We'll see you again in an hour. Our next speaker is keeping the shoulder theme alive, Julie Bishop from the Ohio State University. Thanks, Julie. All right. Well, thanks a lot for having me. And although I'd like to think that my talk is highly important, Dr. Gill is correct. I took my recertification exam last October, so this is all very fresh in my mind. And I have to admit, I'm a shoulder surgeon. My practice is 100% shoulder. And I felt like every shoulder question on the test was the AC or the SC joint. So he's right. But there are a lot of good take-home points from the talk I'm going to give. And I would say overall, given that I just took my recertification exam, this course, I took the whole course, showed up for every single lecture, definitely hadn't thought about foot or ankle or hip in a long time. And this course and practice exams and OKU is what I used. And it really prepared me very well. So I think it's great to be here. So we're going to talk about arthroscopy basics, shoulder instability, and biceps anchor slap today. And as far as shoulder arthroscopy, the main things that they want to ask about are positioning, the portals, what's at risk, and complications. So we'll start with positioning. For lateral decubitus, I think the most important take-home point from this is that there is no increased risk of hypotension or bradycardia, therefore there's better cerebral perfusion in lateral. And they definitely do like to ask that. The disadvantages are neurovascular. So if you pull too hard, too much traction can cause an injury. And then there's increased risk of axillary or musculotaneous nerve injury with your anterior inferior portal in lateral. When you look at beach chair, the advantages is you can do regional with sedation, which you can't do in the lateral position. But really what they like to focus on is that beach chair has an increased risk of hypotension bradycardia, which leads to cerebral ischemia. And there's an increased risk to the cephalic vein with a 5 o'clock portal. But really I would focus on the hypoperfusion. And thinking about the cerebral hypoperfusion, we all practice deliberate hypotensive anesthesia. And what a lot might not realize is that in order to have a clear field arthroscopically, you need a difference of about 50 millimeters of mercury between your systolic blood pressure and the scope pump pressure. So the anesthesia literature recommends that your systolic blood pressure be above 90. So if you have it at 90, that's why your pump pressure is 40, to have that 50 millimeter mercury difference. They also recommend that the systolic blood pressure and the MAP are within less than 20% of baseline measurements in order to prevent the cerebral hypoperfusion. And they recommend cerebral oximetry to monitor this. So they do like to have vignettes where they talk about the CDEs, the cerebral desaturation events. And those occur when you have greater than a 20% decrease in your baseline cerebral oxygen saturation. There's a higher incidence of CDEs in beach chair versus lateral. And again, that I think is a take-home point here. However, don't be fooled in a vignette or a question. Although there's a higher rate of CDEs, there is not a higher rate of clinically relevant effects of doing lateral versus beach chair. So yes, there's more CDEs in beach chair, but that hasn't translated into any clinical outcomes. So the arthroscopic anatomy, I think every joint that has arthroscopy, they like to ask about what's at risk. And I think the thing to take away is that these three structures are what are always the answer for shoulder arthroscopy. So the axillary nerve, the cephalic vein, and the suprascapular artery are the most at-risk structures. Axillary nerve is most at risk with the 5 o'clock portal. Cephalic vein is most at risk with the anterior portal. And actually cephalic vein is the most at-risk structure of all the structures for shoulder arthroscopy. And then the suprascapular nerve is at risk for your releases for a cuff repair if you go too medial for mobilization, and at risk medial to superior glenoid rim. Your higher risk portals then come back to this. So your anterior working portal, cephalic vein. Your 5 o'clock portal, which you use for anterior stabilization, the biggest risk is your axillary nerve. Anterior inferior portal for instability surgery, both cephalic vein and axillary. And then getting posterior for your 7 o'clock posterior labral work, it's the circumflex artery in the axillary. But notice the axillary is closer. So that will be the most commonly asked question. And then your navisor portal, slap, suture, passing, that's the suprascapular nerve. And the arthroscopy complications, they don't ask a lot about this, but I think P. acnes is something that's very relevant and very prevalent. So know that it's gram-positive, non-spore-forming bacillus. You have to hold your anaerobic cultures 10 to 14 days. And recent literature has come out, and I don't know if this will make it to a test question, but it is very relevant that there's an increased risk of infection if you have a cortisone injection within three months of an arthroscopy. And overall, DVT-PE rate is pretty low. So some questions. And again, here we go with the beach chair position. So the minute you hear beach chair in a vignette, if they're talking about beach chair versus lateral, I think they're going for the cerebral hypoperfusion. So the patient had general anesthetic and a nerve block. He had an uncomplicated one-hour case. But at the end of the case, the patient could not be aroused or weaned from the ventilator. And they determined there was an anoxic brain injury. So what is the most likely cause? And if you go down through all of the answers, myocardial infarction, PE, malignant hypothermia and anaphylaxis aren't really things that we talk about, really aren't going to be asked and don't make sense. But cerebral hypotension does. With regard to standard shoulder arthroscopy, the posterior portal is made in the soft spot, two centimeters inferior and medial to the posterior lateral corner of the acromion. If the posterior portal is too inferior to your standard posterior portal, what's at risk? Well, remember we talked about the main things they're going to ask, and I've never seen them ask anything other than suprascapular, cephalic and axillary nerve. So long thoracic nerve doesn't make sense, right? That's always going to be associated with winging, as Tom said. Suprascapular nerve, we're really not near that. That's not at risk. The profundobrachial artery, we haven't really talked about. Now axillary nerve and posterior humeral circumflex are both back there. But remember, the axillary nerve is closer, and that typically is the answer. So moving on to anterior instability, we'll hit the highlights for the exam. So for anterior instability, 23% of all shoulder injuries in NCAA athletes are glenohumeral instability. 