with the content of this talk. So if you look at the journals, all this new, innovative, and controversial stuff, there's a lot of that out there. You go to meetings and journals and that's what you read. But if you look at what's testable, what could you be asked on the exam, most of that is not testable. We're gonna be focusing on this part of the triangle today. All right, so here's the outline of my talk. We'll talk about anatomy, biomechanics, we'll start at the ACL, we'll talk about bracing, and then we'll slip to the LCL, push a lot of corner, and on down. Again, in each of these areas, I'm gonna focus on that which is testable, something that's not controversial, well explained, and well understood. So the anatomy and biomechanics of the knee, we know the knee is a diarthrodial joint. It has many coupled motions. It has rotation and translation in all three planes. Now the biomechanical description of the motion of the knee joint is a four bar cross linkage, all right? And those four bars are the two cruciates and the bony bridges between those cruciates. There you see in that cadaveric specimen there, that's the four bar cross linkage. And what that four bar cross linkage does, it produces a roll-glide mechanism. As you go from extension to flexion, the femur will roll posteriorly, but it slides anteriorly, all right? So there's a distinction there. In fact, it has to slide anteriorly because you know the articular surface, the arc on the femoral condyle, is much longer than the tibial plateau, right? So if it simply rolled, it didn't slide, you'd roll right off the back of the tibia. So you roll posterior, but you slide anteriorly as you flex your knee. So in that result, as the femur does move posterior to the tibial plateau, and in flexion, the condyles are sitting on the posterior horns of the menisci. The ACL. So you need to know the bundle anatomy of the ACL. That's a big thing in the last decade, talking about the two bundles or double bundle of the ACL. The two bundles, the antromedial and the posterolateral, they're named on the tibial attachment. That's different than the PCL, we'll talk in a minute. They're named by the anterior attachment. So you can see the representative there, the AA and the BB. So the first one, the AA, is the antromedial bundle. You should know that it's taught in flexion. It's the larger and stronger of the two, and it controls AP translation. Now, you have to label it on the tibial attachment because when you take the knee from extension to flexion, you can see that those two bundles, their relative orientation on the femur, it flips. In extension, the antromedial femoral attachment's anterior, but with flexion, it's actually posterior to the posterolateral bundle. So conversely, a posterolateral bundle is taught in extension, and it does rotational control. So this is very testable. You need to know this. Antromedial bundle, AP control, larger and stronger. Posterolateral bundle, rotational control. So the blood supply of the ACL is the middle genicular artery. Need to know that. The innervation's by the tibial nerve, and the ACL, as well established, has both mechano and pain receptors. So the ACL is innervated with both pain and mechanoreceptors. It averages about 34 millimeters in length, 11 millimeters in width. It's reported to be somewhere around 17 to 2200 newtons, and to put that in perspective, you should note that the PCL is stronger than the ACL, which is stronger than the MCL, which is stronger than the LCL. How about the femoral attachment? So the ACL attaches posterior to the lateral intercontinental ridge. We used to call that the resonance ridge. And the antromedial and posterolateral bundles are separated by the lateral bifurcate ridge. You need to know this. Very testable. The ACL inserts posterior to the lateral intercontinental ridge, and the two bundles are separated by the lateral bifurcate ridge. On the tibia, it inserts into the anterior intercontinental fossa. It's just interlateral to the medial tibial spine, and something they may reference. The ACL can be seen anatomically as a continuation of the anterior horn of the lateral meniscus. Continuation, anterior horn, lateral meniscus, as far as its tibial attachment. Its function, you all know, is primarily to prevent the anterior translation of the tibia, but understand these secondary functions. It also helps prevent knee hyperextension, and it can resist valgus angulation, particularly if the MCL is injured, and it can resist internal tibial rotation near extension. And that's primarily the posterolateral bundle. Remember, the antromedial bundle does AP translation control. The posterolateral bundle, rotational control, and that rotation is to resist internal rotation. So know that. If the MCL is compromised, the ACL can resist valgus, and it can also resist internal tibial rotation. Secondary restraints to anterior translation. So if the ACL is gone, what are your other restraints to keep the tibia underneath your femur? Well, the static restraints, probably the one you'll be tested on, and has most clinical relevance, is the posterior horn of the medial meniscus. But of course, the MCL and the posterior medial capsule can also contribute, and obviously, the dynamic stabilizers of the hamstrings. Know the posterior horn, medial meniscus. Secondary restraint to anterior tibial translation. And again, we'll talk about, in a chronic ACL-deficient knee, the posterior horn of the lateral meniscus is very commonly torn, much more so than the lateral. Why? Probably exactly because of this. It's bearing the load, because it's preventing the tibia from moving anteriorly. It gets overloaded, fatigue failure, and has a tear. So ACL injuries. No one knows for sure, but approximately 200,000 or more occur every year in the US. The risk factors are participating in the cutting sports, the big five are soccer, football, basketball, rugby, and lacrosse, and then also downhill skating. Females, very well established when you control for other risk factors, they're anywhere from two to four, even greater in some studies, increased risk compared to males. There's a genetic predisposition. ACL tears will tend to run in families. Many other risk factors have been studied with mixed evaluations, everything from hormones to generalized laxity, neuromuscular control, developmental, tibial slope, notch width, limb alignment, and others. The ones that have some evidence that may be one of the multifactorial risk factors are neuromuscular slope, maybe some notch width. But again, the big things is participating in a cutting sport and being a female. What's the presentation when you tear the ACL? The vast majority of them are non-contact, usually in an abrupt deceleration movement. The vast majority of them will feel a pop. The vast majority of them fall to the ground. They're unable to continue to play. They develop an effused knee within a couple of hours, and they often describe a shift or a wobble in the knee. Now here's what you need to be careful of. Beware the patella dislocation, because it can exactly mimic what I just described. 