Our next speaker is Aseesh Bedi from the University of Michigan and he will be giving us an overview of the ELBO. Thanks very much Chris and Bruce for the opportunity to be here. In terms of the ELBO review here, this is really more of the content I think for the test that you'll have and so we'll sort of take this I think in stepwise format, working through some of the pediatric concerns, eventually working through some of the typical fractures, ligament injuries, tendinopathies and then finish up a little bit with the neurovascular issues. So all of this is in your packet but I think it's appropriate to just briefly review the anatomy for the ELBO. We'll talk about this of course in more detail with each of the elements of pathology but of course with regard to the ligaments, when you look at the medial side of the ELBO, the one that gets the most attention is the ulnar collateral ligament. Just note here that there are these three bundles, the anterior bundle, the posterior bundle and the so-called transverse ligament between the two. The workhorse on the medial side of the ELBO as you'll see is the anterior bundle of the ulnar collateral ligament which is the functional valgus stabilizer in anywhere between 20 to 130 degrees of flexion and that will become important for your test with regard to any questions regarding which bundle we prioritize or focus on with reconstruction. As you look towards the lateral side of the ELBO, we'll talk about these ligaments as well. You'll note the lateral ulnar collateral ligament which runs from the lateral epicondyle to the crista supinatoris on the ulna. This ligament becomes important with consideration of so-called PLRI or posterolateral rotary instability. So we'll talk about that during the talk but note that anatomy. You'll also note the annular ligament which is a ligament that again surrounds the radial head. This becomes important with montasia fractures which we'll talk about but also with chronic montasia in which sometimes the annular ligament needs to be reconstructed, a so-called belt house procedure. And then anterior and posterior capsular procedures for elbow contractures. With regard to the muscular anatomy, again we'll talk about these in independent detail but just to review this, remember the triceps in the back of the ELBO innervated by the radial nerve. It has these various heads which have become important. With regard to the anterior aspect of the ELBO, the lateral side of course consists of your mobile wad which includes your brachioradialis, your extensor carpi radialis longus and brevis. Note that that mobile wad is innervated by the radial nerve and the reason that's important is distal to those muscles, the innervation for the remaining extensors is via the posterior interosseous nerve. So that will become important. On the medial side of the ELBO, again note your flexor pronator mass, your pronator teres and then your flexor digitorum superficialis and profundus. Again, important to note those muscles. They'll have relevance when we talk about some of the nerve-related issues as well as the tendinopathies. And then the neurovascular anatomy around the ELBO becomes important. Let's just review here. The radial nerve which we all know courses along the posterior aspect of the humerus and the spiral groove. Then it subsequently wraps between the brachioradialis and brachialis as you can see here anteriorly and then subsequently dives deep and divides into the posterior interosseous nerve and then the lateral cutaneous nerve we're all familiar with. The median nerve here as you can see, of course, innervating the flexors. It innervates half of the brachialis, your FDS, half of the FDP and then distinguishing that from the ulnar nerve which we all know runs posterior to the medial epicondyle and then subsequently between the heads of the FCU. It innervates the FCU, the ulnar half of the FDP and then the intrinsics in the hand. So we'll talk about those again in detail but just a place to start with regard to the anatomy. So again, we'll start with some of the so-called pediatric sports conditions for the elbow. I don't need to belabor this but all of us are familiar with the so-called epiphyses which are the ends of the growth plates. They're the cartilaginous things at the tips of the long bones that ossify over time. The apophysis which is really where the attachments of the tendons or ligaments are, those become relevant as we'll talk about with regard to so-called little Liger's elbow. Remember that at least with regard to the elbow, most of the maturation occurs in this 18 to 25 year time point. You'll all remember this acronym more from pediatric orthopedics but it is relevant with regard to your test questions, so-called CRITO which is the age at which these centers ossify. You can see here this represents the capitellum, radial head, the inner or medial epicondyle, the trochlea, olecranon and then the lateral epicondyle and remember this age at ossification are these odd numbers 1, 3, 5, 7, 9 and 11. So if you remember that mnemonic, you'll remember the typical appearance of these ossification centers but then correspondingly, you need to know sort of when they fuse or start to close and those correspondingly represent the same acronym, just different years. I would draw your attention on this diagram to the medial epicondyle which is usually the one that often gets tested. You can see its age at closure is 15 to 16 years of age. That becomes important because below that age point, it's an apophysis and frequently a source of apophysitis or little Liger's elbow or in some cases in the sports throwing athlete, a medial epicondyle avulsion injury. So just be aware of these numbers and maturation. It's a common test question which ossification center is the last to close and the answer is your medial epicondyle. So with regard to growth plate injury, we'll start with little Liger's elbow which is medial epicondyle or apophysitis. Just note as we mentioned from the crito mnemonic that the medial epicondyle forms at age 5 and fuses at 15 to 16 years of age. This is a pathology that reflects repetitive stress from the flexor pronator mass or group that then places traction on the medial epicondyle and apophysis. It's usually gradual onset and it presents with a complaint of elbow pain, loss of velocity in a thrower and diminished effectiveness. Physical exam findings are pretty typical. Medial epicondyle are pain and swelling. Pain with a valgus stress test, I think the test question here is distinguishing in the maturing adolescent versus adult population. The differential would be your ulnar collateral ligament injury or so-called Tommy John injury. It may often present with a flexion contractor as well which is typical in throwers. If you do have a suspicion for this on the test, they may show you this which is an MRI. You can see here that you'll see this edema at the growth plate and apophysis but you will often see there an intact ligament. Again, demonstrating a more pediatric type of injury rather than a ligament tear, more of an avulsion type of mechanism. The treatment for these is almost always non-surgical. On the test, don't answer for little leaguers elbow surgical treatment. It's usually avoidance of throwing for a minimum of four to six weeks. There's theoretically some association with certain types of pitches but that's soft data. The point here also is if there is an option on your test, note that while the elbow is the source of symptoms and complaints, the problem usually originates earlier or upstream in the kinetic chain. It usually reflects so-called glenohumeral internal rotation deficit or posterior capsular contracture of the shoulder. So the treatment will not just consist of rest but also posterior capsular stretching, improvement of scapular kinematics and hip and trunk stability. So treatment is non-surgical. That is to be distinguished from your medial epicondyle avulsion fracture. So unlike that slight widening that you saw at the apophysis and a gradual onset, this is usually an acute episode, one throw and you feel a pop or perhaps fall with valgus stress to the elbow. There may be a history of repetitive throwing and a history that's typically provided of valgus overload in a young and throwing athlete. Oftentimes, there's limited motion or it may be hard to extend. Why is that? In cases of an associated elbow dislocation, sometimes the medial epicondyle itself is incarcerated in the joint at the time of the reduction. They'll often give a history of swelling, a palpable defect. And the distinguishing feature here as you can see on the x-ray is this considerable gapping and displacement. If all you see on the x-ray is widening and a gradual history, that's more the little leaguer's elbow scenario. In this situation where they're actually demonstrating gapping here, they're demonstrating that it's an elite athlete or a thrower. This is pushing you more of the direction towards potential surgical treatment. A CT scan is often most precise to measure displacement. If you don't see the medial epicondyle