90% of the events are anterior, and the majority of the events are subluxations that don't require a closed reduction. And the mechanism of injury is when a force is applied to the arm in your abducted externally rotated position. So who is at risk? They might ask you this. So of course, prior history of instability. But just in general, patients without a prior history of instability, the contact, collision sports, the military population. Those who have a positive apprehension and relocation test just on the pre-screening physical exam. They've never had instability, but they have apprehension. And then the tall, thin glenoid, that's the anatomy answer, the increased glenoid index they found in the military population is higher risk. So how do you reduce the dislocation? They do like to ask this. I've seen questions on this often. IV sedation versus intraarticular injection. Just know the literature supports the intraarticular injection because of the complication rate. Complication rate is higher for sedation versus the injection, and this seems to be a common theme. So what about the anatomy of the glenohumeral ligaments? Just like there's things like the brachial plexus that harken you back to your OITE days, this is something that you've been asked since you were a resident, and they still ask it on the test and you just have to memorize this. So go through this and commit to memory when the arm is at the side, the primary restraint to anterior instability is your rotator interval superior glenohumeral ligament. In 45 degrees, it's the MGHL. In 90 degrees, it's the IGHL. In 90 of external, it's the anterior band. 90 of internal, it's the posterior band. And there will always be a question about this on the test. So what are your PERT and physical exam findings? So I think for ligamentous laxity, what's important just to take away is BITEN criteria because you might see that in a vignette. And know that the BITEN criteria is 9 points for laxity. And if you see that in a vignette, they're probably telling you if someone has a 7 out of 9 or a 9 out of 9 BITEN score, they're taking you down a ligamentously lax pathway for that patient. For apprehension tests, I think the main physical exam test that they'll talk about and expect you to understand in a vignette is apprehension in the ABER position that's relieved with posterior pressure. Now the Gagee sign, what I think is important, what I've seen for this is they will work the Gagee sign into a vignette. That's why you should know what the Gagee sign is. And the Gagee sign indicates an injury to the IGHL, a Hagel lesion, or inferior capsular laxity. And they compare abduction with the arm in neutral from side to side. If they have greater than 105 degrees of abduction compared to the opposite side, that means the humeral head is going inferior and so the arm is abducting more. That's either inferior capsular laxity or a Hagel lesion. But again, I think this shows up in the vignettes. Imaging, I think it's important to know the true AP is your Grachy. That lets you look at the joint, look for OA. The internal rotated AP view, I've seen them asked several times. That is looking for a Hill-Sachs. You're internally rotated so you see the back of the humeral head posteriorly where the Hill-Sachs is. Your west point axillary shows you glenoid bone loss. The striker knot shows you the Hill-Sachs. And for MRI, that will show, a normal MRI will show your bone bruises, associated pathology, cuff, labrum. MRA is better to define the labrum, capsule, and Hagel lesions. So the pathoanatomy, Bankart lesions are in 90% of dislocation subluxation events. So if somebody had a locked dislocation, they're almost guaranteed they've got a Bankart. The Hagel lesion, they do like to bring up, is in about 9% of instability cases. These are typically a vignette with a much higher level trauma, much higher energy trauma. And the thing about a Hagel lesion is if you miss it and don't repair it, there is a high recurrence rate. And in MRA, they'll show you this classic picture here where the dye is streaming down the medial aspect of the humeral neck because the capsule isn't attached on the humeral side. Past lesions, very common, 40 to 90% of all anterior disability events up to 100% in recurrent events. And I think this is also just a really good picture here. The arrow is on the Hagel lesion that's pulled away from the humeral neck. And they do like to show you arthroscopic pictures on the test. They'd like to give you a picture, put an arrow on something, and ask you what you're looking at. And this picture I've definitely seen, and I think it can get a little confusing if you don't do shoulder arthroscopy very often. But I think what you should take home is a couple things. If you see the humeral head, something looks pulled away from it, and you see muscle fibers. If you, anytime you have the scope in the joint and you see muscle fibers, you're either looking at a Hagel or a reverse Hagel because you're seeing the muscle, the subscap, because the capsule's no longer attached to the neck. Or you're seeing the muscle, the infraspinatus, because posteriorly the capsule's not attached. So just remember, you see muscle fibers, typically it's a capsule or injury because we shouldn't see that. So what are your treatment options for instability? The initial treatment is still controversial despite the well-known recurrence rate. So you're not going to be asked. You're not going to be presented with a first-time dislocator with nothing else and asked whether you should operate. It is increasingly accepted to operate for the first-time dislocators. But more likely you're going to be given a vignette and you're going to be asked to counsel about recurrence rates, and we'll get to that. Treatment, conservative, sling, early motion when they're comfortable, rehab. Return to sport when strength is symmetric. Bracing is controversial. The earlier studies about bracing and external rotation cannot be reproduced. You might see this as an answer, and it's unlikely the answer or to be tested because we can't reproduce