13-year-old girl playing soccer makes an abrupt change, feels a pop in her knee, knee shifts, she falls to the ground, and her knee swells up. That very likely could be an acute patella dislocation. Also sounds like an ACL, so beware of that. So what's the mechanism? There's a couple that proposed, I think for the purpose of this test, rather than getting into the weeds on this, I think you would counter the fact that it entails axial compression and quad contraction, all right, some kind of abrupt stop. One theory is it's predominantly a quad contraction with a relative decreased hamstring counterforce, but that's the one I think you might be tested on, is it's axial compression, quad contraction, the knee slips into valgus with some internal rotation. There's that internal rotation again. Remember, the ACL resists internal rotation. And Elkhorn also resists valgus. So there's that valgus internal rotation again mechanism. The rule of 70, this rough rule, about 70% of ACL tears are non-contact. About 70% of ACL tears are sports-related. 70% of acute hemarthroses are ACL tears. So an otherwise healthy knee has an acute injury, has an acute hemarthrosis, 70% chance that's an ACL tear. Number two behind that is patella dislocation and then osteochondral fracture, and then the fourth is a meniscus tear. But 70% acute hemarthrosis, otherwise normally. 70% of ACL tear patients feel a pop. What about contact injuries? That's about 25% of the injuries result from a direct blow to the knee. Very common to have concurrent injuries, all right? If it's a direct blow, always have to be concerned with other concurrent injuries. Now let's go back to the standard ACL. Let's talk about non-contact. What are the associated injuries of the ACL tear? 40% of ACL injuries have a meniscus tear at the time of the index injury, when they tear their native ACL. 40% will tear an ACL. Much more common laterally, two to one. So of those 40% of the knees that have a meniscus tear, half of those tears, twice as many, will be lateral as medial. So remember, acutely, it's the lateral meniscus that's associated with ACL tears. Chronically, it's the medial. Now why is that? Well, you're all aware of the pivot shift, right? Where the anterolateral rotary translation, where the lateral compartment shifts anteriorly. So during the acute injury, it shifts anteriorly, the ACL tears, the lateral compartment moves much more anteriorly than the medial, so that poster horn lateral meniscus tears. Now you're ACL deficient, and you're active on your knee, which meniscus is more likely to get torn? The medial, it acts as a secondary constraint to anterior translation, we already talked about that. So meniscus tears, ACL injuries, lateral occurs more commonly, acutely, medial with chronicity. So this leads to this next discussion of the tearable triad, described by O'Donoghue. The tearable triad is ACL tear, an MCL injury, fortunately most of them are grade one or grade two, and then a meniscus tear. Now O'Donoghue described the tearable triad as an ACL-MCL medial meniscus, but all the more recent literature says the tearable triad is an ACL-MCL lateral meniscus. Now how do you explain that discrepancy when you read about this? Well, I think O'Donoghue did this many, many, many years ago, and he was seeing ACLs that were chronically injured, or ACL deficient, so he was seeing chronic ACL deficiencies, so he was seeing a lot of medial meniscus tears. Now we're getting MRIs within days or hours of someone getting hurt, and we're picking up that propensity for the lateral meniscus to be torn. So just be aware that this terrible triad, whether it's medial or lateral, may depend on whether you have an acute or a chronic population that you're looking at. Other associated injuries, bone bruises. You have to know this. This is the sine qua non. You're very likely to see an x-ray just like this on the exam, just the x-ray, and they ask you what the diagnosis is. Well, the diagnosis is ACL tear. The bone bruises in the internal sulcus, the lateral femoral condyle, on the posterior aspect of the lateral tibial plateau. Some of this bone bruising can also occur immediately, so don't get tricked by that if you happen to see some immediately. It can't occur immediately, but it's the lateral side that you're likely to get tested on. So this is a great example. Here's the MRI showing the bone bruise pattern, and here you can see in this x-ray how, when the tibia slides anteriorly, it impacts that terminal sulcus, and that's why you get that bone bruise pattern. What about ACL prevention? A brace has not been shown to be effective in preventing ACL tears or protecting a native ACL. Neuromuscular training programs can reduce the at-risk positions that people tear the ACL, and several studies have shown that reduction of ACL injury can occur with neuromuscular training in young, active females. So the answer is yes, neuromuscular training programs can decrease the risk of ACL injury. Braces, no. So if you have a multiple-choice question, and one of the options is to take your team to minimize the chance of an ACL tear, don't choose braces. It'll be some type of neuromuscular training. Physical exam for an ACL injury. We're all familiar with the Lachman test. By far the best exam for an ACL, detecting an ACL tear. Knees flexed 20, 30 degrees. You have to make sure both the quads and the hamstrings are relaxed, and you're assessing two components. You want to know the amount of excursion and the quality of the end point, and you need to know whether the other knee is normal, and if it is normal, you want to compare it side to side. And then they may have some type of question about beware of the pseudopositive Lachman. That's where you have a PCL-deficient knee and the tibia sitting sublux posteriorly because the PCL is out, and when you do your Lachman, you feel like you have increased excursion, but a good end point, but you have so much excursion, you might be tricked into thinking there's an ACL injury, but really you're taking a posterior sublux tibia and just returning it to its neutral position. The pivot shift. So you do the pivot shift by starting out by taking the leg, the tibia, and doing internal rotation, valgus, and axial load. You start an extension and then you flex the knee. So you're flexing the knee. That is an internal rotation, valgus, axial load. And as the IT band passes posterior to the axis of rotation, the tibia reduces because it starts off subluxed. So the tibia goes from an anterior sublux position to a reduced position. That's the shift, or the clunk, or the jerk, whatever term you want to use. So they may ask you, what happens is the, when you do a pivot shift, is the tibia reducing or subluxing? It's actually reducing from a sublux position. Now look at this. What do you see up here? Internal rotation, valgus. All right, remember that site? When it comes to the ACL, you keep seeing those associations. Internal rotation and valgus. Well, plane films, the scone fracture. Here's another. In practice, I suspect most of us don't see this, but they love to ask this on exams. They'll show you this picture and ask for the diagnosis. So the scone fracture is considered pathognomonic for an ACL tear. It's an avulsion fracture from the lateral tibia by the lateral capsule. And a lot of people are now advocating, and this might be testable, enough people believe this, that the capsular ligament, the ALL, anterolateral ligament, which is the thickening of the anterolateral capsule, is what is pulling off that fragment when you have the acute ACL tear. But if you see it, the diagnosis is ACL tear. Now, also x-ray finding. They may show you an x-ray with this very deep