in the x-ray, the answer is a CT scan because in the setting of an associated elbow dislocation, the medial epicondyle can actually be incarcerated in the joint and lead to a slightly non-concentric reduction. So the treatment for these is controversial, but for your test, if there's greater than three to five millimeters of gapping in a throwing athlete, the answer is open reduction internal fixation. K-wires or compression screws are fine. Typically, one or two screws are utilized to avoid rotation and to achieve sufficient compression. Of course, the approach requires protecting the ulnar nerve, as we just mentioned, that lives just behind the medial epicondyle. This is more likely, again, an issue of what the patient does for activity. So the test question will allude to the fact that it's an elite thrower, a displaced fracture with some gapping that wants to return to sport. And the answer in this case is ORIF. What's Panner's disease? This also will show up on the test more than it probably shows up in the clinic. This is a bone development disease or osteochondrosis, maybe analogous to what we see in some other parts of the body, such as Perthes disease in the hip or Kohler's disease in the foot, like Anish just covered. This reflects repetitive microtrauma and stress that can affect blood flow. The bone softens and collapses and then has to remodel. This tends to affect an age demographic similar to Perthes disease, more between 5 to 10 years of age, whereas an OCD lesion that we'll talk about shortly reflects more commonly over 10 years of age. What does this look like in terms of the clinical history? They'll provide you a history of vague lateral elbow pain. It's most common cause of lateral elbow pain in children. So the scenario will say someone in a child who's 5 to 10 years of age who's having some lateral elbow pain, perhaps some stiffness that's worsened with activity. And they'll almost always show you a radiograph that looks like this. The most common location is the capitellum. You'll see fragmentation, even flattening and collapse that does, again, look reminiscent of the findings that we see in the pillars of the femoral head with Perthes disease. Oftentimes an external oblique, AP, and lateral view are diagnostic. An MRI is rarely necessary or provided in these test questions. The treatment is, again, non-surgical. It's rest, avoiding repetitive valgus stress. Remember, with valgus stress, we not only load the ulnar collateral ligament, but also the radiocapitellar joint, which is the secondary stabilizer to valgus stress. So avoidance of throwing and valgus load is critical. It usually just takes some physical therapy for improved range of motion and strengthening. Note that this remodeling back to a normal appearance can take as long as three years. Again, much akin to the other locations in which we see osteochondrosis and remodeling like the hip and the foot. But the answer is not surgery. Let's move on to elbow fractures. Again, a pediatric population most common, but we also will see these in the sports population. One that frequently is tested is the olecranon stress fracture. Remember from that CRETO mnemonic, the olecranon apophysis will appear at age nine, but it will fuse at about 12 to 15 years of age. It can develop a delayed or non-union of that if there's repetitive stress and throwing despite the presentation of symptoms and pain. Oftentimes a contralateral radiograph can be helpful to assess a difference in size and appearance in the physis or apophysis. Again, it reflects micro-stressing from olecranon impingement or tensile forces of the tricep or both. What will it usually present like in your testing scenario? Of course, it'll be pain that's directly posterior. Oftentimes this is misdiagnosed as a triceps insertional tendinitis. It's not a triceps injury. It's pain that reflects early olecranon stress reaction. It's often night pain that's occurring after throwing rather than during throwing. If you're suspicious of the diagnosis, these kind of imaging findings will be provided on the test. The x-ray will be relatively normal, especially if the contralateral radiograph is not provided. You may see some mild gapping at the apophysis, but the MRI is diagnostic where you'll see this edema and stress reaction in the olecranon and at the apophysis. And that, again, can be treated without surgery with rest and rehabilitation. If you do see, however, a more severe stress reaction and even the appearance of the so-called dreaded black line, which is more reflective of a stress fracture that has failed to heal in an elite thrower, that may be tipping you more towards surgery. So again, for the typical test question, the non-controversial, if there's no gapping and early stress reaction, treat it non-operatively. Stop the inciting throwing. Perhaps an evaluation of mechanics for the throwing motion. You may consider a bone stimulator, but that will rarely be a test question. It's operative if it's displaced. Oftentimes, if it is displaced, the treatment will be a single cannulated screw that will compress across the fracture site, plus or minus a tension band construct, either with a wire or a plate. But again, that should be restricted for those cases that are refractory, despite a considerable period of rest or frank displacement for your test question. That's different than your acute olecranon fractures. Those of us are all familiar with these as a different set of mechanics, and this is overlap between the sports and the trauma surgery realm. This is usually a direct blow or fall on a flexed elbow. You'll see pain and visible swelling at the location of the fracture site. Usually, because there's a compromise in the extensor mechanism, the patient or the athlete is able to passively extend, but not actively extend due to incompetence of the triceps and extensor mechanism. These are the typical classification systems that you'll see here. It's not important that you memorize the classification. They'll rarely ask you to classify it. Rather, just note that they're typically non-displaced or displaced or so-called stable or unstable. Those that have comminution usually require some sort of a plate construct to restore length and anatomy. The non-comminuted variety may be treated with a more typical tension band construct. So again, you'll see here, if it's minimally displaced without step off of the articular surface, it wouldn't be unreasonable to treat it with a cast. But most of these in which there's been a direct olecranon fracture and some step off are treated surgically with open reduction internal fixation of the joint surface and restoration of the extensor mechanism. Supercondylar humerus fractures, again, overlap between sports and pediatric orthopedics. These are your most common in your pediatric population. They will typically give you a history of a fall, often from monkey bars or playground equipment, where you're falling on a flexed elbow or a hyperextension type of mechanism. Remember, the main issue associated here is the potential for associated vascular or neurologic involvement. They'll often present you with the scenario of a pulseless elbow. And of course, there is some controversy regarding the urgency of a reduction. But that should allude you to a supracondylar fracture in which the median nerve or brachial artery can be entrapped within or near the fracture site. The Gartland classification remains the mainstay of classification for these. You'll see this angular deformity of extension at the distal humerus. You can see this classification goes from a 1, which is non-displaced, to a type 2, all the way to a 3A or 3B, which reflects displaced with posteromedial or posterolateral displacement. The vast majority of these that are the more displaced variety are treated surgically, most often with a closed reduction and percutaneous pinning. In the setting of neurovascular involvement, you need to be prepared for a potential open reduction to avoid further neurovascular injury and to explore the fracture site. Oftentimes, x-rays will look like this. This is a non-subtle variety in which there's complete displacement of that supracondylar fracture. This is one that could, for example, require a potential open reduction and pinning. Remember the typical relationship that they will be looking for on your x-ray. An adequate reduction has the radial head, a line through the radial head, aligning with the center of the capitellum. So when you're performing your reduction maneuver, you want to see that that's an acceptable amount of alignment. Fixation is typically with K wires. Again, I don't think this will be a test question for you, whether it requires lateral pins or cross pins. There's a number of biomechanical studies in the pediatric literature that the standard of care is at least two lateral pins to confer some rotational control of the fragment. But if it's a type 3 fracture that's grossly unstable, adding in a medial pin adds some level of stability. If you do add in the medial pin, of course, you need to be aware of the ulnar nerve and