So our next speaker is Dr. Julie Bishop from Ohio State University. She's gonna talk about shoulder arthroscopy and labral pathology. All right, well thank you all for coming. And you know, a little less than two years ago, I did my sports board recertification. I took this course. So I wanna encourage you all that this course and OKU Sports had everything that I needed to do well on the test. And the other thing I would tell you, especially in shoulder, the more prevalent topics, there's so much research coming out, so many papers that you see every week in all the journals. Don't be, don't overthink the questions. The answers are all in these courses and in the books. And anything that's controversial is never the answer and never what they're gonna ask you. So I would encourage you just to stick to the basics and not think, oh, I read that recent paper, maybe that's what they're getting at because that's not. So we're going to talk about the arthroscopy basics, all aspects of instability, and then some biceps anchor slap. And for shoulder arthroscopy, the things they really focus on are patient positioning, portals, and really the anatomical structures at risk, and then complications. So as far as patient positioning, really the controversy is lateral versus beach chair. And when they look at the lateral decubitus position, there are advantages like better visualization, improved access to your anterior inferior or posterior inferior labrum. But really the thing they come back to every time is that lateral has no increased risk of hypotension or bradycardia. And that's the consistent theme. So there's better cerebral perfusion in lateral. The disadvantages, you have to do general. If you need to open, you have to reposition. But really what they're worried about is traction injuries. So if you're pulling too hard on the arm and lateral, you can get a neurovascular injury. And then there is an increased risk of axillary and more theoretical muscultaneous nerve injury with the anterior inferior portal in lateral versus beach chair. Now for beach chair, ease of setup. You can do an easy EUA. Easier access to your anterior portal. If you open, you don't need to reposition. But you can use sedation with regional. So that is one thing they might ask you. In lateral, you'll always have to use general. And some people do sedation and an interscalian block and don't need general. You do have more mobility of the arm. But what they always come back to and what the consistent theme I see in the questions is the disadvantages. And really the main thing is the increased risk of hypotension or bradycardia, which can cause cerebral ischemia. That's a very common theme. There is an increased risk to the cephalic vein with a five o'clock portal in beach chair versus lateral. And we'll talk more about the structures at risk in a few minutes. And then you might see a question on the risk of utaneous facial neuropraxia from the padding depending on what kind of beach chair positioner you use. So again, cerebral hypotension, I think there's always a question on this. And realize that we practice deliberate hypotensive anesthesia. And in order to have a clear field, you need a little less than 50 millimeter mercury difference between your scope pump pressure and your systolic blood pressure. So if you ever wonder where the pump settings come from, and the shoulder button is typically 50, that's assuming that you're keeping the systolic blood pressure around 100. The anesthesia literature wants the systolic above 90. And they also feel that your maximum reduction of your systolic blood pressure and your mean arterial pressure, or your MAP, needs to be within less than 20% of baseline measurements to prevent cerebral hypoperfusion. So they recommend using a cerebral oximeter. And so that's something that you might see in the vignette, and they want you to use that. And why? Because that captures your cerebral desaturation events. So know what a CDE is. They might not always spell that out. But that's what they're getting at. And what they've seen is that if you have greater than a 20% decrease in your baseline regional cerebral oxygen saturation, you're gonna get a CDE. And what they've found, and the literature supports, and this is tricky because the question will say, there is a higher incidence of CDEs in beach chair versus lateral. So that's proven. Have they proven that there's a higher incidence of stroke or effects of cerebral ischemia in beach chair versus lateral? No, but there are more CDEs in beach chair versus lateral, and they come back to that and ask that a lot. So know that, and know that hypoperfusion is the risk of beach chair. So what about anatomy? I think you're gonna find on the test every single joint that you scope, they're going to ask you a question about the structures at risk. And I think you just need to make a table and memorize them. But don't memorize all the esoteric ones. For shoulder, they come back to always the answer that they get at. Yes, there's a lot of different structures at risk. But axillary nerves, cephalic vein, and suprascapular nerve and artery are always consistent what they're getting at. So think about the portal, where it is, and then which one of those is at risk. So your axillary nerve seems to be the most common one that is most at risk with the five o'clock portal, and that is about 15 millimeters from the nerve. The cephalic vein is most at risk with your anterior working portal, and it's been found that that's less than one centimeter from the anterior portal in 25% of specimens. And then your suprascapular nerve and artery, they kind of go hand in hand, that's at risk when you're doing releases. So if there's a question that you have a retracted cuff tear that you need to mobilize, you mobilize by doing medial releases, and the nerve and artery are medial superior glenoid rim. So those are the structures that they're getting at and seem to be consistently in the questions. So what are your high risk portals? Those are the anatomical structures. Your portal, your working portal, your anterior central portal, again, cephalic. So that you might think, oh, the cephalic's not that important, but it's the most at risk structure. Your five o'clock portal, your low anchor for your anterior stabilization, the risk is the axillary nerve, and then the hubral cartilage and the cephalic, but the axillary nerve is the closest. Anterior inferior portal, cephalic and axillary nerve. And they're not gonna ask you to pick between the two of them, because they're both at risk, so it's gonna be one or the other. Your posterior portal, your seven o'clock portal, is close to the circumflex artery, but closer to the axillary. So again, it comes back to the axillary nerve. And then your anvisor portal, again, your medial working, your releases, your slap repair, your cuff suture passing for retracted, your mobilization, that is medial, superior rim of the glenoid, the nerve and artery about three centimeters from the supraglenoid tubercle. So if you're working medial, that is when suprascapular is at risk. And then complications, you know, Dr. Gill talked about this a little bit. For arthroscopy, the main thing that they come back to is infection. And P-acnes are really now, it's called C-acnes, is gram-positive, non-spore-forming bacillus. You need to hold the cultures. And whether it's 