terminal sulcus. If it's more than two millimeters deep, they'll want you to think ACL injury. They want to say that terminal sulcus was deepened from that impaction injury when they had the ACL tear. You saw that x-ray, you saw the MRI of how that posterior lateral tibia will impact this, and it can impact it enough to get a little bit of compression. So a deepened sulcus terminalis, again, they're asking you to associate that with an ACL injury. MRI, obviously the most sensitive and specific imaging test for the ACL. You have a high T2 signal, and you see discontinuity, and you have an inability to visualize all the remaining fibers in the ACL. What about a gait pattern? Okay, how do you walk if you've torn your ACL? Again, very testable. This has been well-established for many years. The gait pattern most associated with ACL deficiency is referred to as a quadriceps avoidance pattern. That's very testable. Do you know when your knee is between zero and 60 degrees, and you fire your quadriceps, your quadriceps and patella tendon form this anterior vector that tends to pull your proximal tibia anteriorly. So if you're missing your ACL, your body instinctively doesn't want to pull that tibia anteriorly, right, because it doesn't have anything to check rate it from moving anteriorly, so you tend to avoid using your quadriceps. So quadriceps avoidance in ACL-deficient knee. Again, the quadriceps contraction between zero and 60 produces an anterior vector of the proximal tibia. And this is another reason we'll talk in a minute in rehab. The standard is, whether you believe it or not, this is testable, and it's the answer for the exam, is you should avoid open-chain quad exercises in the early post-ACL reconstruction phase, because that open chain, again, between zero and 60, will generate an anterior directed vector by your quad, and you're simply loading your graft. So question, 22-year-old basketball player with ill-defined deep pain and catching, but no locking in his knee. His MRI's below. What's his diagnosis? All right, you're looking at his ACL. T1, T2. This is a cruciate cyst, all right? So don't get fooled into saying this is an ACL tear. Cruciate cysts can occur in either cruciate. They're more common in the males, and you treat it with arthroscopic excision. But you can see this high, fluid-filled cyst, and it's actually inside the cruciate ligament. You can get other cysts that are synovial cysts in the pericruciate area, but this is, and it's treated similarly, similar symptoms. Treat arthroscopically if you have synovial cysts, but these are also intracruciate cysts. Question, Sagan fracture, pathognomonic for ACL injury is a result of avulsion by what structure? Lateral collateral, medial collateral, popiteous, anterolateral ligament, intermeniscal ligament. Remember, it's the anterolateral capsule because the lateral tibial plateau is shifting anteriorly, right? So it's moving very anterior when you tear the ACL, subluxing. The anterolateral capsule is trying to prevent that tibia from moving so far anteriorly, so the anterolateral capsule, or in this case we'll call the anterolateral ligament, the ALL, is avulsing that little piece of bone off the lateral proximal tibia. So as the lateral tibia subluxes anteriorly, the ligament capsule, or the ALL, is avulsing that little piece of bone. So you tear your ACL, what are your concerns? Who cares? Well, if the exam's asking you how do you counsel the parents of a 14-year-old athlete to tear their ACL, your concerns are they have an unstable knee, they can have further injury to the knee, principally meniscus tears, and the long-term risk for osteoarthritis. So those are three concerns of someone who's ACL deficient, and that's well-established and testable. What are your treatment options? Well, it's either non-operative or reconstruction. For the purpose of this test, repair is not an answer. You're gonna hear more talk recently, and this is exciting stuff about the journals and the meetings about doing ACL repairs. For this test, ACL repair is not the answer. So non-operative management. What are the indications for treating an ACL-injured knee non-operatively? An older patient, a low-demand patient, someone who's having no instability with activities of daily living, and they're able to modify their activities such that they can avoid re-injury episodes. Re-injury episodes is anything that makes the knee become sore, swollen, buckle, or give out. So you can modify the lifestyle, no re-injury episodes. They can be treated non-operatively. So the non-operative treatment is neuromuscular training, working on strength, endurance, balance, agility, maximizing your proprioception, modifying your activities so you can avoid re-injury episodes and you may or may not brace them. So a brace doesn't protect an intact, native, or reconstructed ACL, but it can help an ACL-deficient knee that's having instability episodes feel more secure. So there's a subtlety on the brace. So the treatment may or may not include bracing. Okay, surgical management. What are the indications for doing an ACL reconstruction? Younger patients, the younger you are, the less likely you'll do well without an ACL, the more likely you're gonna have all kinds of problems, principally meniscus tears if you're young. If you have a repairable meniscus, you should consider stabilizing the knee having an ACL reconstruction. If they desire to return to cutting sports, they have instability with daily activities. So the surgical management is reconstruction. Repair is being investigated, but is out. It is not an answer for this test. Timing. So, and this is testable, well-established. You do not operate acutely, immediately, on an ACL-injured knee to do an ACL reconstruction. You need to wait till they have minimal infusion, full range of motion, good quad control, and near normal gait. Statistically, this has been noted to be achieved in the vast majority of patients by three weeks. So if you operate before you achieve these four endpoints, you will have an increased risk of having post-operative arthrofibrosis and range of motion issues. All right, so the reasons you wait is to minimize the risk of post-operative range of motion arthrofibrosis. When do you do it? If they ask for a time period, the magic number here is three weeks. If they ask for clinical exam findings, you want minimal infusion, good motion, good quad control, normal gait. So again, three weeks. That's the magic chronologic number. All right, surgical management. The key concepts in doing an ACL reconstruction, you want a strong graft, you want an anatomically placed, you want it rigidly fixed, and you want to start early motion. So those are the four key things. Now how you achieve those things can vary, but those are the four key things you want when you do an ACL reconstruction. So what about graft choices? You can use an allograft. The advantage of allograft, you have no harvest morbidity. That's probably the biggest one. You can have some decrease in your OR time. Your early recovery can be a little faster, and potentially you can have repeat availability for your allografts. The disadvantage of an allograft, so let me go back to this. Make sure you know these, okay? I'm almost guaranteed they're gonna ask you some kind of graft choice question, and allograft's a nice one for them to test you on. They probably will not test you hamstring