protect it during your pinning. Just know that a single pin would not be sufficient stability. You need at least two cross pins across the fracture site for type 2 and type 3 fractures. Radial head fractures would be the next one in the category. This typically reflects valgus overload or axial load through the forearm, as we mentioned, and will often be a test question in the setting of ulnar collateral ligament insufficiency, which is your primary valgus stabilizer of the elbow. The radiocapitellar joint is your secondary stabilizer, and radial head fractures will occur with these valgus loads. You're probably familiar with this Mason classification. Again, the classification scheme is less important. It's knowing the implications. Most type 1 non-displaced radial head fractures can be treated non-operatively. It's more the type 2 and 3 and 4 fractures that are treated operatively. In general, if they are reducible and one or two fragments, ideal anatomic reduction and fixation is the standard of care. When there is comminution or inability to repair, these are treated either with excision or radial head replacement. That decision-making process, of course, reflects the integrity of the interosseous membrane and distal radial ulnar joint to avoid the so-called dreaded Essex-Lopresti lesion in which there can be shortening with an inappropriate radial head excision. The diagnosis of these can be subtle. If you see x-rays like this on your test, they may be deliberately showing you an oblique view to identify these minimally displaced fractures. There can be overlap. You can see here on the lateral x-ray this could be easily missed, but the oblique view shows the step-off at the radial head that is at least 2 millimeters or more. As we mentioned earlier, non-displaced fractures are treated non-operatively. You do not want to immobilize these elbows. Elbows like to get stiff, so early range of motion is appropriate. In those cases, these are usually stable fractures. When they're displaced, they should be treated with open reduction internal fixation and or excision or replacement depending upon the severity of comminution and integrity of the interosseous membrane. As I mentioned, these will often occur in association with injury to the ligaments given the valgus mechanism. In the setting of a valgus instability, you may not only consider radial head replacement but also MCL repair or reconstruction at the time of surgery. I don't think that will often come up on the test, but just be aware that it's a valgus mechanism such that the ulnar collateral ligament can be involved. This, however, is often a test question, which is if you are going to fix the radial head, what is the safe zone to place hardware? These pictures show it nicely here. There's about a 90-degree quadrant of the radial head that does not articulate with the ulna at the proximal radial ulnar joint. Of course, the location of that quadrant varies depending on what orientation you're looking at the forearm. Note that in neutral rotation, which is the right side of the screen, it's an anterolateral 90-degree quadrant. If they're asking you where that lives in supination, it's posterolateral. So that's the test question answer. You do not want to have your hardware ever placed anteriorly or medially because certainly with pronation, that will engage the proximal radial ulnar joint and can affect range of motion or arthritis of that joint. So note that the safe zone for hardware is anterolateral in neutral rotation or posterolateral in full supination. Capitellum fractures, these are rare, but they're often tested for some reason. I think they're interesting because they do present oftentimes in this athletic population. They're the result of a shear force, usually an outstretched hand with axial compression. They're more common in the slightly maturing athlete age that is achieving near skeletal maturity. As you can see these pictures on the bottom of the screen, you'll hear some typical colloquial acronyms for these fractures. The so-called Hahn-Steinthal or Coker-Lorens fractures, which are either osteochondral in nature or simply chondral in nature. This is the Brian Mori classification system for these and now Mike McKee's classification. Once again, I think the classification for these is less important. That will rarely be tested. What is more tested is how these are managed. And fortunately for capitellum fractures, the answer is usually surgical in nature. If you see here, they'll oftentimes show you an x-ray or a CT scan that looks like this. You can see here the displaced capitellar fragment on the lateral view. In this case, you have a significant amount of associated bone. These require an open reduction and internal fixation. Fortunately, the test question may ask where is hardware often placed. If the hardware needs to be placed through the joint, it's countersunk and headless screws can be used. But note that the posterior 30 degrees of the capitellum is non-articular. So hardware can be placed at that location. You're certainly familiar with this for distal humerus fractures in which the posterolateral plate can extend all the way down and around the bottom of the capitellum without affecting range of motion or extension. So as you can see here, operative fixation techniques can include suture anchors, countersunk screws, headless screws. None of that will be on the test. Just note that if you have a capitellar fracture and it's large or displaced, this requires surgery given the involvement of the joint surfaces. Chorinoid fractures are also tested frequently. And the reason for this is while these are small and seemingly innocuous fractures, they are not, they have a considerable role in the stability of the elbow joint. They're often seen in the setting of an associated elbow dislocation, they may show you what appears to be a simple benign elbow dislocation and then show you after a closed reduction what appears to be a normal elbow joint that's having recurrent instability. And if you look more closely, you'll see a small coronoid process fracture. These can be small but sometimes not benign. So we'll show that here. These usually can involve a twisting, flexion, or hyperextension mechanism. But beware of this on the test if they're showing you a post-reduction elbow that has a small fracture. This is the classification, the Regan-Mori classification system. You'll feel tenderness usually along the joint line, often in the anterior aspect of the elbow. A type 1 fracture is the tip. Type 2 involves less than 50% of the coronoid and the type 3 is at the base involving more than 50% of the coronoid. Certainly twos and threes can be bad actors, not just from the perspective of fixing them because there's little bone stock to work with, but they're challenging because they can simply result in a recurrent instability of the elbow joint. So this is often what they will show you on the test, a lateral view like this where you can see this seemingly benign, small coronoid fracture. This, however, in extension can result in instability and recurrent dislocation. A CT scan may sometimes be warranted to further characterize the size of the fragment in comminution. These are sometimes amenable to a medially placed plate in the setting of comminution. If they're very small, sometimes they require simple suture fixation that are brought through drill holes to the posterior aspect of the ulna, sometimes using an ACL guide. So again, for type 1 fractures, these are usually stable, early range of motion and non-operative treatment is the answer in the absence of instability. If they are type 2 or 3 fractures and there's an alluding to recurrent instability of the elbow, these require surgical fixation. They won't ask you whether it's a plate or a screw or sutures and a guide, but just know that recurrent instability with coronoid fractures do require surgery. Osteochondral lesions of the capitellum or OCDs, these are commonly tested in the sports realm. What this will present as is dull lateral elbow pain that increases with activity. They often will give a history of an overhead athlete or a gymnast. It's repetitive valgus load, as we talked about, that leads to repetitive compressive forces at the radiocapitellar joint. That leads to microtrauma and involvement of the blood supply that leads to softening of the bone. This will be different than the Panner's disease that we talked about earlier. That will be in your 6 to 10-year-old age group and you'll see osteochondrosis of the capitellum. This will usually be in your adolescent population, anywhere between 10 to 16 years of age, and they will give you the following historical features. Typical symptoms of locking and catching, a flexion contracture and swelling, and palpable tenderness, and then usually imaging studies that look like this, where rather than seeing involvement of the entire capitellum, you'll see this area of an OCD, most commonly located in the capitellum, usually centrally and anteriorly, as you can see on the lateral view here on the MRI. These can be so-called