21 days, some say 10 to 14 days, the whole point is that you're holding them longer than your normal cultures, which you hold for about two days. So your anaerobic cultures, you need to hold, because C-acnes is what we worry about. And certainly they may ask about the risk of infection, which is significantly higher if you have a cortisone injection within three months of an arthroscopy. And so those are the infection things to keep in mind. Now there is a small risk of DBT and PE with arthroscopy, more prevalent in those with a coagulopathic state and thrombophilia. However, what they found is that even if you know the patient is hypercoagulostate, prophylaxis is minimally effective in preventing. So I don't really think that they will ask you about the risk of DBT-PE, because overall, it's pretty low and you can't really prevent it even if you know the patient was at risk. So we'll go through some questions. So this is 65-year-old healthy male, and realize there's many, many reiterations of this question, so just get this in your mind because they like to ask it. Healthy male, has a cuff repair in beach chair position. So once they've mentioned the position, you have to know what they're getting at, something about that position, because it's not lateral. He received a general, he had a block, and the case was one hour and uncomplicated. So no medical issues came up. Unfortunately, at the conclusion of the case, he couldn't be aroused and could not be weaned from the ventilator, and was determined that he had an anoxic brain injury, what is the most likely cause? Well, myocardial infarction, pulmonary embolism, malignant hypothermia, and an anaphylactic reaction would not be considered an uncomplicated case. There'd be some kind of anesthetic issue during the surgery. So that really brings you to cerebral hypotension. Again, that's always going to be the answer. With regards to standard shoulder arthroscopy, the posterior portal is normally made in the soft spot approximately two centimeters inferior, one centimeter medial, the posterior lateral corner of the acromion. If your posterior portal is made inferior to your standard posterior portal, what is at risk? Well, first of all, just think about, we talked about it's gonna be cephalic, axillary nerve, or suprascapula. So long thoracic nerve is never at risk in an arthroscopy. Suprascapular nerve, but we're not working medial, right? We're talking about the posterior portal, we're not doing anything medial, so we wouldn't think that. The brachial artery, again, that's not one of the things that's at risk, you have to have some very aberrant portal for that. And posterior humeral circumflex artery, yes, remember that's back there, but the axillary nerve is closer. So if you're at that posterior inferior portal, it's going to be the axillary nerve that's the closest. So now we'll go on to instability. We'll talk about anterior first, and all aspects, etiology, mechanism of injury, anatomy, natural history, options, and outcomes. So anterior instability, glenohumeral instability, is about 23% of all shoulder injuries in NCAA athletes. 90%, so the majority of those instability events are anterior. 85% of them are subluxations not requiring a closed reduction. And the position at risk is a force applied in the abducted externally rotated position. So who is at risk for anterior instability? Because they do like to focus on this. Who is the at risk patient? Prior history of instability, you're at risk. Contact, collision sports, military population is at risk. And then when they did a study of military athletes with no history of instability, if they had a positive apprehension and relocation sign on an exam, this is just they examined everybody, those patients were higher risk for having a first time instability event. And then the tall thin glenoid, the increased glenoid index places patients at a higher risk. So first we'll talk about reducing a dislocation because they do like to ask about level one evidence. And they like to ask, you know, start with the basics, how are you gonna reduce this? IV sedation versus intraarticular injection. And the literature strongly supports an intraarticular injection. Everything else is the same. So they're never gonna ask you which is more effective. They're never gonna ask you which maneuver is the most effective for a reduction because there's a million different maneuvers. But this has been proven that the complication rate is higher with sedation, therefore you want to do an intraarticular injection. Any other answer is kind of leading you astray. But there's more complications with sedation and that is the reason why intraarticular injection is the answer. And how about the anatomy of the glenohumeral ligaments? This goes all the way back to your OITE. This was on every single OITE when I was a resident. They are going to ask a question and you just want to memorize this because there will always be a question. And so when we think about the position of the arm, when the arm is at the side, the primary restraint to instability is your rotator interval and your superior glenohumeral ligament, part of the rotator interval, and that is anterior and inferior instability. When the arm is in 45 degrees, it's the middle glenohumeral ligament. When you're up at 90, the primary restraint is the IGHL, so the inferior glenohumeral ligament. But remember that it's the anterior band when you're in 90 degrees of external rotation and it's the posterior band when you're in 90 degrees of internal rotation. So that is testable material and that's something, again, just memorize it because they will ask it. So what about the pertinent physical exam findings? So I think the reason to know about ligamentous laxity is because it'll be part of a vignette and it'll lead you to the correct answer. So you need to understand just what the BITEN criteria is. You don't have to memorize it, but if they mention the BITEN criteria in a vignette, it's typically because they're telling you this patient either does or does not have ligamentous laxity. It's a nine-point criteria and just for you to know, it's your thumb to your forearm, your MCPs, your elbows, hyperextension, so that's each side, and then your knees, hyperextension, and ability to put your hands on the floor. So it's nine points. So if they say somebody's BITEN criteria is nine out of nine, that vignette is telling you this is a ligamentously lax patient, which is going to take you down a pathway for ligamentous laxity. As far as the apprehension test, there's a lot of tests in instability and they don't really name the individual tests. They're not gonna ask you which one is better. So know the apprehension test. That's consistent and they feel apprehension in the abducted externally rotated position, which again is the anterior band of the IGHL and that's relieved with posterior pressure. That's the most consistent physical exam finding for instability. And then the Gagey sign, why I think this is important is because I've seen this in the vignettes. So they're not gonna ask you what is the Gagey sign, but they might talk about it in a vignette. So the Gagey sign indicates an injury to the inferior glenohumeral ligament and it indicates a haggle, so a humeral avulsion of the glenohumeral ligament lesion. And so if you have a haggle or you have an injury to the IGHL, they can