that. The natural history of instability. So I think this is important. There's up to a 94% recurrence rate. So realize there's a lot of studies out there that have a lot of different recurrence rates. The things they like to ask are, number one, what places somebody at high risk for recurrence? So your younger contact athletes are higher risk. A Hagel lesion, if not fixed, is higher rate for recurrence. But a Hagel lesion that you recognize and fix doesn't make you higher risk for failure. A bony bank guard that's displaced and not fixed is higher risk for recurrence. And the recurrence rates do decline each decade of life after the age of 20. I think the Hovelius paper is probably the best paper to remember when they're asking recurrence rates. So they might give you a vignette, 17-year-old contact athlete had his first time dislocation. You're going to counsel on the risk of recurrence. I think this paper is the best because it's 25-year follow-up on 12 to 25-year-olds that had a dislocation. They have about 60% of those patients had one or more recurrences, 43% had no further issues. The other part they like to ask is about long-term arthritis after a dislocation. This same paper, 25-year follow-up, found that 18% of patients who did not have a second recurrence still went on to get arthritis. So these are not people that had surgery. So this is about a 20% risk of arthritis just from having one dislocation. And then those that had more than one dislocation had a 40% risk of arthritis. So what about return to sport? There's not a lot out there about this. So I think just kind of keeping in mind the studies, there's one or two studies, this is the best one, 75% or so can return to sport if they have an in-season dislocation because they might give you that vignette, in-season dislocation. About 75% can return to sport. They return when they have full symmetric strength and range of motion. Most of the subluxation got back faster. Of those, about two-thirds finished the season. About two-thirds had another episode of instability. So I think those are some general numbers for counseling that you can remember. So what about open versus scope? What is testable? So for Hagel treatment, bone loss, Laterge, it's too controversial. There's not enough literature. You will not be asked to choose open versus arthroscopic. Now for the Bankart repair, though, they're going to try to bait you to take the wrong question or the wrong answer. So the literature suggests there's a higher rate of instability in contact athletes treated arthroscopically. Not all the data supports this. This paper in JBGS had about a 23% recurrence arthroscopically versus open had 11%. But what I think is a take-home is the failures because they can ask, what puts you at risk for recurrence after having a stabilization? Young, male, large, Hill Sachs lesions. But this paper didn't really evaluate bone loss. So the literature cannot support a difference in outcomes, open versus arthroscopic. It cannot support a difference in outcomes for range of motion. Do not say that an open Bankart limits your external rotation. That is not the right answer and they will try to get you to say that. And patient reported quality of life outcomes, none of these are different with open versus arthroscopic. So if you are going to do a stabilization, they're never going to make you choose open versus arthroscopic. So then those two can't be the right answer. They're trying to get you to do something else. What about the outcomes? 90% return to pre-injury level of sport. Overall recurrence rate 4-19% after an arthroscopic repair. Meta-analysis showed about 7. So I think you're safe in that range if you were asked that question about recurrence or failure after arthroscopy. Long-term OA, remember it happens after dislocation with no surgery. And you do see it in up to 40% of patients treated with stabilization. And so it's not a result of our current techniques. It's a result of having the instability event. What are your risk factors for recurrence? I really focus on this. Ligamentous laxity is one, but that's not typically where they're going with the answer. The younger you are, under the age of 20, and glenoid bone loss is one of the biggest things that they're going to ask you, and it's over 25%. Engaging heel sacks does make you higher risk, but it's not the most important. Male sex, contact sports are high risk, but those aren't typically the answers. It's the age and the bone loss is what I see consistently as the right answer. And then post-capsuloraphy arthritis, they do like to ask questions on this. They'll give you a vignette, someone in their 50s, maybe early 60s. They had instability surgery long ago when they were non-anatomic surgeries. They have progressive pain, and they have post-capsuloraphy arthritis. They're going to typically show you a biconcave glenoid because they're so over-tightened in the front, they lose external rotation and really pushes them out the back. And they do like to ask a vignette on this. So what about bone loss? There's the critical amount of glenoid bone loss, the threshold for grafting is 20 to 25%. Now realize, don't listen to any of the current literature when you're taking this test, because the current literature is leading us towards maybe the critical threshold is 13% or 12%. For the test, it's 20 to 25%. It's a bigger number. The predictors of the critical defects, how old you are at your first dislocation, how many dislocations you have. They give you a vignette, suspect bone loss in patients who had failed prior instability because maybe they missed the bone loss. Long history of multiple dislocations, and they dislocate with minimal provocation. So they're just washing their hair in the shower and it pops out. That vignette is probably leading you towards significant glenoid bone loss. I think you should just be familiar with the glenoid tract concept. You don't have to memorize it by any means, but know what it is because they might work it into a vignette. Rarely is glenoid bone loss in isolation. The lesions are bipolar, they're both sides. As you lose more and more glenoid bone, the glenoid tract decreases. That way, the humeral head is at greater and greater risk for engagement of the hill sacs because it has less bone on the glenoid to travel. So smaller hill sacs lesions are more significant, but it's typically not the hill sacs that you're going to address. It's the fact that the glenoid tract is shortened by the glenoid bone loss. So the best