the hind foot deformity. Tarsal coalitions in the rigid caval varus foot. What can cause it? Tarsal coalitions, post-traumatic arthritis, progressive diseases like Charcot-Marie-Tooth, and neuromuscular conditions. Rigid versus supple is the mainstay of figuring out what you got, so you do this Coleman block test where you place the heel and lateral forefoot on the block and then let the first ray drop off the edge. If the heel moves to valgus position, flexible, unchanged, it remains rigid. Surgical treatment, recurrent ankle instability, recurrent sprains, greater than six months, failed physio. Primary treatment would be the gold modification of the brostrum. You take the anatomic ATFL repair and then augment it with the inferior extensor retinaculum. Good success rate. Return to, excuse me, randomized clinical trials, anatomic brostrum better than non-anatomic reconstructions. Chronic ankle instability, tendon graft reconstructions for failure of anatomic repairs. Negatives, they get typically subtalar loss of motion. There is more morbidity and you typically either take or injure the peroneal tendons. Consider hypermobility situation, so use a Brighton score, have them look, assess a hypermobility situation in the question and consider osteotomies to correct the cavus. So ankle malalignment as a cause of ankle instability. Some people, for reasons, preserve articular surface, consider an osteotomy, change the alignment to balance, just like we would do in the, say, the knee, for example. Ankle arthritis, low prevalence versus hip and knee in terms of idiopathic, most is post-traumatic. Most of post-traumatic is chronic instability or direct fracture post-traumatic. Be wary of the tunnel vision, evaluate for systemic arthropathies, hemochromatosis, hemophilia, things that are causing chronic effusions. Indication for painful arthritis in the younger patient is fusion. Create enhanced stress along the adjacent joints. They do get some mobility and increased pain and discomfort in the subtalar and midfoot. This is acceptable for people that are looking for activities like biking, skiing, golf, cycling, and hiking. Technique, position a foot at fusion, neutral plantar flexion, slight or five degrees of valgus, neutral to 10 degrees of external rotation. You wanna match the contralateral side, assuming that's normal. Reduce translations when possible. Arthroscopic and open techniques are described. Arthroplasty, failed, non-operative treatment, severe arthritis, rheumatoids, elderly, low demand, ipsilateral hindfoot arthritis, compliant patient. It's still maybe probably less controversial, but for certain sports except for the lower demand sports. So 24-year-old volleyball player, recurrent ankle sprains, failed PT for greater than six months, considering surgery, modified Brostrom. 39-year-old male, primary complaint of chronic ankle instability, has failed non-operative management. He completes, corrects, he completely corrects with Coleman block test, means he has a supple ankle. Surgical indication, or surgical care includes lateral ankle ligament reconstruction, first metatarsal dorsiflexion osteotomy. So means you could do a soft tissue procedure because he has a supple hind foot. A 10-year-old male with soccer player has a foot pain and flat foot deformity. What is the most accurate physical exam test to differentiate between a flexible foot and rigid flat foot? Reconstitution of the toe arch on heel raise. So he goes up on his toes and does his hind foot correct or not correct. 11-year-old female sustained an inversion sprain to her left ankle 12 weeks ago and is unable to bear weight. Aledania means she's just diffusely pain, swollen. She has a hypersensitivity kind of sympathetic response. Her foot is purple in hue, diffusely swollen. Bone scan shows increased uptake around the ankle, sub-talar joint, talon and avicular joint. Calcaneocupoid joint treatment should consist of decreasing the sympathetic nerve overstimulation and then re-institute physical therapy. 