have inferior capsular laxity. And we'll talk about this later. You don't wanna miss a haggle. And so when you compare abduction with the arm in neutral, if they abduct more than 105 degrees, it's because the humeral head is going inferior because you have a haggle lesion and that allows hyperabduction. So if you hear positive Gagey in your vignette, that's taking you down a haggle pathway. And that's why I think that's important. So imaging, true AP, the Gracie view, that lets you see joint congruity and OA, which is important for the instability patients. Your internal rotation AP lets you see posteriorly, so it's the best view for the hill sacks. Your west point axillary lets you look at glenoid bone loss, and they really rarely ask that or have that in any vignettes. And your striker notch is for your hill sacks. MRI, normal MRI, labrum, capsule, bone bruises, associated pathology. But the MRA better defines your labrum, your capsule, and your haggle lesions. Bankart lesion is in up to 90% of dislocation subluxation events. A haggle is about 9% of instability cases, so it's not common. And a haggle is always going to be a high-energy trauma. And the reason why haggles and then the gaugy sign are important, because if you miss a haggle, there's a 90% recurrence rate. So if you know somebody has a haggle, that is a decision, that is a reason to operate because the known recurrence rate. And you need an MRA to best view the haggle because normally you have a U-shaped pouch where down here your capsule normally asserts right here on your humeral neck. When a haggle occurs, the capsule rips off and the contrast can stream down immediately. And I'm sure Dr. Yu will touch on this during his radiology talk. Hill-Sachs lesions are 40 to 90% of all anterior instability events, so you almost always have a Hill-Sachs. And on a recurrence, you're always 100% gonna have a Hill-Sachs lesion. And this is just a nice picture of a haggle. Here is the capsule. It's sitting down here because it pulled off the humerus. You can see the end not attached and you see the contrast streaming down. You see that picture, you know that's a haggle, that's why they're showing me that picture. And then here's an arthroscopic picture. I've seen them put a bunch of pictures on the questions and they'll always orient you. You'll tell you what direction you're looking from. And the scope here is posterior and what you'll always see is that there's a thickened tissue because you can get pretty, you know, the test is going, the clock is ticking and you all of a sudden think, I have no idea what I'm looking at. But if you ever have a camera in a shoulder and you see muscle fibers, you should never see muscle fibers, and you always see muscle fibers with a haggle lesion because the capsule is pulled away from the neck and you will see the fibers of the subscapularis. And it's hard to see them well here, but the pictures that they put on the exam, you see muscle fibers, you know that's not normal, it's because the capsule is detached. So what are our treatment options for instability? So the initial treatment is still non-operative, it's controversial despite the known recurrence rates. It's a controversial topic and it is very unlikely you will be asked this unless it is clear as day, like there's a haggle lesion, there's a large bony bankart that's displaced. And although there's an increasing acceptance of surgery as the initial treatment for your first time dislocator for this test, you do not operate on the first time dislocator. So conservative treatment, sling, early motion rehab, return to play when strength is symmetric. Bracing is controversial, certainly there's some early studies that show at a lower recurrence rate when you brace an external rotation versus internal rotation. But those studies can't be reproduced and they will throw those studies into the answers to throw you off, but we can't reproduce that and that's not going to be the answer. So you're never gonna answer brace an external rotation because we can't reproduce that. So that's just, you'll see that as an answer and you'll say, okay, that's not the right one. The natural history, they do like to talk about this. So there's up to a 94% recurrence rate. Younger contact athletes are higher risk for recurrence. They do give you questions with a bunch of different options. Why is this patient the highest risk? Young and contact athletes, haggle lesions, bony bankarts, especially if they're displaced, and know that the recurrence rates decline with every decade of life after 20. The Hovelius study is a really important study. I did my mock recertification this year online. That's one of the articles they chose, which shows you they think it's important and they pull questions from it. And this is one of the best studies that has a 25-year follow-up on the 12 to 25-year-old with a dislocation. And they have, the number is 57%, had one or more recurrences. So if you look at this population, you follow them for 25 years, that's the recurrence rate they like to stick to. There's a million recurrence rates out there. This is the best done study. 43% had no further issues. And then long-term arthritis after dislocation, they do ask about this, and this study let them follow this. And so they found moderate to severe arthritis in 18% of patients without a history of recurrence. So one dislocation, never occurred again, about a 20% rate of moderate to severe arthritis. And people who had more than one recurrence had a 40% rate of moderate to severe arthritis. So sometimes they'll try to get you to say that the surgical intervention caused the arthritis, but we know from this long-term study that you get arthritis just from having one instability event. So unless you see a picture of a terribly done surgery with a screw in the joint, the surgery is not going to be the reason that somebody gets arthritis. So conservative treatment for return to sport, there's not a lot out there. And I think this is the most quoted study, prospective of 45 athletes, 75% return to sport. So if they ask you, what's the chance of an athlete getting back to sport if they have an in-season instability event, about 75% can get back to the sport. However, I would just kind of round the next two, get in your mind two-thirds. Two-thirds finished the season and two-thirds had recurrent instability during the season. So I think that's kind of a good ballpark to remember. And we really can't say, and they can't ask you, if delayed surgical management is going to affect outcome. We really can't prove that, so that won't be an answer. How about open versus scope? I think that what's testable, Hagel, bone loss, Laterge, it's too controversial. There's minimal literature. They're never going to ask you whether you should do your Laterge open or arthroscopic or your Hagel open or arthroscopic. Now they're gonna trick you or try to trick you on open versus arthroscopic bank art repair. The literature suggests a higher rate of instability in contact athletes who are treated arthroscopically. However, not all the data supports this. And the best done study of open versus scope had a 23% recurrence rate arthroscopically versus an 11% open. And they found the scope failures were male, less than 25 and with a heel sax. However, this study did not incorporate bone loss, but it does bring up the recurrence rate. The