way to evaluate is 3DCT. Treatment options for bone loss, you're unlikely going to be asked to choose one over the other. So you're going to be asked to choose a bone augmentation procedure, a bone grafting procedure. You won't be asked to do open versus scope Latter Jay or Iliac crest or distal tibia. You're not going to be asked. That's too new. Literature cannot really support one technique over another, and this won't be asked. So what about the Latter Jay? This is very popular now, and what they focus on is complications. And that's the biggest thing that I see with the Latter Jay questions. The complication rate is up to 30%. The recurrence rate of a Latter Jay is very low. So I think that that's very quotable, up to 8% recurrence rate. That's associated with a medial graft position. So they like to say, if the graft is too medial, what can happen? It can dislocate. If the graft is too lateral, they like to ask that. You get arthritis if the graft is too lateral. I think you should be familiar with issues with the coracoid, lysis of the coracoid, resorption of the coracoid. That is very prevalent. It happens, but it hasn't translated into negative clinical outcomes. The nerves at risk, 10% risk of reported, mostly sensory from musculocutaneous, and for axillary nerve, motor and sensory from retraction inferiorly. I think those are the most important things to take home. And for Latter Jay, yes, the literature supports a loss of external rotation. So you do lose some external rotation, and that would be a correct answer. Remember, open bank art, no support for loss of external rotation. So what about the Hill Sachs lesion? So glenoid bone loss with a large Hill Sachs, most of the evidence is still pointing towards addressing the glenoid side to prevent engagement. You're unlikely to ever be asked to address both of these in the same patient on the test. For really large Hill Sachs with minimal bone loss, there's a lot of options, but there's no good guidelines for indications. There's no good data. There's a high complication rate. So I don't think the correct answer is ever going to be allografting, grafting the Hill Sachs, putting a metal implant in because the literature is fraught with complications. Remplissage, I think you might see. You could see in a vignette. It's to fill, that's the French word, suturing the infraspinatus into the Hill Sachs. And it's a viable option in the absence of glenoid bone loss. And I don't think that they're at the point where remplissage is going to be an answer, but it's going to be one of the answers, and understanding why you would use it will be helpful in sorting out the correct answer. Some studies have shown a decreased rate of recurrence when you do a Bankart and a Remplissage compared to just a Bankart. Studies show that it heals. You do lose some motion. So this, again, you lose about 8 to 10 percent external rotation with Remplissage, at least with the literature that they use for the test. So let's look at some questions. 25-year-old ice hockey player sustains a shoulder dislocation after being hit into the board. See, they like ice hockey players. A lot of these vignettes for shoulder are ice hockey. Which of the following is associated with an increased risk of recurrence after an arthroscopic stabilization? So bony Bankart, but realize if you fix the bony Bankart, having a bony Bankart in and of itself doesn't place you at higher risk. We'll jump down to capsular labral complex injury. Well, they all have them, and you're fixing it. So that doesn't place you at higher risk. And engaging Hill Sachs doesn't place you at higher risk. It's something to think about your glenoid track, and it could lead you to realize there's glenoid bone loss, but that in and of itself doesn't make you higher risk. And ALPSA, I've seen this several times. They try to fool you and get you to answer ALPSA. So ALPSA is a stripped Bankart. So it's very medialized. So periosteal sleeve avulsion of the anterior labrum. And if you miss an ALPSA, they're going to be high risk for instability, but it in and of itself doesn't place you higher risk because if you mobilize it and fix it, it doesn't increase the risk. So your inverted pair, your glenoid deficiency is the reason, is the answer. So now you have a 20-year-old football player, presents to the emergency room 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. And see how this answer makes sure that you know, oh, wait a minute, you get arthritis with even one dislocation without surgery. So that's not the answer. Surgery is not going to prevent the development of arthritis. The best technique is traction-counter traction. Well, there's 5 million techniques. None are proven really to be better. They're not asking you that. If he declined surgery, play is at the player's discretion. Well, that's just not the answer because the team physician is involved. And open surgery has a better success rate than arthroscopic surgery. That's not the answer either because we haven't proven that. Even though some still feel open is gold standard, literature hasn't proven that. So there you go. You get to premedication with lidocaine, which is less complications than premedication with IV sedation. This picture is viewing from posterior. Again, they like to have pictures. They like to put an asterisk on it and ask you what you're looking at. So when you're looking at this, I think just they really like to ask you about the middle glenohumeral ligament. They often like to ask that. Maybe they think you might confuse it with the labrum. But it's always coursing transversely or obliquely across the subscapularis. It's not near the labrum or near the glenoid. And I think it's just a matter of just having a visual in your mind of what the anatomy looks like. But again, they really do like to ask that. I've never seen them put an asterisk on superior glenohumeral ligament because that's just really hard to define, to see well. And so they always like to ask this or put an arrow on the capsule for a haggle. And then here you are when the arm is abducted 90 degrees and fully externally rotated, which of the following is responsible for resisting anterior translation of the humerus? So coracohumeral and superior glenohumeral ligament, remember that's the rotator interval. That resists anterior translation with the arm in adduction. Middle glenohumeral, that resisted in 45 degrees of abduction. So the anterior band of the inferior glenohumeral ligament is the correct answer in 90 