18-year-old male presents with recurrent bilateral ankle instability. Symptoms have been slowly progressive, denies problems with coordination, complains of easily fatigue when he types. Exam is notable for bilateral cable varus foot with perineal weakness. So we know we got something going on here. He has intrinsic muscle weakness in his hands. He should, evaluation should include EMG. 35-year-old female who's an avid runner complains of progressive, worsening bilateral leg pain over the last six months, which has reached a point where she's unable to run. States she wears quality running shoes, stretches regularly, physical exam, pain along the posterior medial half of her tibia. She has normal knee and ankle exam, slight pronation of both feet. Radiographs are normal. Bone scan reveals longitudinal uptake along the posterior medial surface of both tibia. So she has medial tibial stress syndrome and rest orthotics and calf stretching. Almost there. Tendon problems. So tenonopathy. Tenonitis is rare. Tenonosis is a histologic diagnosis. Peritonitis, tenonitis with peritonitis, most common symptomatic tenonopathy. Partial tears and complete tears. So rupture of the Achilles. Sudden complete mechanical failure associated with fluoroquinolone usage. Average age around 35. History of tenonosis may or may not be present. Tenonosis frequently is asymptomatic, true tenonosis. Paratenonitis, chronic insertional or proximal tenonus can be present. Thompson test is obviously the mainstay of diagnosis if there's a disruption of the continuity between the gastrocnemius attachment to the heel via the Achilles tendon. Obviously if you squeeze the muscle mass, you should see a corresponding plantar flexion response. You could do this like this. You could have them lay prone. Whatever works best and most comfortable. If you squeeze this and there's disruption, there is no movement. So you can cast, brace, early movement to prevent dorsal flexion, loss of motion. There is no risk of infection with this. There is a risk of DVT, typically slower to initiate weight bearing. You could argue that there was classically a reported higher re-rupture rate. This is probably, may not be true with some of the newer randomized clinical trials. There's obviously with open repair, increased risk of infection, lower, potentially lower risk of re-ruptures. The strength is really what we're talking about in the power issue with more aggressive in the younger patient, the higher demand patients, probably is what this comes down to. Open repair, typically in a prone position. Medial approach favored, secondary to wound healing as well as the seronerve. Repair of the tendon and tendon sheath is key. Terms of risks, the medial approach, there is wound infection and healing issues. Wound healing as well as infection. In the percutaneous, the seronerve is at most at risk and most commonly injured with this procedure. Tendinosis, degenerative process, may or may not be painful. Palpable nodule is typical within the tendon. Treatment is eccentric loading during physical therapy. Sometimes you can use a use of nitrites which decreases the vascular inflow. These can be percutaneous and maybe will decrease some of the inflammation. Achilles insertional tendinopathy, nutritional condition, encephalopathy would be attachment of the tendon to the bone. Tendonitis, bone spurs often present, broad, often broad plate of the bone. Ossification within the tendon itself can be found. Tenderness at the insertion of the bone and bony prominence of the heel is found on exam. Obviously non-operative management, modify the routines, you can put them in a boot, heel lifts, stretching, injections for this area are very rarely recommended. Longitudinal tendon incisions for surgical treatment of tendinopathy, concentrate on the most painful area, excise the degenerative tendon and bone, reattachment, use of FHL as augmentation, prognosis, guarded, improved symptoms, but typically not a cure. Most of these patients at the insertional aspect will have a Hoagland's deformity, which is a mechanical cause of tendinosis, posterolateral bump typically present, often associated with a retrocancanial bursitis, which is a fundamental component of this. Etiology is to decrease the area of vascularity. The tendon degeneration or tendinosis with peritendinitis is present. This can often happens at non-insertional tendinitis in this quote-unquote watershed area, which is anywhere from two to six centimeters proximal to the attachment of the heel. At this point, they have a less capacity repair secondary to this watershed area. They have pain, swelling, warmth, and crepitus. Typically in runners, athletes oftentimes have gradual onset. You'll often notice a bulbous area that will move up and down with the ankle because it's attached in part of the tendon. Good response rate overall with non-operative management. NSAIDs stretching, eccentric stretching is key. Ionophoresis, which we kind of mentioned. No steroid injections directly into the tendon and modify activity across train. Operative peritendinitis, a longitudinal medial incision, release of the adhesion, stripping of the thickened peritenone, and immediate mobilization for the post-operative course. With tendinosis, you wanna make sure that you debride the thickened peritenone. You