people who are at biggest risk are young male contact athletes. And what's really important is the literature cannot support a difference in outcomes, range of motion or patient reported quality of life in open versus arthroscopic. So if a question tries to get you to say that you will have better range of motion with a scope versus an open, that's not the right answer. They're not going to say, oh, you're going to lose external rotation with an open bank art versus a scope because we can't prove that. So don't be fooled by those answers. They cannot prove a difference between open versus scope and they're not going to ask you to choose one over the other. And the outcomes, I think it's important to know that 90% return to their pre-injury level. And the overall recurrence rate taking everything into account is a range of four to 19%. Recent meta-analysis says 7%. So I think if you're kind of right in the middle of that range, that is an expected, if you're counseling a family, there's a vignette about that because there was one year, that's a pretty acceptable recurrence rate. Long-term OA, remember that OA happens after dislocation with no surgery. So yes, 26 to 40% of patients treated with a stabilization go on to get arthritis, but no one can prove it's the surgery because we have the natural history without surgery is about the same amount. What are risk factors for recurrence? Ligamentous laxity, but that's never gonna be the answer because the younger you are, that's an important one. Contact sports and glenoid bone loss. So if you ever see glenoid bone loss more than 25%, that is the risk for recurrence. Certainly heel sacks, male sex, less than three suture anchors used are all factors, but the thing they come back to is the younger the patient and bone loss. And then a little bit on postcapsulorathy arthritis. I know Dr. Gill touched on this. They do like to give you a vignette of an older patient who had instability surgery years ago, so you know it's a putty flat or a magnuson stack, something that was non-anatomic, progressive pain, and they will show you an axillary with a biconcave glenoid. The humeral head is sublux, it's sitting on the posterior glenoid. That is postcapsulorathy arthritis, and they do like to have questions on that. So how about instability with bone loss? The critical amount of bone loss that they accept for grafting is 20 to 25%. Now I know there's studies out there now, they're talking about the critical number is 13.5%. Put all of those aside, it is clear on the test it's gonna be a big number. So if you have 20 or above 20, 25% bone loss, they are leading you down a bone grafting path. What are the predictors of critical defects? How old they are at the first dislocation, so you remember, the younger you are, the worse everything is at your first dislocation. How many dislocations you've had. And if they give you a vignette where you have a patient with failed prior surgery, long history of multiple dislocations, and instability with minimal provocation, so it comes out in their sleep, they're taking you down a bone loss pathway. And I think the glenoid tract concept is important just to know what it is. They're not gonna ask you a question on it, but it might be in a vignette. So rarely is glenoid bone loss in isolation. The lesions are bipolar, that's kind of the buzzword that we use now. And as the glenoid bone loss increases, the glenoid tract decreases, thus the humeral head is at greater and greater risk for engagement. The more glenoid bone loss, the smaller the hill sacs needs to be in order for it to engage, and it slips off track and dislocates. So just be familiar with that, so if you see that, you're not thrown off in a vignette. The best way to evaluate is 3D CT, that's the most accurate, and you can detect hill sacs with over 80% accuracy. Treatment options for bone loss, you're not gonna be asked to choose one over the other. So there's Latter-J, open or scope, there's ILLIAC, CREST, there's all kinds of allograft choices, such as distal tibia, they're really gonna say bone block, or they're gonna lead you down a path where they're going to tell you the bone block of choice is a Latter-J, but you're never gonna choose one. If they're asking you what would you do, Latter-J, distal tibia, or ILLIAC, CREST, then none of those are the right answer, because we can't prove one is better than the other. And the Latter-J, most of the questions focus on complications, because it's a technically challenging surgery, so I think you should be familiar with the complications. Know that you do a Latter-J or a bone block when there's greater than 20 to 25% bone loss, and then know the complications. So the overall rate is anywhere from 25 to 30%. The recurrence rate with Latter-J is very low, so one to 8%, so certainly there's a documented lower recurrence rate, and recurrence is associated with a medial graft. So your graft is medial, they show you a picture with a medial graft that is leading you down a path of, okay, the complication was probably recurrence. You can see coracoid fracture, interoperative fracture, lysis, non-union, coracoid resorption. They probably won't ask as much about that, because the nerve vascular injuries are more prevalent. Musculocutaneous is mostly a sensory deficit, and axillary nerve, motor and sensory from retracting inferiorly. So if they also give you a picture of a graft really low, that can be leading you down a pathway. Oh, the graft is really low, it's pushing on the axillary nerve. And then very important is lateral graft position. If the graft is lateral, if you see it overhanging, that is iatrogenic arthritis. So that's the one time that the surgery is gonna cause the arthritis from the instability. If your graft is lateral, or again, if it's something like the screws are in the joint, then the surgery did cause the arthritis. And it is accepted that you will lose external rotation, average around 13 degrees. What about the hill sacs? When you see glenoid bone loss with a large hill sacs, most of the evidence still points to addressing the glenoid side to prevent engagement. So you're unlikely going to be asked both on a test. They're gonna lead you down a clear pathway of one versus the other. For large hill sacs with minimal glenoid bone loss, there's a lot of different options, allograft, arthroplasty, metal caps. There's really no guidelines for indications. They're high complication rates. I really do not believe you're gonna have an answer that's correct, which is bone grafting and hill sacs. I don't think that's the path they're gonna take you on. That's probably going down the wrong pathway. Remplisage, I think you need to know what it is because it's gonna be one of the answers. And remplisage means to fill. So you suture the infraspinatus into the defect. It's a viable option in the lack of glenoid bone loss. And the one study that showed that it was better than Bankart alone was instability surgery with no glenoid bone loss, remplisage versus no remplisage. There was a lower rate of instability with remplisage. Studies do show that it heals, but there is a documented external rotation loss. So I think those are the important aspects to know about that. So some questions about instability. We have a 25-year-old hockey player who sustains a shoulder dislocation after being hit into the boards. Which of the following is associated with an increased risk of recurrence after arthroscopic stabilization? So bony Bankart, no, we haven't really talked about that because as long as you fix it anatomically, that's not gonna put you at higher risk. Capsidolabral complex injury, well, that's basically what a Bankart is, so that's not gonna put you at a higher risk. And realize Haggle, let's say they threw Haggle in here. As long as you fix it, that does not put you at higher risk for recurrence. Haggle is only if you miss it, your higher rate. And engaging heel sacs, well, no, we haven't really talked about that. And an ALPS lesion is a periosteal sleeve avulsion. So it's when the Bankart is stripped and sitting really medial. And as long as you mobilize it and bring it back anatomically, ALPS is not the right answer. But inverted pair, that is the classic word for glenoid bone loss, because it looks like an inverted pair. So that is the answer. 