versus patella tendon. Disadvantage of allograft, risk of transmission of HIV or hepatitis is roughly one in 1.6 million. If you want to kill the HIV, you have to irradiate the graft with three megarads, but the problem with it, when you start getting that level of radiation, you weaken the cross-linking of the collagen, you have a weakened graft. Allografts have been shown by numerous studies to have a higher re-tear rate in young, active patients. It's been shown in animal models to have a longer time to bioincorporate. Allografts heal or mature biologically into the knee joint more slowly than autografts. It can be more expensive, it is more expensive. It's been shown by several studies to have a low-grade immune response. One other comment about allografts, the less processed the allograft, probably the better it is. They may ask you, is a highly processed graft better than a fresh frozen? They may or may not go down that line, but the fresh frozen is probably better, the less processed. So definitely, if they're gonna ask you a question about disadvantages, it's probably gonna be the higher re-tear rate in young, active patients and the fact that if you radiate it to kill the HIV virus, then you have an impaired graft. Autografts, you have bone, patella tendon, bone, patella tendon, hamstring. All right, the two of them, for all practical purposes, have very similar clinical results, all right? So patient satisfaction between the two of them are essentially the same. What they can test you on that is different is the patella tendon is more stiff than the hamstring, but the hamstring has a higher ultimate strength. The patella tendon has been shown by numerous studies that long-term, it's more likely to have kneeling pain, and the hamstring has, on average, if you look at some of the meta-analysis, about a .5 millimeter increased laxity, so small increased laxity, but doesn't appear to be clinically relevant, all right? So these are the five points that they may test you on about patella tendon versus hamstring, all right? Bottom line is that patient-approved results and the vascular, all the other endpoints are essentially the same. A quad tendon is a very viable option. If they show you a case that they've lost their patella tendon, hamstring, for whatever reason, isn't an option, they don't wanna do an allograft, they may ask you what other graft is very viable, quad tendon's a very acceptable graft to use. All right, graft complications, patella tendon. Patella fracture, well-documented. You have numbness laterally in incision. That's because you very typically transect the infratellar branch of the saphenous nerve. This nerve runs from medial to lateral, so the lateral side of the knee will be numb, and you can have the kneeling pain long-term. Hamstring graft complications. You can injure the saphenous nerve during harvesting. You can have weakness in terminal active flexion, and you can have premature amputation during the harvest. This is where you're cutting the indirect attachments of semitendinosus, and the semitendinosus is your go-to graft, and if you can cut that prematurely, you end up too short, and you have a problem. So those are the complications of the patella tendon and the hamstring. Now, double bundle, and they very likely ask you about some things about double bundle. So here's what you need to know about double bundle, all the other noise and discussion. The bottom line is, in the basic science studies in cadaveric or in the lab, when they do a double bundle versus a single bundle, they've shown that double bundle will increase rotational control and more closely replicates normal knee kinematics. So they're really adding that post-lateral bundle. Post-lateral bundle, remember, helps control rotation. So in the lab, double bundle does show some benefits, but clinically, no difference. Maybe, if you're gonna look closely, maybe a little bit pivot-shift results, but really for all practical purposes, I think for the board exam, it's gonna be, it's shown no clinical benefit in your living patients, but in the cadaveric basic science studies, there is some benefit. So no difference clinically. So what is the evidence of what an ACL reconstruction does? We can say with certainty, there's evidence to back this up, that our patients that have an ACL reconstruction, they have increased knee stability, they have a decreased incidence of meniscus tears, but we have not shown to decrease the long-term risk of OA. So we still need to work on that. So, but if that's a very testable thing, they may ask, you know, what's been documented to be the benefit of ACL reconstruction? Stability, decreased risk of meniscus tears, but not decreasing long-term OA. All right, what about complications? Loss of motion. That used to be one of the most common complications. It's much less common since we started aggressive rehab. So you wanna start motion right away. That's a key ACL tenant of ACL reconstruction. If you're still stiff, despite therapy at six to 12 weeks, the answer is, you know, start to think about doing a manipulation anesthesia. Another loss of motion is cyclops or complication, less common than it used to be. It's this fibrous mass at the base of the ACL graft. It can cause, it may or may not have pain. You can have clicking, and it occurs at terminal extension. You're pinching this ball here of a fibrous synovial tissue in the front of your notch when you go into terminal extension. So if someone has pain on passive terminal extension after an ACL reconstruction, look for a cyclops lesion. You treat it with arthroscopic excision, and they do well. Graft retears. Why do grafts retear? They have a successful reconstruction, and they retear. Number one, and this is, people are starting to debate this now, but for the purpose of this exam, the number one reason, if they ask you why ACL reconstructions fail, it's gonna be a technical error. Another reason they can fail is lack of biologic incorporation, lack of biologic healing, or they can have a repeat traumatic episode. What's the overall retear rate? Well, if they ask for a number, you use a number, the number's all over the place, but I use a number somewhere around 6%. If you are a teenage soccer player, it could be as high as 12 or 16%. If you're over the age of 35, and you just work out in the gym, it's less than 1%. But you take all comers and average them, it's somewhere around 6%. But it's important to know that the younger cutting athletes have a higher retear rate than those who don't. The number one predictor or risk factor for tearing a successful ACL reconstruction is returning to a competitive cutting sport. You should also know that the contralateral knee has equal or greater risk for ACL tear. The first two years after ACL reconstruction, you're more likely to tear the ipsilateral, the reconstructed ACL. After two years, you're actually more likely to tear the contralateral native ACL. So early, you tear the reconstruction, late, you tear the contralateral. And overall, the retear rate when you look at those, if you start going like six years out, is roughly the same. So risk factors for well-done ACL reconstruction, it could be use of an allograft, that's a biologic failure, that's what we think it is. Or you could be someone who's young and you're participating in high-cutting activities, and that would be traumatic. So how about