wanna remove any necrotic tissue excised and then do a primary tendon repair and recirculation. Undiagnosed ruptures, these can come in chronic. The tendon does heal, but it heals in an elongated position. So the issue is pain and weakness and muscle dysfunction. They often can present with functional limitations, inability to go up the hills, stares with a limp. I don't often complain of pain. They can have weakness and difficulty with running, and as I said, stares. Defects from two to five centimeters, you often have to consider a FHL transfer. Into the repair, defects greater than five centimeters, you often have to even do something more proximal in addition to the FHL transfer in terms of myotendinous lengthening, VY lengthening. Perineal tendinopathy and ruptures. Longitudinal split along the tears are common. The brevis is the most common involved. MRI not uniformly predictive due to angle of the travel of the tendon and the cuts of the MRI. May see small avulsions, fracture on x-ray. Check if the perineal tear is there and then fix it. Superficial perineal retinaculum is the most important to secure, to reduce any perineal subluxations which often lead to this in the first place. So you wanna address the etiology as well as the tear. So perineal tendon subluxation dislocations commonly associated with ankles with recurring ankle sprains. Tears are commonly associated with dislocations of the tendons. Disruption of the superficial perineal retinaculum is part of this etiology. Whether it's acute disruption, but usually in these situations it's a chronic attenuation. Posterior tib teninopathy, posterior tib dysfunction. So evaluation of this is tenderness along the tendon with swelling. Too many toe signs as you're looking like this picture is from the back of the person. Hindfoot valgus, radiographs can show degenerative changes and tailored tilt. MRI changes in and around the tendon. Classifications are listed here. Late stage classifications or fixed deformities and oftentimes result in fusions. One and twos, they're much more supple and can be treated from a classic tendinopathy standpoint. 18-year-old high school basketball player treated for Achilles tendonitis. What type of strengthening exercises? Eccentric. 30-year-old sedentary male evaluated for increasing pain near the insertion of the Achilles. Denies change in activity level. Chronic sinusitis, seasonal allergies being treated with Cipro. Family history of diabetes. Management should discontinue the fluoroquinolones and then conservative management. 40-year-old female recreational runner develops increased pain along the Achilles tendon for four months, preventing her from running. Episodic pain when she exercises. Tried ibuprofen, little relief. Exams palpable painful thickening of the mid portion of the Achilles tendon. What is the best treatment recommendation for her to return to activity? PT and include eccentric stretching. 35-year-old male sustains a fall while rock climbing. Notes immediate pain, deformity of the ankle. Diagnosed with a closed bimal fracture. Surgical fixation and medial mal fracture. A disruption of the mid substance of the posterior tibialis tendon was identified. You're, of course, you're gonna fix that. 50-year-old male recreational tennis player. Medial pain, weakness of his left ankle. Persistent for three months despite conservative treatments, including a cam walker, physical therapy and orthotics. Transient improvement, corticosteroid. Tenderness with chronic swelling, posterior to his medial mal. Has mild, flexible, dynamic flat foot. Ankle dorsiflexion extension of five degrees. Stable anterior drawer. Difficulty with a single toe raise. Here's your x-rays. He's got posterior disruption of his tibialis. So posterior tibialis tendon debridement and repair. All right, intraarticular issues. Ankle impingement. Anterior ankle pain with activity. Mechanical block to dorsiflexion. Anterior impact sports like gymnastics or basketball with sudden stops or explosive things. Weight-bearing lateral x-rays and maximum dorsiflexion helps with this. Treatment, heel lift, NSAIDs, corticosteroid injection locally. Typically with ultrasound so you can maximize its localization and use it as a diagnostic tool. Rest. Surgical debridement for those failing non-surgical care. Remember we talked about in the very beginning that beset's ligament. Oftentimes that becomes hypertrophied and needs to be removed. Anterior osteophyte may be successfully imaged with oblique radiograph. Dorsiflex position, CT scan or MRI. Arthroscopic or open debridement within the gutters can be done. And consider using C-arm fluoroscopy while you're doing this to make sure you get enough of the debridement of the distal aspect of the tibia. Anterolateral impingement lesions are common. Low risk for arthroscopy. High success for defined impingement lesions. Most common complication with this is cutaneous nerve injury to the superficial perineal nerve. Effective ankle arthroscopy is effective at removal of acute chondral loose bodies. Sinovial biopsies, debridement of impingement lesions. OCD of the talus is unfortunately relatively common. Size of defect tends to indicate outcome. Review of the literature comparing debridement versus grafting or OATs. Debridement and drilling microfracture is primary option. 