20-year-old football player presented the ER with a dislocated shoulder. Which of the following would you tell the player based on level one evidence? Surgery will prevent the development of arthritis. So we know, right, so we know that's not true. So that's not the answer, because we've talked about that. Best technique is traction-counter traction. There's a million techniques. They're never gonna ask you which one is better. We can't prove that. If he declines surgery, play is at the player's discretion. Well, that's not true. That flies in the face of a team physician. So that's not the answer. And then open surgery has a better success rate than arthroscopic. So see, your answers, when you do your self-assessment test and you do the AOSSM online tests, the answers show you clues as to what they're thinking with the questions and what they feel is important. Because they're baiting you here, right? But no, open surgery doesn't have a better success rate. But we do know that pre-medication with lidocaine has fewer complications than sedation. So when you're taking the test, don't just go to the answer. Read all the other answers, because it's a clue of what they're thinking about and what they're gonna focus on. This figure shows an arthroscopic view of a left shoulder. So you're looking through the posterior superior portal in the beach chair position. The asterisk indicates one anatomic structure. And this is a pretty common picture that we see on the test. And so first, look at your upper rolled border. Here's your subscapularis. So that can't be it. Superior glenohumeral ligament. Well, that's really all the way superior in the rotator interval. We can't even see the rotator interval. The anterior labrum. Well, here is your glenoid cartilage. Here's your anterior labrum. So just always stay committed to get your bearings. And then your biceps. Well, you can't see the top of the glenoid. So it can't be the biceps. So by default, that's your middle glenohumeral ligament. And they ask that a lot. And just think, it always courses in an oblique fashion against the subscapularis. When the arm is abducted 90 degrees and fully externally rotated, which of the following is responsible for resisting anterior translation of the humerus? Well, it's not the cortical humeral or superior glenohumeral ligament because they're both contents of the rotator interval. And we know that they function with the arm at the side. The middle glenohumeral ligament, remember, is at 45 degrees, provides you some anterior translation. The anterior band of the IGHL? Yes, that's the correct one. Because the posterior band is when you're fully internally rotated. And again, this is just one of those memorization questions. Which of the following plane radiographic views best reveals a hill-sax deformity on the humeral head? Well, the lateral scapular Y, first of all, they didn't even call it scapular Y. So we don't really talk about that for hill-sax. Your scapular AP is really your Gracie or your true AP. And that is more of a slightly externally rotated, lets you see the greater tuberosity and better profile. External rotation AP, no. Neutral rotation AP, we didn't talk about that. But internal rotation AP lets you see posteriorly and lets you see the hill-sax. So this is a 22-year-old male hockey player, presents for management of recurrent right anterior shoulder instability. His index dislocation occurred when he was checked into the boards a year ago. Since then, he's had dedicated PT, but three repeat dislocations. Exam shows positive apprehension, so you need to know apprehension in this position. MRI has a Bankart lesion with 25% attritional bone loss. Which is the following is the most appropriate? Well, you just saw that, 25% bone loss. They want you to do some kind of bone block procedure. So open Bankart, no, because there's bone loss. Arthroscopic Bankart, no, there's bone loss. Remplisage, that's for the humeral head. We didn't even talk about the hill-sax. Humeral head allograft, again, we didn't talk about the hill-sax. But Laterge, yes, that's one of the bone block procedures. So now moving on to posterior instability. 10% of instability events are posterior. 2 3rds are trauma, a traumatic event where the arm flexed, adducted, and internally rotated. About 1 3rd are seizure disorder related. You need the axillary, you don't want to miss the locked dislocation. But most of the athletes, most of the questions are really the microtrauma of posterior instability for the at-risk position of the arm. So the positions, linemen swinging a bat, golf swing, where you're at this at-risk position. Flexion, adduction, internal rotation, I see that at-risk position in a lot of the vignettes. They're leading you down posterior instability. At-risk athletes are people who have more glenoid retroversion. And with every one degree increase of glenoid retroversion, you have a 17% increased risk of posterior instability. And the exam and the presentation, typically it's vague. So you'll have a vague pain during the at-risk position, posterior loading. So when they give you someone who's benching, blocking, doing push-ups, and they have this pain, that's putting you in that at-risk position. On the exam, pain with that at-risk position recreates, or putting you in that position recreates your pain. There's a lot of different tests. Just be familiar with these words. If you see that in the vignette, that's what they're getting at, but they're not gonna ask you which test is better. And then always check all directions of instability and laxity, because some of these people are posterior inferior unstable, and the rotator interval is important in posterior inferior instability. How about the imaging? MRI, with or without contrast, evaluates the pathology, and it's accurate in about 68% of cases. The CD, the CT with 3D recons will let you see if they have a reverse Hill-Sachs. If it's retroverted, like this picture right down here, that's the best way to look at the bony anatomy. So what is the pathoanatomy? Most people have a patchless capsule. So again, there's an element of the posterior inferior instability and a posterior labral tear. You can also see a deficient rotator interval, reverse Hill-Sachs, or you can see a raggle. So that's a posterior band IGHL injury. So remember, 9% of instability have a haggle, and of those haggles, 7% are the reverse Hill-Sachs, or the reverse haggle. And again, if they orient