patient-reported outcomes? The most common reason that a patient would say they're unhappy with a knee is a technical error. So predictors for poor outcome after a well-done ACL reconstruction is a revision surgery, having a meniscus tear. So these are predictors of a poor prognosis. Regardless of how well you do the surgery, it's a revision they don't do as well. If they have a meniscus tear, they don't do as well. Graph type does not predict patient-reported outcomes how well they do, with the exception of allografts and young, highly active patients, they have a higher retear rate. Technical errors. The most common technical error is tunnel placement on the femur. The most common misplacement on the femur is placing the tunnel too anteriorly. So you're gonna be tested on that. So if the frontal tunnel's too anterior, which is the most common one, your knee is tight in flexion. If, for whatever reason, the tunnel's too posterior, you could be tight in extension. Vertical tunnel. So this vertical tunnel concept kinda came out of the double bundle discussion. So having your tunnel at the noon position of the notch is considered vertical. It's considered to be less anatomic, and it'll have less rotational control, because again, you don't have that post-lateral bundle. So they may ask you about a, they may show you an x-ray with the graft very, very vertical, straight up and down, in line with the anatomic axis. And the answer is it's less anatomic, and they have less rotational control. Patient may still be happy. They may have good AP control, but they'll have less rotational control. OK, how about the tibial tunnel placement? So landmarks on a lateral plane film for appropriate tibial tunnel placement after an ACL reconstruction is this. This is testable. This is what they may show you. They'll show you a lateral x-ray, and you're going to be able to see Blumenshott's line. And the tibial tunnel, the anterior wall of the tibial tunnel should be posterior to Blumenshott's line. If it's sitting near anterior, then it's going to be a tibial tunnel that's placed too anteriorly. So they may show you this, be prepared for this. The line of the tibial tunnel should be posterior to Blumenshott's line in full extension lateral x-ray. Yes. I have a comment still on the newer technique of anatomy of the spine. It's not the same as insertions in the anterior. I've had a lot of insertions in the tibial tunnel, and that's why I'm a little doubtful about the anterior wall. So I don't know if you can hear this. We'll take the questions afterwards. But he's asking about some of these newer techniques that are going to come down the wall. They're not going to be questioning you on these newer techniques. If they show your lateral x-ray and ask about the tunnel placement, this is what you're looking for. That's my point. The tunnel is posterior to Blumenshott's line. Again, I'm not saying this is, I'm getting you ready for the exam. ACL reconstruction rehabilitation. Avoid open chain work from 0 to 45 degrees in early post-op phase. Again, that has to do with the quadriceps generates an anterior directed vector from 0 to 60, so you avoid that. Whether you think that's clinically relevant or not, if they ask you for tenets for post-op ACL reconstruction guidelines, that is a yes. You pursue early motion. You have early weight bearing. That's been shown that early weight bearing decreases telephone pain. There's no evidence that a CPM machine or bracing provides you a long-term benefit. Short term, a couple weeks, or a month or so maybe, but no long-term benefit. So questions about how you should pursue the rehabilitation after ACL and what the evidence is. Avoid open chain. Pursue early motion. Pursue early weight bearing. No CPM or brace. Question, what gait patterns are associated with ACL deficiency? So we talked about that. Quadriceps. In an ACL deficiency, what structure provides sigmoid restraint to anterior tibial translation? We hit this a couple times. Anterior horn, posterior horn, medial meniscus. And this may explain the increased rate of medial meniscus tears in a chronic ACL deficiency. Pediatric considerations. Younger adolescents are more likely to do poorly long-term if they're ACL deficient. You must consider the fiseal injury during the ACL reconstruction, concerned about growth arrest. And there's a high rate of meniscus tears in young patients who are ACL deficient. Look at this, tibial eminence fracture. You can attempt to reduce it in full extension, but I think the board answer now is you have to do an open reduction of internal fixation. The fixation could be suture or screw. I don't think they're going to test you on what type of fixation, but they're going to say you need to recognize it. You want to recognize it as an ACL evulsion. You want to reduce it. You want to fix it. You do it arthroscopically. They may ask, well, what's the status of the ACL collagen in someone who's had a tibial eminence evulsion? That's been shown that the collagen has actually been injured and compromised to a certain extent as well. All right, treatment. If the fysis is closing, which fortunately most of them are, you're a 10 or 4, then just go ahead and do your adult operation. No one even questions that. If the fysis is wide open, they may imply it's safest to avoid crossing the fysis with your surgery. That means you either stay entirely intraepiphyseal or you stay entirely extraepiphyseal. I'll show you some examples of that in a minute. I think people move away from this, but they may, in a 10 or 1 or 2, a really young kid, they may say try to buy some time to let them mature more, do the reconstruction. The problem with that is that that's been shown to have a very high chance that that youngster is going to tear a meniscus. So there's some movement against it. But what could be testable is you have an 8 to 10-year-old ACL injured patient. You decide to try to wait a couple of years. What's the downside of waiting a couple of years? The downside is the high chance they're going to have a significant meniscus tear. So here's a fysal spurring reconstruction technique. This is the all-epiphyseal or all-intraepiphyseal technique. See, they don't cross the fyses. Another fysal spurring technique is all-extraepiphyseal. Now, you're going over the top and over the front. Both of them, if you're going to do a fysal spurring technique, either one of those is fine. So surgical considerations, if you're doing a trans-tibial technique in someone with open fyses, you want to drill the smallest possible tunnel across the fyses. You want to put a big enough graft to meet the purpose, but as small as possible. You want to fill the tunnel completely. So you want a nice, snug fit of a soft tissue left in your tunnel across the fyses. And you do not want to cross the fyses with a bone plug or fixation device. A lot of studies show that there's growth arrest in doing ACL reconstructions in people with open fyses is because there was a technical error and they crossed the fyses with a staple, or a bone plug, or a screw. If you do a trans-fyseal reconstruction in someone who's a 10, or 3, or 4, the risk of a growth abnormality is very, very low. We don't know what the risk is in a 10, or 1, or 2. That hasn't been studied. But a 3, or 4, it looks like the risk is very low. ACL bracing may be effective in facilitating functional stability in ACL deficiency. OK, so if you have no ACL and you have some instability, a brace has been shown to be effective. But it has not been shown to benefit to protect your graft after an ACL reconstruction. And it's not been shown to prevent tears in a native ACL. So question. 