contained or uncontained lesions. This shows a contained lesion here that does not involve the lateral column of the humerus versus uncontained lesions that can involve the lateral column of the humerus. The reason this becomes important is it affects how you might treat it. The vast majority on the test will be contained lesions, where you'll see that there's an appropriate shoulder and margin. These can be treated with excision and drilling or microfracture. When it involves the lateral column and are uncontained, or it's had a previous microfracture and failed, the treatment of choice is an osteochondral transplant, autograft or allograft. Most of these, however, on your test will be mechanical symptoms, a first-time injury or presentation, and the appropriate treatment is elbow arthroscopy, removal of the fragment, and drilling or microfracture. In the setting of failure, significant bone involvement, or involvement of the lateral column, it's an appropriate answer for an osteochondral autograft transplant, usually using a harvest from the knee joint. Just be aware of that presentation for mechanical symptoms in the throwing athlete. Now we'll move on to some of the tendinopathies, the most common dreaded tennis elbow or lateral epicondylitis. I've highlighted here in yellow the key terms for your test. We know this as tennis elbow, but of all the different muscles and tendons that are involved in the mobile WAD, the pathology lives in the ECRB. The extensor carpi radialis brevis is where the pathology lives here. This is good work from Nurschel that describes this pathology as angiofibroblastic hyperplasia. So they may ask you a test question, what might you see at the time of surgery in the tissue? You will not see an inflammatory infiltrate. They may lead you to see a test answer that says lots of white cells. In fact, it's relatively devoid of inflammatory cells. It simply looks like bland hypocellular vascular tissue. And just be aware of that buzzword as the pathology or test question answer. Usually it's repetitive or vigorous use of the forearm muscles. Usually the pain and exam will be pain with resisted wrist extension or extension of the index or the long digit. It often presents with weakened grip strength as well, but that's a confounder that they're throwing at you. It's not involvement of the ulnar nerve. It's pain related weakness in grip strength and swelling. That's what you might see on imaging studies. If they show you that, you'll see disorganized tissue on an MRI. On an ultrasound, you'll simply see thickening at the ECRB. The treatment options are all of the following. Again, no rocket science here. If it's a first time presentation, the answer is non-surgical. They probably won't have you distinguish between corticosteroid or PRP. But do note that there is now at least level two quality evidence for PRP for treatment of patellar tendonitis and lateral epicondylitis. So that is in some level our strongest level of evidence for platelet-rich plasma. So it is now an acceptable answer if provided on the test for tennis elbow. But all of those would probably be grouped under a form of non-operative treatment strategy. Surgery and debridement is indicated for these only if non-operative management fails. They may have given you a history that the patient used a counterforce brace, had multiple series of PRP injections and physical therapy, and the answer would be an arthroscopic or open debridement of the ECRB. This can be done arthroscopically or open. That won't be a distinguishing factor on the test. Both have been done and demonstrated effectively with good outcomes. This is just showing you that angiofibroblastic dysplasia here from Nurschel's initial study when he reported on over 1,000 patients in this. Again, 97% improved. It didn't matter what surgical technique was used, whether or not suture anchors were placed. So those will not be test factors. It will simply be treating the pathology in the ECRB tendon. What about medial epicondylitis or so-called golfer's elbow? The key factor here will be that this involves the flexor-pronator origin, most commonly the pronator teres, FCR, or palmaris longus. So for your test, if there's a question as to which tendons are involved, pronator teres and FCR will be the test answers. It's repetitive stress that leads to tendonitis, again can lead to avulsion fractures like we've already discussed in the younger patient population. So if they're getting at the diagnosis of medial epicondylitis and not little leaguer's elbow or an avulsion fracture, it will be in a slightly older patient. Again, the pain, as you would imagine, is over the flexor-pronator group. There's weakened grip strength. If there's paresthesias, you need to consider involvement of the ulnar nerve and associated neuritis. Same imaging and treatment considerations as lateral epicondylitis. These have normal radiographs, and the treatment course is the same. Alternative treatment is the first line, physical therapy, ice, compression, bracing. Surgical debridement is rarer than it is for lateral epicondylitis, but it can be effective. And again, it would be in the FCR and pronator teres muscle groups. You may want to look for tendon degeneration. Ultrasound may be appropriate to look for tendon thickening. X-rays are really more to rule out confounding diagnoses such as osteophytes, OCD, or fracture. Already covered here, rarely surgery. And PRP or corticosteroid injection would both be acceptable answers for this pathology. You need to distinguish this, however, from a flexor-pronator strain. This is commonly tested, and it tends to be tested, as I highlighted here, in the older throwing athlete. So this is commonly reported as an associated pathology beyond your typical ulnar collateral ligament injury. They may give you a history of an older or aging pitcher who now has sudden onset pain and weakness in the forearm with repetitive microtrauma. They're alluding to potentially an ulnar collateral ligament injury. But as you look further in the history, you'll get pain distal to the media epicondyle, but also weakness with flexion and pronation. If you do see associated ecchymosis, this is alluding to more than an ulnar collateral ligament injury. So just beware if you see a palpable defect, pain, and swelling in an older thrower. They're alluding to a flexor-pronator strain. Usually they'll show you an imaging study that looks like this. This is to have you distinguish between an ulnar collateral ligament injury, where they're looking for the so-called T sign that I'll show shortly, and looking more for this, where you see proximal myotendinous injury and edema in the flexor-pronator mass. The x-ray should look normal. The MRI will not show an injury, at least in the cuts they provide to you in the UCL, or it will show a UCL injury and these findings in the muscle. Generally speaking, these are treated non-operatively unless you're doing an associated ulnar collateral ligament reconstruction or repair. In that setting, if there's an associated flexor-pronator avulsion, it can be fixed surgically. But most of the time, they're looking for non-operative treatment unless it's an avulsion mechanism with greater than two and a half centimeters of retraction. In that setting, those can be repaired, particularly in elite throwers. Distal biceps tendon ruptures, these deserve some attention because these are very, very commonly tested, not just in terms of what the pathology is and what deficits result, but also with regard to the surgical repairs. So these are your demographics here that are commonly tested from Mark Safran's paper in AJSM. It's usually one to two out of 100,000 patients, but it tends to be your mid-aged male athlete tends to have predisposing factors of smoking or a high BMI, but usually a physical or manual laboring job. And a history will be provided to you of an eccentric load on a flexed elbow. So they may tell you that the patient is lifting a heavy object with a flexed elbow, felt an acute pop and the elbow extended to give you a mechanism of an eccentric load in a tendinopathic or potentially a tendinopathic patient. You need to know this tuberosity anatomy. George Athwell has described it. It's a cam-shaped appearance to the radial tuberosity. First be aware of this orientation because the tendon only inserts on 30% of that radial tuberosity and that will become important here shortly when we talk a little bit about the anatomy and reconstruction or repair for distal biceps tendon injuries here. As you can see here, why is that important? Because when you're placing back the distal biceps on the footprint, you want it to be not just on any anterior aspect of the radial tuberosity. You can see here it's actually on the relatively ulnar aspect of the tuberosity in a supinated elbow that you're placing the tendon footprint back. There are two heads to the biceps here. This is sometimes tested that the short head can rupture in isolation, so-called partial injury to the distal biceps. The reason that's important is because the short head is the stronger