you, the scope is anterior, you're looking posterior, and you see muscle fibers, that's because you have a reverse haggle, and the capsule is torn away, and you're seeing the muscle fibers of the infraspinatus. Posterior labral tears are often in combination with other lesions. So 24% are isolated, but 19% are combined, so they often extend up and around. So what are your treatment options? So for this, it's pretty clear. Systematic reviews have shown that you start conservatively. So the answer, if it's the first presentation for posterior instability, the treatment is conservative, you do start conservatively. And a good prospective study found that, of 112 patients, they were treated conservatively, 82% did not develop recurrent instability. And the factors that are predictive of recurrence were age, how big was the reverse Hill-Sachs, and if the dislocation was seizure-related. Most of the scenarios you're going to have are going to be athletes, and I don't think you're going to really get into the seizure aspect. So your treatment options. So this, unlike Bankart, most prefer arthroscopic. This is supported by systematic reviews and meta-analyses. You do a posterior labral repair, anchor repair. You can do plications. You may or may not do a rotator interval closure or anterior plications. The literature's unclear on this, so you're not going to be asked whether you need to add a rotator interval closure or plication. Open versus scope, overwhelming literature for doing this arthroscopically. So open stabilization is definitely not the right answer for posterior instability, unless there's some significant bone loss posteriorly, and they'll take you down that path. And the outcomes, I think what's important here is that the satisfaction's good, recurrent instability is low, probably lower rate of recurrent instability than anterior. But down at the bottom, the most important thing for posterior instability is that the return to pre-injury levels is not nearly as good as anterior. So return to pre-injury levels for anterior is about 90%. Return to pre-injury levels for posterior labral repairs is more in, you know, kind of the 65% range, and even less for overhead athletes. And what about bone loss for posterior instability? It's a rare problem. And again, while we keep harping on posterior inferior instability, checking the rotator interval by checking the sulcus sign by externally rotating, it's because for patients who have posterior inferior instability, who fail a posterior labral repair, a bone block is not going to stop that inferior instability. So that's something that they'll try to kind of bait you on on the questions. You want to have a good exam. But if they really have bone loss, allograft or iliac crest is reasonable, but the complications either open or arthroscopic are high. And there's a lot of significant complications, and so I think that's the take home. Yes, if you have bone loss, you can fix it, iliac crest or allograft, but the complication rate is high. So questions. Figure 23. So this figure is an axial MRI scan of a 21-year-old male who was injured playing college football. His pain was aggravated with blocking maneuvers. So again, blocking is they're trying to get you, when you see that, they're taking you down a posterior path. He was alleviated. His pain was alleviated with rest, and he had to stop playing because of pain. So what maneuver will most likely reproduce his pain? And just think, always orienting yourself, find the coracoid. You're in a hurry. You're kind of panicking on a test. Find the coracoid. It's anterior. So here is a posterior labral tear. He has pain with blocking. So flexion, adduction, and internal rotation recreates posterior instability. Flexion and abduction really doesn't. Forward elevation in the scapular plane actually centers the humeral head. And external rotation and abduction is for anterior instability. Which of the four muscles of the rotator cuff provides the most resistance to this patient's direction of instability? So remember, he has posterior instability. So supraspinatus, no, not really. That's not the big factor. Your infra and your teres are both posterior. So you might think, oh, I'll strengthen them. They'll stop the humeral head from sliding out. But even if you're thinking that, they're both about the same, so they wouldn't make you pick. But truly, the subscapularis, the stronger it is, it's a tether. It stops the humeral head from coming out the back. So that is the correct answer. 19-year-old college defensive lineman. So there you go. He's a lineman. So that's, you know, when they give you a lineman, it's going to be posterior. He felt the shoulder come out and spontaneously reduce. On exam the next day, he has moderate pain at rest, and he's guarded in a sling. He has limited mobility because of pain. Here is his imaging. What's the next most appropriate treatment for this lesion? So here's your subscapularis. Here's the humeral head. The head is sitting subluxed on the back of the glenoid, and you see this little piece of bone with the posterior labrum. So look at the answers. Because you might think, oh, I'm not sure. Should we treat it operatively or not operatively? Because maybe this isn't displaced. And they're going to lead you down the pathway. So sling immobilization and external rotation, so they're trying to throw you off. That's the bracing study for anterior instability. Immediate PT focused on cuff and periscopular strengthening. So remember, the treatment for posterior instability is PT. But immediate PT, when he's in this much pain, tells you that's not the right answer. That's their trick in there to let you know that that's not the right answer. Arthroscopic anterior labral repair, well, this is an anterior. Arthroscopic posterior labral repair and capsulography, incorporating the bony fragment. That sounds promising. And then open posterior labral repair with bone block, we just know that those are bad. So here's the correct answer. And I think where you might get confused on this question is, do I do PT or do I fix it? Because maybe it's not really clear how displaced that is. But it's the immediate PT that tells you this isn't the right answer. And they want you to fix this. So now going on to multidirectional instability. They do like to have vignettes on these. Most of these are atraumatic. You can have a traumatic onset, so don't be thrown off by that vignette. Doesn't rule out the diagnosis. Most are in their second and third decade of life. They have a patchless capsule. They have abnormal patterns of rotator cuff muscle activity. Abnormal scapular kinematics. They're going to want you to watch their scapular kinematics. And the symptoms are kind of vague, nonspecific, neuro, pain, weakness, and popping out of place. They're going to have normal or increased motion. They have apprehension. Their cuff is weak and painful. They really want you to check their scapular dyskinesia. They want you to focus on scapular stabilization programs. This is where Bighton's criteria comes in. They want you to check that. That's going to be in these vignettes. So most of the time when you see a Bighton's criteria, it's in a vignette for a ligamentously lax MDI patient who they don't want you to operate on. Always watch for volitional components and connective tissue disorders like Ehlers-Danlos. The anatomy of