30-year-old athlete has continued instability two years after ACL reconstruction. The most likely cause is tunnel malposition, unrecognized post-lateral corner, failed graft, cyclops, recurrent trauma. For the purpose of this test, the number one reason for failure is going to be tunnel malposition, an anteriorly-placed femoral tunnel. Another question. 14-year-old cyclist injured his knee. The exam is compromised by swelling and pain. So you look at the MR, and what do you see? What's your next best step? So we're seeing a tibial eminence factor, right? Arthroscopic, open reduction, internal fixation, tibial spinal invulsion factor. All right, we'll move on to the PCL. The PCL is intra-articular, but extra synovial. Little anatomic tidbit, but they may ask you about that. It's extra synovial, but intra-articular. It originates off the lateral border of the muofomal condyle. It has an insertion in the posterior tibial cortex about 1 to 1 1⁄2 centimeters below the joint line. It averages 38 millimeters in length, a little bigger than the ACL. 30 millimeters in width, again, a little wider than the ACL, and it's stronger than the ACL. It has two bundles, just like the ACL, and it is named off the origin on the femur. Remember, the ACL has two bundles named off the tibia. The PCL has two bundles named off the femur. It has an anterolateral bundle and a posterior medial. The anterolateral is stronger. It's twice the cross-section of the posterior medial bundle. So the anterolateral bundles are stronger and more important of the two. Blood supply for the middle geniculate, more generous than the ACL. The PCL, as opposed to the ACL, has some significant healing capacity. The innervation is from the posterior tibial nerve. If you look at these, it's essentially the same as the ACL. What about the meniscal femoral ligaments? They go from the medial femoral condyle to the posterior anterolateral meniscus. You have the ligament of Humphreys, which is anterior to the PCL, the Risberg, which is posterior to the PCL. They act as secondary restraints to posterior tibial translation. They can be anywhere from 5% to 20% the strength of the PCL. There's variable occurrence. You may only have one of them, or the other, or both. But most people have at least one. I think one good thing to know is Humphreys and Risberg, one is in the front, one's in the back. It's alphabetical, Humphrey, Risberg, front to back. And whether you spell Risberg with an R or a W, it's still alphabetical. Humphreys is in the front. So PCL, primary restraint to posterior tibial translation, 94% if you're between 30% and 90%. Secondary restraint to external rotation, OK, so that's different than the ACL. Remember, the ACL is internal rotation. PCL is secondary to external rotation. The post-lateral corner is the primary restraint to external rotation. We'll come to that. The two bundles, the anterolateral is tight in flexion, the posterior medial is tight in extension. And they have reciprocating tension as you take the knee through the arc of motion. PCL, we've all seen the dashboard injury, high velocity. Anytime you see dashboard, think PCL. Low velocity, it's kind of all over the place. You can be contact, non-contact. It could be a posterior directed blow to the proximal tibia, as you see here, or it could be hyperflexion or even hyperextension. So there's no one clear mechanism. But I think for the purpose of this exam, they'll probably be looking at some kind of posterior directed blow to the proximal tibia. So here's the poster drawer. It's the physical examination of choice. You want to assess the medial tibial shelf. So here you can see in this x-ray stress test, this is a normal knee. You have this usually about a 10 millimeter shelf there. And here's a PCL deficient knee that when you do the poster drawer, that shelf disappears. So the poster drawer is the most accurate exam. You normally have about a 10 millimeter step off. A grade one, if you test them, you have an injury. But the tibial plateau remains anterior to the medial formal condyle. A grade two, it's flush. And a grade three, it's posterior to the condyle. A grade three PCL is very likely to involve the post lateral corner. That's some point they may hit. A truly isolated grade three PCL, you need to rule out a subtle injury to the lateral side of post lateral corner to make that statement. So clinical exam, a posterior sag sign, the ski slope sign, pretty clear. Quad active test, every year it goes by, they seem to be less concerned about this. But it might be on the test. So it indicates PCL injury. It can help differentiate whether you have posterior laxity or anterior laxity. You put the knee in 30 degrees, I'm sorry, 80 degrees of flexion. You hold the foot fixed. And you ask the patient to fire the quad, attempt to straighten the knee. And the tibia will move anteriorly. So this is described by Dale Daniels. It's called the quad active test. It's taking the posterior suboccipital tibia and pulling it anteriorly. Again, it's more evidence of how the quadriceps the patella generates an anterior directed vector. MRI is the gold standard for acute PCL injuries. A chronic PCL tear may actually look normal in ACL because it's in that thick synovial sheath with lots of vascularity. You can have a grade one or two PCL injury and six months, a year later, your PCL and MRI may look normal. So what are the issues with a chronic PCL laxity? This is highly likely to be tested. They may ask you something like, gee, you have a patient who's been PCL deficient for 15 years. You sculpt their knee. Where are you likely to find chondral erosions? Well documented, medial femoral condyle and the patellofemoral joint. Chronic PCL deficient knee, these two areas have been well documented to show chondral wear. The other problems with chronic PCL deficient knee are kind of vague pain. And they don't have the gross buckling that you have with an ACL injured knee, but they have this lack of confidence and class liaise with going downstairs or down an incline. So if you think about it, if I'm walking down a step with my lead leg, my femur wants to go off the front of my tibia, right? Or conversely, the tibia wants to come behind my femur. And what stops that from happening? My PCL. So if I don't have a good PCL, I'm a little cautious or tentative walking down a slope or down steps. So they talk about vague knee complaints, and uncertainty, et cetera, walking downstairs, think PCL deficiency. The treatment, an acute isolated PCL, if it's a grade one or two, four to six weeks of relative rest, a grade three acute one, if you put them in full extension for about four weeks or so, you can kind of, when you take the knee in extension, it tends to reduce, you can hopefully get the thing to have some potential healing. You might consider surgery, we're gonna talk about it in a minute, the two indications for a acute surgery in a grade three. A chronic isolated PCL, again, a grade one or two is all quad rehab, activity modification. Again, quad rehab, right, because the quad pulls the tibia anteriorly. If you're PCL deficient, you wanna pull the tibia anteriorly so a lot of quad work