degrees. This is the anterior band. If you were 90 degrees of internal rotation, the answer would be the posterior band. And I think you can be guaranteed one of these questions will be on the test. And then which of the following plane radiographic views lets you see the Hill-Sachs deformity on the humeral head the best? Well, the lateral Y, no, really that doesn't show it very well. Scapular AP, no, that's not even a study. Neutral rotation AP, no, remember the Hill-Sachs is posterior. And internal rotation AP, yes, that brings the Hill-Sachs into view. And an external rotation AP, no, that doesn't bring it into view. So then we'll move on to posterior instability. About 10% of instability events are posterior. And you have macro and microtrauma. And I'll say for the test, because it's sports, they're mostly going to ask you about microtrauma. But you should always realize that macrotrauma, two-thirds of posterior, frank-locked posterior dislocations, are typically a trauma. So they might give you someone who falls with a high load on a flexed, adducted, and internally rotated arm. Or a seizure. Any time you see a seizure, if a football player has a seizure on the sidelines and then cannot externally rotate their arm, they have a posterior dislocation until proven otherwise. But the majority that we see are microtrauma, the at-risk position position. They like to have a lot of vignettes with this at-risk position. So flexion, adduction, and internal rotation is the at-risk position. Football linemen, if you see a vignette with a football lineman, it's posterior instability. It's always the answer. Or it seems to be. Swinging a bat, golf swing, again, you're at that at-risk position. Who are the at-risk athletes? Increased glenoid retroversion. So dysplastic glenoids. And you definitely might see that. For every one degree increase in retroversion, you increase your risk of posterior instability by 17%. And the physical exam, a lot of times the vignettes are vague. So they have a vague pain. It's not like anterior instability where they will say, I am unstable. I feel my shoulder subluxing. This is typically a vignette with vague pain during the at-risk positions. Posterior loading, they might say they're a lineman, they're having increased posterior discomfort with bench press and push-up. On physical exam, they have pain with the position of risk, adduction, internal rotation, and flexion. There's a variety of different tests for posterior instability. They're never going to ask you to choose between them. I think Kim has about seven tests, all slight variations. But they're going to give you a situation where they're loading the posterior labrum. And always on your physical exam, check all directions of instability and laxity. Because the rotator interval will tighten in external rotation. So a lot of these players have posterior inferior instability. Remember your GAGI exam test for inferior instability. If they have a positive sulcus sign that is minimized by external rotation, that means you're externally rotating, you're tightening your rotator interval, and you're minimizing that inferior instability. So imaging, they like to show the picture right here on your left. They like to show this picture a lot. It's the axillary view, and there's clearly contrast between the labrum and the glenoid. And this is a nicely formed glenoid. Over here, you have a CT of a dysplastic glenoid. They might give you some variation of that. CT is best to look at the bone loss. MRI is best typically with contrast to look for intra-articular pathology. And the anatomy, pathoanatomy, most of these patients have a posterior labral tear and a patchless capsule. You might also see a deficient rotator interval, because remember the rotator interval, if you tighten it, will limit inferior instability. So if the rotator interval is deficient, they might be more prone. They might have a reverse Hill-Sachs if they had macrotrauma. They might have posterior capsule or posterior band injury to the IGHL, so your reverse Hagel. And that's again, if you're viewing from anterior, if they tell you you're viewing from anterior, you're looking towards posterior and you see muscle fibers, you're seeing the teres minor, the infra, that is a reverse Hagel. And often the posterior labral tears are in combination with other injuries. So only about 25% are isolated posterior, 57% anterior only. This is instability surgeries and 19% are combined. So there's a lot of anterior and posterior pathology together. Your treatment options. Now this I think is very clear that physical therapy and conservative treatment is the way you start, unless there's some kind of bone injury for posterior instability. And so the duration of PT is unclear, but it's accepted that most patients undergo rehab and physical therapy. And one study looked at 112 patients with posterior instability and recurrence did not develop, recurrence didn't happen in 82% of them. And so I think the answer on the test, if they haven't had therapy yet, is therapy for posterior instability. And again, the vignette is going to lead you down the path that it's posterior instability, but we start with therapy. Now for surgical, different than anterior instability, the gold standard is arthroscopic. So that is supported by meta-analyses and systematic reviews. You repair the labrum. If the capsule is patchless, capsulolabral placations. It's questionable whether you should or shouldn't do a rotator interval closure. They're not going to ask that on the test. The literature is unclear. But you need to understand the anatomy of the rotator interval and that it is responsible for posterior inferior instability. Open versus scope. There's been studies that have looked at both. And there's a high complication rate with open, lower patient satisfaction, lower rate of return to sports with open. So for posterior instability, arthroscopy is your treatment of choice, barring bone loss. And that is pretty consistent. The outcomes are good. The recurrence rate is low. But the one thing to differentiate posterior from anterior, remember for anterior, return to prior level of play was 90%. For posterior, about 65-70% return to pre-injury level. So I think that's significant and worth noting. They don't return to their prior level of injury, especially throwers, the way anterior stabilization does. And bone loss is pretty rare. And remember that your bone block will not address the inferior instability. And most of these posterior cases have posterior