flexor and supinator in pronation and in neutral position. So if they do give you a history of a partial distal biceps injury with weakness and supination, it may be that there's an isolated rupture of the short head. And you can see here when you look at the footprint anatomy, it is also the larger portion of the footprint of the distal biceps. I'll also pay attention to this. This is commonly tested because it's an anatomic finding that is pertinent to this area, the so-called Lacerdus fibrosus. We're all familiar with it. You can see it originates from the short head of the biceps, but it inserts along the medial ulna and acts as a cover to the neurovascular structures. The reason it's important in this area is because when it is intact in about 60% of these tears, it prevents further proximal retraction of the tendon. This is an important finding because it allows you to access that and repair that with a single incision, sometimes not requiring a counter-incision proximally for those that are retracted above the elbow flexion crease. So they may ask you, what is this anatomic structure that has prevented the tendon from retracting proximally, and it's an intact Lacerdus fibrosus is the test answer. What is the neurovascular structures at risk here in order of frequency? Note that number one, if they ask you the number one injured structure, it's actually the lateral anabrachial cutaneous nerve. The reason I highlighted in yellow the PIN is that's often the one that we by mistake answer because it's the one we're most worried about as surgeons. So the PIN is the most catastrophic, but the LABCN is the number one injured nerve. That's because it lives right beneath the mobile wad when you do your proximal dissection. We tend to dissect between the brachioradialis and pronator teres. If you do vigorous retraction on the mobile wad, you'll almost always note some cutaneous paresthesias after surgery. But the PIN is the most catastrophic of the nerves involved. So test answer LABCN if it's a choice in terms of most commonly injured. Well, what about the PIN? They will ask this very commonly because our newer techniques often do involve drilling through the radial tuberosity and flipping on the contralateral cortex or even with suture anchors. Just note that 25% of the time, the PIN is within five millimeters of the radial tuberosity. So if the history tells you the doctor is dissecting during your dissection, you encounter a nerve in and around the supinator. The nerve that they're alluding to is the PIN. And they'll often ask you, what position do you want to place the forearm during your dissection? That, of course, depends on your surgical approach. If it's a volar approach, you want it to be in maximal supination. If it's a dorsal approach or a two-incision technique, it will be in maximum pronation. And you can see that here in this diagram that shows how the PIN changes in its relative position within the supinator in pronation and supination. So just note that when you do a transmuscular approach or you're dissecting between the heads of the supinator, the PIN is at risk. And for that reason, if they tell you with a volar approach, what position do you want the forearm in, just know that anatomy to be able to answer that question. If you are using a drilling technique or they describe that the surgeon uses a drilling technique, it's a very common test question to ask what direction do you want your drill or your pin to aim to avoid or minimize risk of PIN injury? That comes from these papers here. You can see when you're talking about proximal versus distal, there's a pitfall there. We tend to think distal, aim at distal. It'll be away from the nerve. It actually turns out the more distal you aim, the closer you are to the nerve. As you can see here, the actual correct answer is 20 degrees proximal from this study. On the other hand, what about radial versus ulnar? You want to decrease your risk by aiming ulnarly. So if the test question asks, in general, you want to angle your pin proximal and ulnar. If there's not a choice of proximal, distal, aim ulnar. And that, again, reflects these dissection studies about the proximity of the PIN with a transcortical approach. So what are the validated tests? This is a commonly tested question, which is how can you diagnose or confirm the diagnosis of a distal biceps rupture? You do not need an imaging study. The hook test is diagnostic. It's 100% sensitive, specific, and predictive. If you note here, as it shows in the video, you need to perform that test working from medial to lateral. And that's important so you don't mistake an intact lacertus fibrosus or lacertus for an intact distal biceps tendon. You can see here that you can place the shoulder in an abducted position and just perform this hook with your index finger. An absence of a hookable tendon is diagnostic of a distal biceps rupture. And you can see that anatomy here, how that's being shown, and how you can avoid the lacertus in doing that with this technique. Diagnostic imaging may not be provided on the test. If it is, it's usually more to distinguish it from a myotendinous injury. Why is that important? If there is intact tendon on the radial tuberosity, that's a red flag for a surgical repair. You'll see that more commonly in diabetic patients or in the setting of a partial tear. What they're alluding to here is that that can be effectively managed non-surgically, much akin to the way we treat proximal myotendinous or distal myotendinous injuries anywhere in the body. For example, a hamstring tendon avulsion versus a myotendinous injury. What's the considerations for repair? Again, a reason I mention this is because typically the standard of care in a young active patient will be surgery. So if they show you a full rupture in a young manual laborer, the answer is surgery. And we'll explain why here. Before we do that though, let's talk a little bit about the safety aspects of this procedure. We mentioned that bone and tunnel and button methods appear to be safer than anchor or screw methods. So those have become more the standard of care. Doesn't really matter which of those you use though. Just know that when you're using any VOLAR approach, the LACN is at risk. They will really test the historically that a two incision approach is more commonly associated with heterotopic ossification. Any exposure of the ulnar periosteum increases your risk of HO. Whereas a VOLAR approach increases your risk of PIN injury. We talked a little bit about this, but this has now shown up more often on the test. They may show you or give you a history like this, where a distal biceps tendon repair was performed, but a patient lacks full restoration of supination strength postoperatively despite an intact repair. What may have been the error during the surgery? And it's this. You can see here that the repair was placed anteriorly on the radial cortex, but not anatomically on the radial tuberosity. And you can see what that results in. A loss of that moment arm, and as a result, an incomplete restoration of power. So even though a repair of the distal biceps was performed, this subtle location or error in where it's placed on the tuberosity can lead to a lack of supination strength postoperatively. So the answer on the test is a non-anatomic repair on the radial tuberosity. One incision technique, if you do this, this is kind of your step order. Protect the LACN, follow the bicipital tunnel to the tuberosity, supinate the forearm to protect the PIN, limit your lateral retractors. A test question that is often asked is that a Bennett retractor is placed on the radial neck during the exposure. The patient postoperatively has inability to extend their wrist. That reflects a PIN injury from direct retraction. Again, it's alluding to the fact that 25% of the time, the PIN will be resting directly on that radial neck. So avoid direct retractors on the radius at that location. What I've highlighted here in yellow is an important test question. If you leave a distal biceps tendon to be treated nonoperatively, what does the patient lose in function? The answer is 40% of supination and 20% of elbow flexion strength. They often lead you down the path of answering elbow flexion, but remember the brachialis can be a considerable elbow flexor, and in this regard, a compensator. It's really supination you're losing. The supinator can offer some strength, but most of that is being provided by your biceps. So that is why in your manual labor, if this is treated nonoperatively, it's unacceptable because of this 40% loss of supination and 20% of flexion strength. As I mentioned earlier, what they're leading you down a pathway for if you use a single incision technique and an inability to extend the risk is PIN injury versus your two-incision technique has a higher risk of heterotopic ossification. So if they give you a test question that says the patient has a loss of pronation and supination passively after a two-incision technique, they're alluding to HO and involvement of the proximal radial ulnar joint that's now restricting