in the PCL deficient knee. If you're a chronic grade three, you do the quad rehab, and if they fail the rehab and they're a grade three chronically, then you do a PCL reconstruction. So the two indications for acute repair, so if you have a grade three on exam and the PCL's clearly pulled off the femur, you can do an acute repair of that PCL back up to the femur, and if you get to it acutely, there's a decent chance you'll get a good result. So nonabsorbable suture through a bulged fragment, passes through bony tunnels or bony bridge, but it does not work with a chronic or a mid-substance tear. It has to be a nice, clean, acute tear right off the femur. The second indication for a surgical repair of an acute injury is if a tibial bony avulsion at the posterior tibia where the PCL attaches on the tibia. You can go in there and put a screw and washer on that and repair it, and they do pretty well. All right, so if you're gonna do a PCL reconstruction, they may ask you about two different techniques. You have two technique decisions to make. Are you gonna go trans-tibial or tibial inlay, and are you gonna do single bundle or double bundle? All right, so there's two decisions you have to make when you're talking about doing your PCL reconstruction. And your post-op protocol, you wanna keep it in extension early on to help maintain your reduction. You wanna really push the quadriceps hard, but you wanna delay any active hamstrings for several months. Now remember, you avoided open-chain quads for the ACL. PCL's the opposite. You push the quads very early on the PCL division, again, because the quad pulls it in too early. Whether you do trans-tibial or tibial inlay, do a single, double bundle. No clear clinical advantage to either one. So the answer is it doesn't matter which of those two you use. Let's talk real quick about what they may ask you about trans-tibial versus tibial inlay. The trans-tibial, the risk is drilling the tunnel through the tibia is you may damage the neurovascular bundles, and you have something called the killer corner, which can fray the graft. We'll talk about it in a minute. Tibial inlay, you have to do a posterior exposure. They may ask you about how you protect neurovascular structure. The answer is you pull the medial gastroc laterally to protect neurovascular structures, but you have to do an intraoperative repositioning. So here's the killer corner. You can see this when you go through the tibia, you have this nine degree turn here, and there's a concern that you go fraying and stretching of the graft. It was this concern about the killer corner that led people to develop this tibial inlay in which the graft has a less acute turn. So that's where the killer turn is. The tibial inlay, what's the advantage of tibial inlay? You avoid the killer corner. What about double bundle versus single bundle? If you're going to do a double bundle PCL, you tension the anterolateral bundle at 90, you tension the posteromedial bundle at 30. The basic science studies show some improvement in restoring normal biomechanics when you do a double bundle. But again, patient report outcomes, no difference between single and double bundle PCL reconstructions. So that's very similar you saw with the double bundle ACLs. In the lab, show some advantage. In the patients, no clear advantage. So some miscellaneous concepts about PCL. Meniscus tears and bone bruises are seen much less commonly with PCL tears compared to ACL tears. The pathologic posterior tibial translation unloads the posterior horn of the meniscus and that protects the menisci. Combined PCL and postulated corner injuries are more common than initially believed. So you see the more severe the PCL injury, the more you need to look for postulated corner injury. Failure to address a postulated corner injury can contribute to an increased PCL graft tension and ultimate failure. So they may ask you what puts you at risk for your PCL reconstruction to stretch or fail. One of the things to put at risk is failure to recognize a postulated corner injury. All right, so PCL injury, postulated corner, keep those tied and linked together. Question, posterior instability is diagnosed by the quad active test with tibia translation. What happens? It's gonna be anterior translation right there between 79 degrees. Again, anterior vector produced by patella tendon pulls the posterior suboccipital, I mean, tibia anteriorly. All right, how about tibial slope? A couple of things you just need to know. If you increase your tibial slope, that will encourage the tibia to slide forward, which is good for PCL and bad for the ACL. If you decrease the posterior tibial slope, the tibia will wanna slide posteriorly, that's bad for the PCL, good for the ACL. So they talk about whether you're born with a certain tibial slope or whether you'll do an osteotomy to change it or not. Those, just know this slide right here. MCL, you guys have all studied the anatomy. You may wanna review the anatomy. MCL knows primary strength of valgus throughout the arc of motion. It's usually an injury from a bloated lateral knee with the foot planted. When you do the exam, the key exam is test for valgus laxity at 30 degrees. Because why do you flex knee at 30 degrees? You wanna unscrew the screw hole mechanism. When you take the knee to full extension, you have the screw hole mechanism, which means the cruciates are wrapped tight around each other and the posterior capsule's tight. If you flex at 30, you've taken the posterior capsule out of the equation and you've minimized the cruciate's contribution and you can isolate the role and contribution of the MCL. So you also wanna check for valgus laxity at full extension. If it's lax in full extension, your posterior medial capsule's torn and you really need to start looking at your cruciates. So if you have grade three laxity at 30 degrees, that's your first test. Now you need to test them at full extension. If they're lax in full extension, you have at least a posterior medial capsule injury and you need to start looking for associated ligament injuries, mostly looking at the one or both cruciates. A grade three MCL is very, very commonly associated with other ligament injuries. So if you have a grade three wide open, start looking for other things. So what about the location of the MCL? Well, they may test you on this. A femoral-sided injury tends to heal better, but it can also lead to some stiffness and some pain syndrome. A tibial-sided injury will heal less readily and you're more likely to have some chronic laxity. So that's been established. You may get tested on the implication of the location of the MCL injury. MCL treatment, non-operative treatment indications, any truly isolated injury, if they're stable at full extension, you treat the MCL non-operatively. Surgery indications are a combined grade three MCL injury. So if you've got a grade three and it's combined with another ligament injury, you probably do a surgery. Or if you have chronic laxity. So combined or chronic laxity. The surgical technique, if it's acute, you can do a repair. If it's chronic, you have to do a reconstruction. So pediatric considerations, and they love to ask this type of question. Beware of valgus laxity in a knee with a wide open physis because they can have a distal femoral physis injury. So they love to tell you about that 10 or 12 year old boy playing soccer, injures his