inferior. The graft of choice is allograft or iliac crest. There's been both types of techniques reported. The complications are high. So this will probably not be addressed on the test unless they give you a CT with significant bone loss. Then you've got to do some kind of bone grafting procedure for posterior bone loss. So some questions. This is, again, MRI axial cut, 21-year-old injured while playing college football. His pain was aggravated with blocking, alleviated with rest, and he had to stop playing because of pain. What examination maneuver will most likely reproduce his symptoms? Well, remember the position of risk. And that is flexion, adduction, and internal rotation. So forward elevation in the scapular plane is wrong because that actually is stabilizing and centering the humeral head on the glenoid. So if somebody raises their arm in straight forward elevation and they sublux out the back, a positive circumduction test is raising the arm in the scapular plane. So that's wrong. External rotation and abduction is anterior instability. Flexion and abduction is wrong because you're raising them out to the side. That's not the position of risk. It is adduction, internal rotation, and flexion. And that is consistently seen in the vignettes. Which of the four muscles of the rotator cuff provides the most resistance to this patient's direction of instability? And I think sometimes this might be a little counterintuitive because you might be thinking, oh, they're coming out the back. I need to strengthen the infra and the teres. But that can't be right because not one is more important than the other, and they're both listed. So even if you're not sure, those both do the same thing. So you can't pick one or the other, subscapularis, the stronger the subscapularis is the more it can tether or prevent the head from coming out the back. Now this is a defensive lineman, see they did mention that, 19-year-old, pain during off-season drills. He felt the shoulder come out, spontaneously reduced. On exam he has moderate pain at rest and he's guarded, so he's really painful and he's in a sling. He has limited range of motion secondary to his pain and here's his imaging, what is the next most appropriate treatment for this lesion? So one thing, I would look at this, remember they do like to hone in on bone and issues with bone. And so here is your axillary, there's the head. The head is preferentially sitting on the back of the glenoid, here's your glenoid, and you can see this gap right here, this is a posterior bony vanguard that is displaced. And whenever there's a bony vanguard that's displaced, they like you to fix that. So when you look at this, sling immobilization and external rotation for six weeks, well that was something that maybe worked for some long ago with anterior instability. But that hasn't been proven in our literature, so that's not correct. Immediate PT focused on cuff and periscopular strengthening. Now remember I did say, typically you start with therapy for posterior instability. So two things, one there's a bony lesion and second, I think it's the word immediate that tells you this isn't the right. Because look, he's in a sling, he's guarded, he has a ton of pain. You're not going to start immediate PT on that patient. So I think that is the word that tells you that's not the right answer. And anterior labral repair, well it's not anterior. And open posterior labral repair with bone block, well remember open doesn't go so well for posterior, so that's not typically your answer unless you've lost bone. And so the correct answer is posterior labral repair incorporating the bony fragment. But I think the correct answer is this, because that fragment is displaced. So now we'll go on to MDI. And most of the cases, most of the vignettes are atraumatic, but it can be traumatic, so it doesn't rule out the diagnosis. They might try to fool you and give you a vignette that had a traumatic onset. Often the second and third decade of life. And the etiology, and this is what they like to come back to, is your patulus capsular complex. Your abnormal patterns of rotator cuff muscles and abnormal scapular kinematics. That is really the focus of the vignettes, is the scapula. The patients complain of popping out of place, pain, weakness, nonspecific neurosymptoms. So they will give you just kind of paresthesias. So they're not leading you down a path for some kind of cervical problem. Typically, it's the young female with complaint of popping and just a non-dermatomal distribution of paresthesias. And they often can't continue in sports. They have, on their exam, normal or increased shoulder motion. They will have apprehension. They'll have a weak and painful cuff, but don't be baited into doing a decompression or doing some kind of surgery on the cuff. The cuff is weak and painful, because it's trying to stabilize a shoulder that's very loose. Check for scapula dyskinesia. That's a big part of these vignettes. This is where the biting criteria might come in. So you see a young female with a nine out of nine biting criteria. They have MDI until proven otherwise. Watch for volitional component and check for a connected tissue disorder like Ehrler's Danlos, cuz that's very common. The pathoanatomy, I think you need to memorize this as well. Memorize the rotator interval comment, just like you have to memorize the function of the glenohumeral ligaments. These patients have a patchless capsule. They have increased glenohumeral volume. They have laxity of the IGHL, so they could have that positive gaugy sign. They have rotator interval laxity or incompetence. And you could test that by no change in the sulcus with external rotation. So sulcus sign is the same whether they're in neutral or external rotation. That means the rotator interval is lax. And these are the contents of the interval, superior glenohumeral ligament, coracohumeral ligament, the capsule, and then the long head of the biceps. And I think you just need to memorize that. And then they also like to ask the borders of the rotator interval. Again, this harkens back to OITE. So superior border is your anterior edge of your supraspinatus. Your inferior border is your upper border of your subscapularis. Medially is the coracoid, laterally is the transverse humeral ligament. And the function of the rotator interval, just to kind of drive it home, is posterior inferior glenohumeral stability when the arm is in adduction. So treatment is always conservative. Always, always, always, it's