range of motion, and that may require a subsequent open incision, debridement of the HO, and radiation postoperatively. Triceps tendon rupture, the anatomy of the triceps inserts on the posterior aspect of the olecranon. Again, pretty straightforward history. They'll usually tell you that it's all of a sudden a pop that occurred with extension during weightlifting, often due to trauma or fall on an outstretched arm. They may give you a history of a deceleration injury in a javelin thrower or a baseball pitcher. History and diagnosis is usually pretty straightforward. There is pain on the posterior aspect of the olecranon, but to distinguish this from your olecranon stress fracture, it's usually a single traumatic event, a palpable defect, but most importantly, an inability to actively extend the elbow, but an ability to passively extend it with gravity assistance. If they give you an x-ray, usually what they're alluding to here without the MRI is this fleck sign. So you can see it here. It appears seemingly benign, but it's much akin, for example, to a patellar sleeve injury in a child where the bone fleck is representing the more significant involvement of the tendon and an inability to extend. These are always surgical. So these are surgical repairs and reattachment of the triceps tendon to its footprint. And usually there's involvement of both the medial and long head. If there's options regarding techniques, anchors, two row, one row, none of that will be tested. It's really more about drill holes and or anchor repair of the tendon to the footprint. Elbow dislocations I want to briefly cover here. These are sports injuries. Posterior dislocation is the most common. I think all of us know that test, question, answer. But every now and again they'll show you one that's a so-called divergent dislocation where there's involvement of the proximal radial ulnar joint. Just be aware of that because that also requires treatment of the PRUJ, not just reducing the ulnar humeral joint. These are most commonly simple and a closed reduction is an acceptable standard of care with brief immobilization followed by rapid mobilization to avoid stiffness versus complex dislocations. History will be that the patient dislocated their elbow. They may have a transient period of pulselessness or neurovascular injury, but these are treated usually with a closed reduction and a rapid return to motion. I wanna show here, this is your typical x-ray. Note here, when would an MRI be indicated? It is not necessarily the standard of care to MRI, a simple concentric closed reduction, but they may allude to it with something like this here where you can see the risk for entrapment of that medial epicondyle fragment within the elbow or when they're alluding to injury to the ulnar or lateral collateral ligament in a throwing or overhead athlete. This is really the most common aspect of what's tested here is this so-called Hoareye circle. The concept here is there's a progression of injury when an elbow dislocates and it starts from the lateral side of the elbow. So if they ask you a test question of which ligament may be intact after an elbow dislocation, it's the medial side of the elbow that may be intact. An easy way to remember this is that posterolateral rotary instability, which is involvement of the lateral ulnar collateral ligament is the simplest form of a subtle elbow dislocation or subluxation. And then there's propagation of injury through the anterior and posterior capsule, ultimately to the medial side of the elbow. Why is that important? Because all of us know with some of these quote unquote simple elbow dislocations, if they are unstable, we will sometimes immobilize them in a fully pronated position. The concept here is that you're tightening those medial structures to confer some stability to the elbow. So treatment, closed reduction is always the answer for a simple dislocation with a brief immobilization followed by early range of motion. But again, if it's unstable, you may need to immobilize them in some flexion or pronation to try to tension those medial structures. Why is that different than your terrible triad? This is frequently tested. If they give you this history of an elbow dislocation with an associated coronoid and radial head fracture, that's a bad actor. That's no longer simple. Those need surgery often to treat the coronoid, radial head, and associated ligaments. They won't ask you necessarily which of these to perform because they're highly variable. Some need a radial head replacement. Some need reconstruction or repair of both the medial and lateral side. That has to be individualized. Just know the terrible triad are these structures. It's an elbow dislocation with the radial head and coronoid. They may give you test answers that say radial head and UCL, radial head and olecranon. Those are not the right answers. It's the radial head and the coronoid. I mentioned montages. These are fracture dislocations that involve the ulna as well as a radial head dislocation. I'll move through this quickly. The key answer is here is that the vast majority of the time, montages are anterior dislocations of the radial head. It's the type one that's the most common. These are almost always surgical injuries in adult patients where you plate the ulna to restore length. But again, the key issue here with the test is to make sure that you restore the reduction of the radial head. If they show you a plated ulna, in this case non-anatomically, and the radial head remains subluxed or dislocated, that's an unacceptable result. And of course, that leads to chronic radial head dislocation and at times a so-called Bell-Towes procedure to reconstruct the annular ligament and restore the reduction. PLRI is commonly tested. This is one of those phenomenon where it sees us more commonly on the test than it sees me in clinical practice anyway. But what is PLRI? This is this mechanism of valgus hypersupination with axial load and compression. So take a look here at this mechanism. They often test this. Somebody has an LUCL injury with a so-called positive tabletop test. What mechanism occurred? It's axial load, hypersupination, and valgus that leads to injury of the LUCL. The LUCL takes origin off the lateral epicondyle. It inserts on the crista supinatoris, as you can see here. There's tenderness over the lateral elbow joint. You can see the diagnostic test as shown here, this rotary drawer test that's done with reproducing that valgus and supination. Under fluoroscopy, you'll see gapping of the joint. Oftentimes, the test question will give you a history that the patient feels it's subluxing sitting up from a chair. That's because that's conferring that valgus supination load with that mechanism. X-ray or imaging finding may show you gapping with stress of the LUCL if they provide you that. Know that the answer for this is usually surgical. So if there's gapping and subluxation, it's any one of these docking or overlay techniques, but it's reconstruction of the LUCL ligament. You may also get a test question that describes a lateral or posterolateral exposure to the elbow. A surgeon has done a Coker approach, or a lateral approach to the elbow. When their approach veers to posterior, they've injured the LUCL, and now the patient has secondary instability symptoms. What they're alluding to is a posterior dissection that compromised the LCUL, and now it requires a reconstruction or repair for rotary instability. I'll move through this part quickly, but this does get a lot of attention in sports elbow, the UCL, or so-called Tommy John injury. I already mentioned this earlier in the talk. Remember that the UCL inserts from the anterior inferior aspect of the medial epicondyle to the sublime tubercle on the ulna. Remember that this is the primary stabilizer against valgus instability of the elbow, and it's in particular the anterior bundle. That's the critical bundle that we're stabilizing. So if you look at this anatomy here, and they tell you you're picking between the anterior bundle, the transverse ligament, or the posterior bundle, it's the anterior bundle that's the critical bundle for most of our functional range of motion that we're reconstructing. Where does it live? It lies superficial to the capsule and within the capsule, but deep to the FCU and FDS. So the flexor pronator mass is a secondary dynamic stabilizer, but cannot supplant for the function of a UCL in a thrower. The mechanism of injury, usually they'll give you a history. When does it most commonly occur? The answer is late cocking to ball release. Why is that? The angular velocities are somewhere between 2,400 to 5,000 degrees per second. We know that the ligament is experiencing a force in excess of 200 to 300 newtons. That's usually when these are failing. If they give you a history of an acute pop, it's between late cocking to deceleration. What's valgus extension overload? This is commonly tested. When there's some subtle laxity in the ulnar collateral ligament, as you can imagine, that leads to compression in the lateral structures and reactive bone