26 year old male has a posterior medial talus OCD. Posterolateral approach for ankle arthroscopy is made during surgery. The portal is created between the Achilles and the perineal longest tendon. 31 year old male hockey player comes into your office. Four year history of anterior left ankle pain. Been getting worse over the last few months. Is now interfering with simple activities. Initial injury was a forced dorsiflexure of the ankle landing on a jump while snowboarding. He has an MRI. At the time of injury it showed a contusion. Four injections, several rounds of therapy and only one transient improvement. MRI shows this OCD. On the medial side, what's the best treatment option? So unfortunately at this point, the best treatment option we have for him is ankle arthroscopy debridement with or without marrow stimulation as a primary treatment. 29 year old professional tennis player who has had multiple ankle sprains. Complains of anterior ankle pain, popping, locking despite PT, NSAIDs, MRI shows medial OCD. What's the next appropriate step? So as you can see, there's a commonality with this. 14 year old female dancer presents with ankle pain. She has persistent effusions, mechanical symptoms despite appropriate conservative management over the seven months. MRI. Again, she has mechanical symptoms. So operative arthroscopy, removing the mechanical symptoms, potential treatment at that time. You are counseling a patient considering ankle arthroscopy for loose body removal. What is the most common complication associated with ankle arthroscopy? Superficial perineal nerve. All right, heading home. Stress fractures of the distal tibia and talus. Relatively rare overuse or metabolic issues. Presents with vague pain but limits activity. Common in gymnasts, skiers, runners. Non-athletes really work up the metabolic side. TSH, vitamin D, PTH, testosterone. X-rays and then repeat two to three weeks later as just like in the hand. Sometimes you can see development of a fracture that was done acutely as it starts to resorb. MRI scanning if you want to do it acutely. Consider DEXA scan if multiple recurrent, i.e. there's a mineral issue. Immobilization and weight bearing is, immobilization and limited weight bearing is treatment. Triplane fractures, ankle instability for cavus or hind foot varus and then Charcot-Marie-Tooth, which is again progressive perineal dysfunction, anterior lateral compartments, weakness, intrinsic hand atrophy, and cavo-varus deformity progressive. Triplane fracture, this occurs in the distal tibia physis as the physis is closing. Early to late adolescent ages, different fracture planes on AP and lateral X-ray, hence the triplane. Typically requires surgery, especially if displaced. Painful osteogonum, this happens fairly common. Common sources of test questions. Clinical problem, ballet dancers, trauma, their pain is often lateral to the FHL. You want to treat them like an ankle sprain first. Injection or incision if it fails, arthroscopic or open. 23-year-old ballet dancer is felt to have chronic pain due to osteogonum syndrome. Is to undergo surgery relative to FHL, the tendon is lateral. The osteogonum is lateral to the tendon, sorry. 23-year-old ballet dancer notes hind foot pain when on point, which obviously means when they're up on their toes. Which of the following is most likely the cause of her pain? Osteogonum. 17-year-old female high school track athlete has posterolateral ankle pain associated with sprinting, jumping, events. Progress to the point she can no longer compete. Examination tender to the Achilles tendon, medial and lateral, just above the insertion. No swelling. Pain with full plantar flexion. There is minimal discomfort and resistance in aversion. Radiographs show ossification, posterior talus. MRI shows fluid around the posterior talus and ossification density. You still wanna rest in NSAIDs with alternative training regimen. That's it. Good luck, thanks. Thank you.

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