always the right answer on the test. Strengthen the cuff, work on the scapula, improve proprioception. And the definitive length of time isn't known, but on the test you better have given them at least three to six months of rehab. They will never ask you, if the correct answer is surgery, it will always be after this vignette of this ligamentously lax female has failed six months to a year of therapy. Then surgery might be the right answer. But do not be fooled into operating first on the test, no matter what they tell you about the traumatic onset or the paresthesias. If they take you down the path of MDI, it's conservative treatment. And surgery, only if a non-operative has failed. And again, a good six months of non-op. The goal is to decrease the capsular volume, tighten your IGHL. And basically, is open better than arthroscopic? Open has been considered the gold standard. What I've seen as I've followed the test questions over the years, is it used to be the answer was always open. Now, sometimes the answer is scope, but open will not be one of the answers. So it will either be open or it'll be scope and the other one won't be there. You'll never choose between an open and an arthroscopic plication. And if they're both on there, then they're both wrong. They're leading you towards a different answer. So both are considered safe and effective. And you're really not going to be asked about whether you should or shouldn't close a rotator interval. Know the contents, know the borders, know what it does, but they won't ask that. That won't be an answer to a question, won't be adding a rotator interval closure. That will not be the answer. So some questions. What structure is the primary restraint to inferior translation of the shoulder? So remember, the middle glenohumeral joint or middle glenohumeral ligament was a restraint to anterior translation in 45 degrees. Your subscapularis is a main restraint to anterior translation. The long head of the biceps is totally controversial, whether it has any role in the shoulder at all. So that's not going to be the answer as far as stability. Your coracoacromial ligament is a restraint to superior translation in the massive cuff-deficient shoulder. So that takes you to the coracohumeral ligament. Even if you're not sure, you can rule out all the other ones. So on to slap lesions. Mechanism of injury for a slap lesion. They're going to give you a forceful traction to the arm or direct compressive load, a traumatic fall onto the hand or elbow. They might also give you a scenario with repetitive overhead throwing. So excessive, they'll give you a physical exam, excessive external rotation in the late cocking phase. That puts increased torsional forces on the long head of the biceps root. Result in a peel back injury to the posterior superior labrum. And it's proposed an internal rotation contracture is an essential lesion. So pay attention to any time they give you a differential in internal rotation. So excessive external, loss of internal compared to the other side. They're taking you down a slap pathway and a glenohumeral internal rotation deficit pathway. So they present with pain, about half with mechanical symptoms. They have fatigue, they're unable to throw, maybe a sense of instability, but not overt instability and weakness. And on physical exam, again, as Dr. Gill talked about in his talk, they're always gonna ask you, there's always gonna be a question on a spinal glenoid notch cyst. So you have to inspect, look for dyskinesia. If there's dyskinesia in a patient with a clinical vignette of a slap, you're doing therapy to fix that dyskinesia. Anytime you see dyskinesia, you have to do therapy to address it. You track their motion, and typically their strength of motion are intact. But if there's external rotation weakness, you're going down the spinal glenoid notch cyst pathway. If there's an internal rotation deficit, so a side-to-side difference in internal rotation when you're in 90 degrees of abduction, there could be predisposed to internal impingement and a slap. But that takes you down the pathway of rehab to stretch out the posterior capsule. Instability exam, you perform it, but it's rarely overt. And then you check a biceps exam, which is sensitive but not, or specific but not terribly sensitive. So no physical exam is 100% accurate for a slap tear. So you're never gonna be asked to choose. The clinical exam alone is unreliable, so it's multiple tests, interoperative findings, and the vignette. And they will take you down a clear vignette for a slap if that's where they're going. The O'Brien active compression test is most commonly used maneuver. And as Dr. Gill's question showed earlier, they didn't even call it O'Brien, they just called it the active compression test. So they're going down the biceps slap pathway when you see that physical exam finding. But you're not gonna be asked to differentiate because these physical exam findings or maneuvers for slap are unreliable. Your imaging, x-rays always rule out your joint abnormalities. MRI can find other pathologies, but there's a pretty poor correlation between normal MRI and interrupt biceps findings. MRA is most sensitive and specific for diagnosing long head of the biceps and slap pathology. Associated findings, again, we're beating a dead horse, I know, but we're coming back to looking at the cysts. You'll see it on the scapula lateral, you'll see it on the axillary, and that again is your suprascapular nerve neuropathy from compression at the spondynglenoid notch. So your anatomy, just know that the majority of the long head of the biceps originates from your supraglenoid tubercle. The remaining fibers insert into the superior labrum. It's a primary posterior dominant insertion, superior labrum's avascular. And the stability of the long head of the biceps, I think it's important to know what stabilizes as it enters the groove, to see if there's subtle instability of the long head of the biceps. It's the pulley, the corcohumeral ligament, and the superior fibers of the subscapularis. So if you saw a picture that had tearing of the upper lateral board of the subscapularis, and what appeared to be subtle subluxation of the biceps, with biceps pain and a positive biceps exam, that's probably what they're going down the pathway of. Now there's normal variants. They like to show you these pictures on the test. Know the normal variants, sublabral foramens, the Buford complex, or an absent anterior superior labrum. If it looks nice and