formation in the posteromedial aspect of the olecranon. So you will see patients or athletes that will complain of lack of terminal extension and pain along the posteromedial joint line. They may show you an X-ray that shows this buildup of osteophytes at this location. This is alluding to subtle laxity of the ulnar collateral ligament. These are often treated surgically. If there's a test question about treating valgus extension overload and excising osteophytes, it's that an overzealous resection of more than three millimeters of bone leads to catastrophic strain in the UCL and a secondary UCL tear. That's a paper from Camanini and others at the Mayo Clinic that showed excessive resection of that bone can then lead to a secondary injury to the UCL. So valgus extension overload is that finding of those osteophytes. And just be aware that if they give you a history of treatment or resection, it increases the strain in the ulnar collateral ligament. What's the diagnostic test of choice for a UCL injury? It's the moving valgus stress test described by Sean O'Driscoll. This is the gold standard. These other tests that have been described here, a milking maneuver, gravity stress test, are certainly OK. But a moving valgus stress test locks the elbow by externally rotating the humerus. And then in a functional range of motion from 30 to 130 degrees of flexion assesses for stress and pain at the ulnar collateral ligament with gapping. You also want to, of course, assess for associated ulnar nerve symptoms or a flexion contracture. Why is that important? If they give you a history of preoperative ulnar neuritis and an ulnar collateral ligament injury, they're alluding to the fact that the ulnar nerve will need to be addressed at the time of your surgery, either with an in situ decompression or transposition. So what does it look like? I may give you this type of an imaging study here. This is probably in some ways more the exception than the rule, but it's nonetheless the popular one to test. You see this so-called T sign, where fluid extravasates between the sublime tubercle and the distal aspect of the UCL. They're demonstrating a distal UCL injury here. This combined with gapping on a valgus stress radiograph is diagnostic. So just be aware of this finding. T sign is, again, what they're testing here is an ulnar collateral ligament injury. Treatment for this used to be more physical therapy and non-surgical. Really, I think if they're giving you a UCL injury in a thrower, the treatment and standard of care is now surgical. Why is that? Art Rettig was the one who published this non-operative protocol of treatment for UCL tears. And if you look, the mean return to play after a non-operative protocol was 40%. So that was felt to be not a high standard of successful return to play with non-operative treatment. For this reason, if they give you a history of an elite overhead throwing athlete, standard of care is surgical reconstruction. A non-athlete or non-thrower non-operative treatment is still very reasonable. This was Art's protocol, which is in your slides there. Not really critical. What I wanted to show here is this is the ulnar collateral ligament reconstruction. This happens to be the docking technique described by Dave Olchek, but certainly the figure of eight technique described by Dr. Andrews and others are acceptable here. You can see in this approach, the FCU heads are split, a muscle splitting approach preserves the innervation of the FCU. This allows you to perform the surgery with or without exposure of the ulnar nerve, depending on whether preoperative symptoms are present. Either a palmaris or gracilis autograft is utilized and a reconstruction is performed, docking this to the anatomic footprint on the epicondyle. One test question that is often found here is what happens if the palmaris longus is absent? There is a risk of median nerve injury with harvest, so it's critical that the patient is tested for a palmaris longus presurgically. That involves a simple test where the thumb and the small finger are brought together and the wrist is flexed. If history is provided that a test for a palmaris longus is absent, what graft should be utilized? The answer is a gracilis tendon from the leg to avoid risk of injury to the median nerve. Systematic review here, I just put here to show that with ulnar collateral ligament reconstruction, the successful return to play to throwing athletes is significantly higher than non-operative and the reason that that's the standard of care. I'm gonna finish up here by briefly talking about neurologic conditions. Ulnar neuritis still falls on the test. We all know what that presents as, as symptoms in the ulnar one and a half digit of the hand. Usually it's the cubital tunnel, which is the fibro-osseous canal formed by the medial epicondyle proximal ulna and cubital tunnel retinaculum, which is the source of compression, but beware that any of these other sites can be the location. So-called arcative struthers, FCU, intermuscular septum, or osteophytes. The typical test question is what is the finding? It's a drop in 10 meters per second in nerve conduction velocity across the elbow on an EMG. If they give you that, that's cubital tunnel and they're alluding to a surgical treatment with decompression and or transposition. They may also give you some history of weakness of the intrinsic muscles of the hand, as well as weakness in the ulnar one and a half digits. Rarely will they give you imaging studies of this. If you see perineural edema and nerve thickening, that's what they're alluding to, but usually that's not the case. And again, the treatment can be conservative for a period of time, like night splints, which keep the elbow in relative extension. We know that flexion places more traction or stress on the nerve. Surgical treatment can be in situ decompression, transposition, or even a medial epicondylectomy was a historical treatment. The reason you can do an epicondylectomy is remember the ulnar collateral ligament inserts on the anterior and inferior aspect of the epicondyle, so you can still remove that inner aspect of the epicondyle and not result in an instability of the elbow. They shouldn't really test or ask you which of these, whether you need to do a transposition, decompression, et cetera, because all of them have had effective outcomes. They will simply test that some surgical decompression of the nerve is warranted. What's pronator syndrome? It shows up on the test sometimes. It's proximal entrapment of the medial nerve. Possible structures that are involved are the ligament of Struthers, which is from this associated accessory process off the humerus. The Lacerda's fibrosis we talked about earlier. Remember the medial nerve passes beneath the two heads of the pronator teres, beneath the fibrous arch of the FDS. So any one of those locations can be the location of pain and compression. Usually it's vague anterior forearm pain, but they're gonna test this by seeing whether you know what the medial nerve innervates. So they're gonna say it's involving the radial FDS tendons and muscles. It's gonna involve the thenar muscles, and EMG is generally inconclusive, and they're gonna allude to the fact that medial nerve is involved, and this may sometimes require a decompression. An ultrasound or MRI like this may show an area of potential entrapment. They may show you an x-ray, and if you see an associated accessory process off of the humerus, they're alluding to a ligament of Struthers that will require decompression. Surgical decompression is indicated when conservative management fails, no different than the cubital tunnel. Radial neuropathy, there's a couple to discuss here. We already talked about the PIN when it comes to the distal biceps, but you gotta know it here. PIN compression syndrome is different from radial tunnel. What's the distinguishing feature here? Radial tunnel syndrome is pain. There's no weakness. There's no physical exam findings of loss of extension in the digits. Poster interosseous compression syndrome also has motor findings, and you have to distinguish them because they'll give you both answers on the test. Wartenberg syndrome is different. That's compression of that superficial radial nerve, which is isolated sensory symptoms of the dorsal branch of the radial nerve. So where can the radial nerve be compressed? At the leash of Henry, at the arcade of Froge, along the edge of the ECRB, and then at the distal edge of the supinator, so you need to know those. But in general, just know where it runs. We already talked about the fact that it runs along the posterior aspect of the humerus, then subsequently between the brachioradialis and the brachialis. Know that the radial nerve is innervating the mobile WAD, which is your BR, as well as your ECRB and ECRL. Distal to that point, it's the posterior interosseous nerve that's innervating the supinator and the remainder of the digital extensors. Why is that important? Because this is what they're gonna give you here. It's a PIN compression in somebody with big forearm muscles, a