the rotator interval is just as important to know as your glenohumeral ligaments. So the superior glenohumeral and the coracohumeral ligament are part of the rotator interval, the capsule, and then the long head of the biceps courses underneath. And they want you to know the borders. So if here's your rotator interval, superior border is your anterior edge of your supra. The inferior border is the upper border of the subscapularis. Internal is your coracoid and then lateral is your transverse humeral ligament. And the function of the rotator interval, primarily posterior inferior glenohumeral stability and adduction. Conservative treatment is always, always the answer. Strengthen the cuff, strengthen your scapular muscles, improve your proprioception. Rehab is always three to six months. So if somebody initially presents and they haven't had rehab, you absolutely need to do rehab. Definitive length of time isn't known. And some of the studies are showing that maybe these patients don't do as well as we hope with rehab. But do not be fooled into operating on the test if they don't tell you six plus months of rehab. You gotta rehab these people. And then surgical treatment, if rehab fails, and they're gonna tell you that rehab failed. They're gonna say they've done six to nine months. They're gonna have at least that much. If someone's done six to nine months, they're leading you down a surgical pathway. And they are not going to ask you to pick open versus arthroscopic plications versus open capsular ship. Open is the gold standard, but there's really no evidence to support this. And systematic reviews have shown that they're really similar in return to sport and recurrent instability rates and loss of external rotation. So they're both safe and effective. They're both right. And every vignette I've ever seen, if they lead you down a surgical pathway, they either give you an open answer or they give you a scope. But it's okay to answer the scope plications if surgery is what they want you to do. So don't think a scope plication is wrong and believe that the only option is open. But they're not gonna make you choose. So which structure is the primary restraint to inferior translation of the shoulder? So remember your middle glenohumeral ligament, which they like to show you the pictures of, is anterior restraint in 45 degrees. Your subscapularis, we just talked about that, that helps restrain posterior. Long head of the biceps, very controversial. Shoulder surgeons don't believe it has any function. If it has any function, it's a humeral head depressor. So it's not a restraint to inferior translation. Corical humeral ligament, oh, well that's part of the rotator interval. We keep talking about the function of the rotator interval is inferior stability. And then coricoacromial, right, you don't want to cut that in a massive cuff tear because you're afraid of superior migration. So corical humeral, content of the rotator interval. Sixteen-year-old female swimmer has several episodes of atraumatic lenihumeral instability that occur in different arm positions. So it's kind of telling you all different positions she has instability. Exam has generalized ligamentous laxity, positive sulcus sign, and she can go out the front and the back. Thermal management should consist of thermal capsulography, I don't think that's ever the right answer. That's something from long ago. Inferior capsular shift, well, she hasn't had therapy. A glenoid osteotomy, as Dr. Gill said, that's never the answer. I don't think that's ever the right answer. And then a putty plat is something from the dark ages. So, and I apologize if anybody in here did one of those and it's from the dark ages. But we don't do those anymore. So a strengthening program for cuff and scapular muscles, that's what they want you to do. So now moving on to slap lesions and the pathophysiology. And you know what's funny is even though, as Dr. Gill said, they don't want you to operate on slaps, they're on the test all the time. Everyone wants to talk about them, but they don't want us to operate on them. So you need to know the mechanism is forceful traction to the arm, direct compressive load, so traumatic fall onto your hand, and then repetitive overhead throwing. So increased external rotation in the late cocking phases increases the forces on the long head of the biceps root, where it results in a peel back injury to the posterior superior labrum. And a lot of people believe the internal rotation contracture is the essential lesion. And we'll come back to that because that's important to focus on. The presentation is typically pain, maybe mechanical symptoms, fatigue, unable to throw, weakness, a sense of instability, kind of vague, they just can't throw. They don't have the same force. Physical exam, always check dyskinesis and atrophy because as you heard from Dr. Gill, the one time they want you to go after these, slap tear leading to a spinal glenoid notch cyst pressing on the suprascapular branch of the infraspinatus, you will see atrophy posteriorly and they'll often have dyskinesia. And so you want to check those two things. Range of motion and strength is typically intact unless you have external rotation weakness, you're going to think that's in the vignette, you're thinking spinal glenoid notch cyst. And then the important thing is they ever give you a vignette where there is a loss of internal rotation from one side compared to the other, they'll always give you the other side's mobility. And if one side there's a drastic loss of internal rotation, they're leading you down a pathway that this patient is predisposed to a slap because they have internal impingement because they have glenohumeral internal rotation deficit. So they have GERD, they're tight posteriorly and that predisposed them to the slap. They ever give you that vignette, you had better do aggressive physical therapy for the posterior capsule before you ever operate on it because again they don't want you to operate on these. Instability overtly is rare, maybe subtle. And then you want to check the biceps exam but it's really not very sensitive so it's kind of part of the whole picture that they're looking for. There's no single exam finding that's 100% accurate. Single exam alone is unreliable so if they compare multiple tests for slap with intraoperative findings there's really not a reliable test. So they're never going to just say pick the best test. O'Brien's is most commonly used but given the unreliable nature of all the slap exams you're not going to be asked to differentiate and you're going to be given a history, an exam and an MRI finding that's all consistent with slap. Imaging radiographs just to look at the joint. MRI can show other pathologies but there's a core correlation, a poor correlation between your MR findings and your intra-biceps findings. An MRA is more sensitive and specific for diagnosing slap tears. Associated findings, again, your infraspinatus, we keep harping on this but it's on every OITE and it is on this test so that'll be like a gimme when you get that. You see that big cyst, you know that it's pressing on the suprascapular nerve. The anatomy of the slap tear, the normal anatomy, the majority of the biceps originates from the supraglenoid tubercle, the remaining fibers into the superior labrum and it has a dominant posterior insertion. It's avascular