clean, so it's a nice clean picture, there's no fraying, there's no erythema, there's nothing that looks like it's torn, there's no fraying of the cartilage. And they show you these pictures, it's probably an anatomic variant, they're trying to get you to operate on it. And that will lead to significant external rotation loss. So just know what the pictures look like of these anatomic variants. For SLAP classification, I think the take home point is knowing the top, the type one through four, and knowing what you do for a type one versus a type two, versus the rest. So type one, know what it looks like. There's gonna be fraying, degeneration, you debride it. The type two will be detachment of the superior labrum, biceps anchor. There'll be abnormal mobility of the complex, right, the peel back sign. And you just know that you repair it. You are not gonna be asked, SLAP repair versus bicep stenodesis. There's a lot of controversy. Do we do SLAP repairs? Do we just do a bicep stenodesis? You will never have to choose between them. It's gonna be some kind of repair. And that will just be the answer and either SLAP repair will be there or bicep stenodesis will be there. They will not both be there. You just know type two gets a repair. Type three is a bucket handle tear just of the superior labrum. The anchor's intact, so all you do is debride. So type three is debride. Type four is you repair. Again, how you repair it, you're not gonna be asked to choose between. But know that the bucket handle tear extends into the long head of the biceps anchor, so you're gonna be doing a repair on that. You start non-surgically, indicated in almost all cases. Activity modification, the posterior capsular stretches really wanna drive this home. They like to ask this. You wanna stretch out the posterior capsule if they have a presentation of glenohumeral internal rotation deficit. Scapular dyskinesia, you've gotta correct that. So again, you see that, you see posterior capsular tightness, therapy is the answer. Surgical management, again, this is controversial, especially comes to the age of the patient and the sport. You're not gonna be asked anything controversial. It's gonna be really clear cut for SLAP. Know the basic tenets. Type one and three, scope and debride. And they like to show you a picture and ask you what you would do. Types two, four, and then five, six, and seven, which you won't be asked about. You're gonna scope and do some kind of repair, tenotomy, tenodesis, but you're not gonna be asked between those types. You're just gonna do something versus debride for those. So how about the outcomes? They're inconsistent regarding satisfaction, return to play, and revision. The revision rate is high, so I definitely see them have questions about somebody who's had a SLAP repair and is not doing well. And so it is accepted, this is the correct answer. If someone had a SLAP repair, they've done their proper rehab, their post-op management, and they are still symptomatic, biceps tenodesis is absolutely the right answer in this situation. And it's generally accepted that the results of a cuff repair and a SLAP repair are not acceptable. So you are not going to do those two together on the test. Complications, you have anchor-related problems, synovitis, cartilage damage from the anchors, recurrence, persistent pain, stiffness. And they can give you vignettes with and without stiffness, but they're still gonna have all the positive bicep signs, biceps exam is positive. The belief is that you over-constrained the long head of the biceps during the repair of the superior labrum, and that's why the stiffness occurs. And then also there's a belief that some people have pathologic long head of the biceps tissue that's left in the groove, and that's why they can still have pain. And so this picture shows an ugly looking biceps, and you couldn't see that part in the joint. So questions for the biceps. The figures below are the MRI scans of a patient with shoulder pain and weakness. What muscle and nerve are most likely affected? Well, you've been over and over and over this, so you know it's the infraspinatus muscle and the suprascapular nerve, and that's always the answer. We never talk about the subscap and nerve injuries of the subscap. Supraspinatus and suprascapular nerve, you would see that, but the cyst would be in a more superior location, near the transverse humeral ligament, and both muscles would be affected. Terry's minor and axillary nerve just isn't the right position for this, cuz the Terry's minor is lower. And deltoid and axillary, they're really not ever talking about with cysts very often. Which of the following SLAP lesions are best treated by repairing the labrum to the glenoid? And see, this is the way that they will frame it for you. So a type 1, remember, we debride. So you take out A and D, cuz you debride them. And then remember, type 3, we debride type 3. So you take out D and E, and so there you go, that leaves you with C. Type 2, you repair. Type 2 gets a repair, type 4 gets a repair, 1 and 3 get a debridement. And I think that's all you really need to remember there. Here's a 35-year-old male, recreational tennis player. His shoulder had pain for six months despite appropriate rehab. MRI shows a SLAP tear, and so he undergoes, so he did his rehab. He did the appropriate thing. He's 35, he had a SLAP tear, he had a repair. Despite compliance and six months of PT, he still has similar symptoms without stiffness a whole year out from surgery. Further imaging didn't show any cuff pathology, and this intraoperative picture was found. What is the appropriate management of this patient? While irrigation and debridement, if he was infected, they would be taking you down a different pathway. There would be more clues in his vignette if this was a P-acnes infection. Revision labral repair, but we're never going to do another labral repair for biceps for superior labrum, but the first one didn't work. More therapy, well, the scope's already in his shoulder, so we're probably not going to do more therapy and just take the scope out. And he's already done therapy. And hemiorphidoplasty, that's a little aggressive. So that leads you to biceps tenodesis, which again, remember, is what you answer if the SLAP repair fails. So thank you very much, and good luck on the test. Thank you.

shoulder surgery

treatment

arthroscopy basics

shoulder instability

slap lesions

conservative treatment

surgical interventions

complications

multidirectional instability