bodybuilder or a laborer. They're gonna present with physical exam findings of pain, but here's the key point. They're gonna tell you the wrist is radially deviated with extension. That's alluding to the fact that the ECRL and ECRB are still intact from radial innervation, but the PIN is deficient, such that they'll have difficulty extending their fingers. So that's really your critical finding to answer PIN. As I mentioned earlier, you need to distinguish that from your radial tunnel syndrome, which we're gonna mention here in just a moment. Imaging is rarely positive here. You might eventually get an MRI like this that shows edema in an area the radial nerve is passing. I don't think that's gonna be your typical test finding. Treatment, like all these nerve compressions, is usually conservative, period of rest, splinting, physical therapy. If none of that works, then it's surgical decompression, and it's exploring all of these potential sites of compression. Arcata-froge, supinator, et cetera, et cetera. Radial tunnel syndrome, again, one of these things that's commonly tested. It's a small subset of patients that are often misdiagnosed as tennis elbow. The challenge, of course, here, is that many of the symptoms that are positive with the PIN syndrome are positive with radial tunnel, but again, the key distinguishing factor is it's all pain. There's no real weakness because of the preservation of the motor function of the nerve. It's worsened with pronation and supination. Usually, it's pain with palpation, about three to five centimeters, distal to the lateral epicondyle. You won't really see much on imaging. They might try to allude to some edema and a location of potential compression, and same deal here. Non-operative treatment is the standard of care. Surgical decompression when it's not responding. Again, the surgery is, in some ways, the same as for a PIN syndrome because you have to decompress the nerve in any location. I'll finish up here very briefly with elbow contracture. Remember, the elbow's a joint that likes to get stiff. Actually, much of this great work comes from Buddy, who's in the audience. There's intrinsic contractures and end-strixon contractures. All of these things can be a source of contracture. You need to distinguish which ones are the cause because certainly that will affect your approach for a release. What will this usually present as? There'll be muscle atrophy for the patient, paresthesia, swelling and skin tightness, limited range of motion. What this is alluding to is that you usually wanna initially get some imaging studies to identify what may be the cause. As you can see in these images, there's osteophytes in the coronoid and olecranon fossa. These are loose bodies that can be excised. This may be treatable also with the so-called outer bridge Kashiwagi procedure in which you deliberately create and deepen the olecranon and coronoid fossa with a clower drill to improve range of motion. You need to distinguish that from extra articular sources such as soft tissue contracture. The standard of care, if it's extrinsic, is gonna be the static and then dynamic braces that gradually improve elbow flexion and extension. If those fail, then they're alluding to some surgical approach such as a column procedure where you will excise or release the anterior or posterior capsule versus intraarticular procedures like we talked about such as the outer bridge Kashiwagi. Very quickly, bursitis here. As you know, elbow bursa and olecranon bursa is tested. It's a bane of our existence and not anything that the surgeons wanna treat, but nonetheless, it usually will have a history that a patient had a direct blow to the elbow or repetitive force on the elbow with flexion and extension. Often will present in this way. They'll give you a history of a red, warm, swollen, painful bursa. Aspiration can be done to assess the cause of bursitis. Just be aware, though, that aspiration carries the risk of a persistent sinus track and drainage. So if you're approaching this, you usually wanna go through a thick, fleshy area of the elbow to close off that track. They may show you an x-ray like this or an MRI like this with an associated spur off of the olecranon, an enthesopathic spur. In those situations, what they're alluding to is you wanna not only treat the bursa after you've eliminated any infectious associated etiology, but maybe subsequently remove the bone spur that is the inciting reason for formation. Treatment is rest, ice, anti-inflammatories. It's almost always non-operative when possible, particularly with an infectious bursitis. If it's a septic bursitis that's giving systemic symptoms or when it's no longer inflamed, surgical treatment is appropriate. Finally, elbow arthritis, most common in males. You'll see it with heavy lifting. Again, as we already mentioned, ulnohumeral arthroplasty in the setting of limited flexion extension in the form of an Outerbridge-Kashiwagi procedure is reasonable, but beware when it's post-traumatic arthritis and there's associated loss of pronation and supination. Why is that important? Because your OK procedure will only help flexion extension. It will not help rotation. In that setting, it really needs to be elbow arthroplasty. They won't really get into the various types of arthroplasties on your test. There's constrained and semi-constrained implants. Really, the key idea is that a total elbow is indicated for elderly, lower-demand patients with involvement of the ulnotrochlear joint that have failed non-operative management. It can also be used in rare cases for non-reconstructible comminuted fractures, such as a distal humerus nonunion or a comminuted proximal radial ulnar joint injuries. Again, unlikely to be tested. Generally speaking, this will show up as your test as a treatment for end-stage osteoarthritis and loss of motion. I'm gonna finish up here with radiocapital or plica syndrome because this is often tested. What is this? This is lateral elbow pain. The differential includes your tennis elbow, but it usually is a history of innocuous trauma or repetitive microtrauma in young and throwing athletes. You can see it here as shown on this imaging study. They will often have this plica that you'll see entrapped within the radiocapital or joint. It's thickened over time, much similar to a knee synovial plica. They may show you some chondromalacia on arthroscopic views involving a portion of the radial heterocapitalum. They may give you a history of popping and clicking and show you an MRI that appears normal. This is trying to lead you down the path of answering an OCD lesion, but you don't see an OCD lesion. If it's mechanical symptoms, lateral elbow pain, and no OCD, start thinking about a plica. Again, treatment is always non-operative for a period of time, and usually the imaging studies are negative. So they're giving you these imaging studies and showing you normal studies. The thickened plica is in some ways incidental, and the treatment is an arthroscopic excision when conservative management fails. So first line of treatment, rest, physical therapy, corticosteroid injection, but if none of those things work, it's an arthroscopic excision of the plica. So I'll finish up here very, very quickly. These questions that sort of are in your packet, and I tried to highlight the other important test question items as we went through. Eight-year-old baseball player, medial elbow pain has decreased power and effectiveness. What are you concerned about? As we talked about medial apophysitis or little leaguers elbow. Collegiate baseball player has posterior elbow pain. His x-rays are pretty much normal. New x-rays show a fracture. What do you suspect? Electron stress fracture. So posterior elbow pain, triceps normal thrower, MRI starts to show edema, then subsequently gapping or a fracture line. Remember CRETO, at what age does the olecranon apophysis appear? Nine, so we should just remember that mnemonic because it's a simple test question. What's the terrible triad? As I mentioned earlier, they'll lead you down these other paths. The terrible triad is an elbow dislocation, a coronoid fracture, and a radial head fracture. That's your bad actor for instability. What's the difference between PIN and radial tunnel syndrome? Remember here, the PIN has motor symptoms. The radial tunnel syndrome, no motor symptoms, just vague anterior elbow pain. Which x-ray view is beneficial for identifying radial head fractures? You won't often see it on your lateral x-ray. You need to get this radial capitellar view to identify displaced type two mason fractures. What's a divergent elbow dislocation? We talked about this. Most common are simple. Divergent means involvement of your proximal radial ulnar joint. And that, of course, is a bad actor, requires more ligament reconstruction of the PRUJ, not just the ulnohumeral joint. So, thanks very much. Thank you.

elbow pathologies

fractures

ligament injuries

tendinopathies

neurovascular issues

anatomy of the elbow

diagnostic methods

treatment options

surgical interventions

ulnar nerve-related conditions