and you should understand a little bit about the stability of the long head of the bicep as it enters the groove. There's a medial pulley, the coracohumeral ligament, part of the rotator interval, remember the comma sign, superior fibers of the subscapularis are all important. There's anatomic variants and they're gonna try to get you to operate on an anatomic variant. So know that repairing any anatomic variant will lead to external rotation loss and the best way to think about it is that if you see something that looks like the labrum, it's not attached to the glenoid but you don't see disruption in the cartilage, you don't see fraying of the cartilage, it doesn't look like it just tore off. You know, the cartilage looks smooth and normal here. This is an anatomic variant, do not operate on this or on the test. The types, type 1 and type 3, all you need to know is that you debride them. Type 2 and type 4, you do some kind of repair. They're not gonna ask you, it's so controversial now, do you do a slop repair versus a bicep tenodesis, that is, they're not gonna ask you to differentiate. Just know 2 and 4, repair, 1 and 3, debride. And then here's some good pictures of the differences, 1 is just frayed, 2, it's detached, so 2, repair, 1, debride, 3 is bucketed, so you just debride that piece, and then 4, it's bucketed and it extends into the biceps and that is a repair. So that's just a simple way to remember. Always start non-surgical, posterior capsular stretches, really important, scapular stabilization, correct the dyskinesis, at least 3 months of therapy, and definitely recognize internal rotation deficit. And then if you do operate, again, just know the basic tenets, they're not gonna ask you anything controversial, it's just gonna be repair or debride. And outcomes, they're inconsistent, they're not that good, the revision rates are high, so it is generally accepted on the exam, if they give you a failed slop repair and they've gone through all their rehab and they're still painful, the one case that Dr. Gill showed, they were stiff, you did a capsular release, but if their mobility is good and they're painful, you do a tenodesis, that's the accepted revision and that is a good answer and then it's generally accepted you shouldn't do a cuff and a slop repair together, so that is not the right answer. Complications, stiffness, pain, persistent pain, anchor-related problems, trapping pathologic biceps in the bicipital groove, so again, biceps tenodesis is definitely the accepted treatment. So a couple questions, these figures below are MRI scans of a patient with shoulder pain and weakness, see again, they keep coming back to this, what muscle and nerve are most likely affected? Well, this is posterior, here's your coracoid, here is your nice muscle belly of your supraspinatus, here's your nice muscle belly of your subscap, here's your teres minor down here and you know, I can't see the infrab really well, so deltoid and axillary, this cyst is nowhere near your axillary nerve, teres minor and axillary nerve, again, the cyst is above the teres minor, the nerve comes underneath, so that's not it. Supraspinatus and suprascapular, where the cyst is posterior, so it's missed the branch to the supraspinatus, infraspinatus and suprascapular, oh, we keep talking about that, that is the correct one, and then subscapularis, well, we're all posterior, so that can't be right. So here is a good, and this is like a good question to kind of show you how they ask about repairs, which of the following SLAP lesions are best treated by repairing the labrum to the glenoid? So remember, type 1's, we debride, so you get rid of A and you get rid of B, because we debride type 1, type 3, remember, is the bucketed piece that you just debride, so you get rid of 3 and you get rid of D and you get rid of E, because we debride 3, we debride 1, so that leaves type 2, and that is where you do a repair. This is a 35-year-old male, recreational tennis player, he's had shoulder pain for 6 months, he's had appropriate rehab, MRI shows a SLAP tear, and he has a scope repair. Despite compliance and 6 months of therapy, he has persistent similar pain without stiffness, so he's at the 12-month mark, the rehab has gotten him his motion back, he's not stiff, MRI shows no cuff pathology, his image has shown what is the appropriate management of this patient, so they're basically giving you a failed SLAP repair. You don't even really have to look at the image to know that biceps tenodesis is correct, right? You're not going to do a hemi-arthroplasty, there's no arthritis, you're not going to do more PT, he's already done 6 months, they've kind of already told you no more PT. We're definitely not going to do a revision lateral repair, because if it didn't work the first time for a SLAP, the results aren't that good, they're inconsistent. We're not going to irrigate in debris, they're not taking you down an infection pathway, they're not saying that the anaerobic cultures were positive, so you are definitely going to do a biceps tenodesis. And this is an interesting question, because I think it lets you know, when you read the questions, just read the whole thing, don't start thinking about your answer until you read the whole thing, because this question takes you off on a whole different pathway. 19-year-old hockey player presents after 6 months with a type 3 AC separation. He's missed a few weeks of the season, he was able to return without restrictions with motion and strength. However, he continued to have pain at the AC joint. Here are his radiographs, and there's this little fleck of bone right here. An MRI confirms a small bone fragment about the inferior and lateral aspect of the distal clavicle. His season ended, and he wants to have this bone fragment removed prior to the start of his season. Figure 2 was taken during the routine diagnostic scope of his joint as part of his surgery. So think about that, they just told you all this stuff about the AC joint, and your mind is racing, AC joint, AC joint, what should I do, it's a type 3. And they want you, they show you a scope picture, so it's a long, convoluted way to get you this picture of an anatomic variant. So here's your humeral head, here is your glenoid, here is your biceps, here is the anterior inferior labrum, and this is a cord-like middle glenohumeral ligament. So in addition to removing your loose bone fragment, what other treatment should be performed during, given this arthroscopic finding? So labral debridement, oh that's a little frayed, maybe they want me to debride that. That's tenodesis, oh maybe that's a type 2 slap tear, and they're trying to tell me to tenodesis. Labral repair, that's what they really are trying to get you to say, but it's wrong. Capsular release, no one's talked about tightness. Or no treatment, again, you see this image, they're always trying to present to you an anatomic variant, and they want to know, do you recognize an anatomic variant? So just keep that in mind, don't do anything. If this is an anatomic variant, leave it alone. And then there's more questions in your packet that I put in there that you can go through on your own. So thanks a lot for your attention.

shoulder arthroscopy

labral pathology

patient positioning

complications

treatment options

shoulder instability

glenohumeral ligaments

rotator interval

slap lesions