knee, has an effusion, and he tends to have valgus laxity, but his x-ray is normal. What they want you to do is, they want you to rule out a physio injury. So they want you to get an MRI or stress x-rays. So someone, either varus or valgus injury, physis wide open, get an MRI or a stress x-ray. How about post-lateral corner? So the poppeteus inserts distal and anterior to the LCL on the femur, 13 to 16 millimeters. They may ask this. So poppeteus is somewhere 13 to 15 millimeters anterior and distal to the LCL. So know that. LCL injury. Isolated LCL, much less common than MCL. It's a varus contact injury. You have an open physis, just like the MCL. Beware of physis injury, get an MRI, stress films. Test for laxity at 30 degrees and then full extension. If lax at full extension, you have a post-lateral corner injury and have to start looking at cruciate injury. Very analogous to what we talked about with the MCL. Similar to the MCL. So treatment of the LCL. If it's truly isolated, it's treated non-operatively. If it's a combined injury, you need surgery. Again, acutely you repair it, but what's a little different than a repair of the MCL, I think there's enough evidence out there that the exam, if they ask you what you're gonna do in acute LCL that you're operating on, if you either augment it, do a reconstruction from the get-go, or if you repair it, you need to augment it with a graft. So that's what makes LCL a little bit different than MCL. Post-lateral corner. Again, you guys can review the anatomy. They'll be very big on the popatial fibular ligament. It goes from the posterior aspect of the proximal fibula to the popatious tendon. So mechanical injury, it can be a blow to the anteromedial knee, producing hyperextension, various deformity. Very commonly associated with LCL and PCL injuries. So sitting there between the LCL and post-lateral corner makes sense. So any kind of PCL injury, LCL injury, always be looking at that post-lateral corner. So the dial test, you need to know this. How do you do the dial test? Well, you put the patient prone. The feet are externally rotated at 30 and 90 degrees of knee flexion. And then you look at the foot-thigh angle. So if you have 10 to 15 more in the contralateral side, then it's positive. So if you have a positive dial test at 30 degrees of knee flexion, your post-lateral corner is torn. If you're lax at both 30 and 90, your corner and your PCL are both injured. So this right here, they're very likely to ask you. So if you have a post-lateral injury, you wanna do the dial test, you wanna do it at 30 and 90 of knee flexion. 30, post-lateral corner, 30 and 90, corner and PCL. So isolated post-lateral corner, it's rare but can treat non-operatively. Combined injury, repair, augment with a graft. Chronic, reconstruction of the popliteal ligament, and you're commonly associating this with some kind of reconstruction treatment but LCL, PCL. And again, augmentation, better than repair alone. So chronic lateral side injuries, so they're likely to ask you this, this is well-established. If you have chronic lateral instability of the knee, they're gonna want you to get a standing long-legged film because if you're mechanical varus, they want you to consider osteotomy because if you have a big varus thrust, your reconstruction lateral is gonna stretch out and fail. So they want you to take a valgus-producing osteotomy to take you out of varus. So lateral-sided ligament laxity, check for a varus knee, you got a varus knee, the treatment for that has to include or maybe simply an osteotomy. Varus, osteotomy, lateral-sided knee injuries. Question, flag football player, three days after injuring his knee, he's got a symmetric Lachman, varus stress at 30s, asymmetrically, actually a pretty good endpoint. Dial test is positive at 30, but it's negative at 90. What's the best management? Looks like he has an isolated post-lateral corner, so he's a brace in physical therapy. So multiligament injuries. That's two or more ligaments that are injured that classify by direction of the tibial displacement. The most common knee dislocation is anterior. The posterior has a very high risk for vascular injury and the lateral has a very high risk for peroneal nerve injury. Associated injuries, popularity about 30% of the time, peroneal nerve, 20 to 30%. The most commonly injured nerve is the peroneal nerve. And you have a tibial plateau fracture of some type up to 60% of the time. So be aware of these associated injuries. Classification all depends on the cruciates. KD1, one cruciate, KD2, both cruciates, KD3, both cruciates and a collateral, KD4, both cruciates, both collaterals. Five is a four with a fracture, then you can put a C for vascular injury and for a nerve injury. So classification. Popularity of artery injury. Eight hours or more of ischemia likely result in amputation. So that's the number, eight hours. Some people say six, but eight. Eight hours of ischemia. Must repeatedly check pulses. Your ankle brachial index, you want to at least 0.9. And you also want to keep checking your leg compartments. Admit for monitoring. Have a very low threshold to obtain an arteriogram and vascular consultation if you suspect an arterial injury. That is the key thing on multi-legs. How to treat a multi-leg is all over the place. You're unlikely to get a question on that. In fact, the treatment they're gonna push you on if they present you with a multi-leg is assess and monitor neurovascular status. That's what you need to know. So treatment, assess neurovascular status, pre and post-reduction, do a timely reduction. You need AP level films, pre and post-reduction, you get an MRI. Admit for monitoring of vascular status and the compartment syndrome. Again. When would you do acute surgery on a multi-leg injured knee? So the indications are a vascular injury, an open dislocation, a compartment syndrome, or an irreducible dislocation. So those are the four indications to do an acute surgery. Other than that, it's reduce and monitor. Vascular status is number one priority. All right, just remember that. Vascular, vascular status, assess, monitor, follow up. Do not send them home. You're gonna admit them and observe them. So what's the treatment of multi-leg injured knee? In an active individual with a good surgical candidate, you can repair the medial side if you're acute. You can repair and augment the lateral side and post-lateral corner if it's acute. You can reconstruct the cruciates either early or stage it, do it later. And if you're doing them chronically, you have to reconstruct the medial lateral sides. So that's about, I think, the extent that they'll push you on surgical treatment of multi-leg knee. The rest of it's not enough consensus. A poor surgical candidate, you wanna maintain the reduction. A lot of times that means applying an external fixator, allow it to get just a lot of scar tissue around the knee with delayed protected motion, put them in a hinge brace and protected weight bearing. Lateral avulsion injuries. All right, you see some kind of fractional outside of the knee. You need to look for a LCL or biceps avulsion of the femur or head. It could be that Sigan fracture. You can also look at a popates avulsion of the femoral groove. So any kind of little bony avulsion over here in acute injury, look for one of these three. Medially, the pellegrini-stegiata lesion, they may ask you what it is. It's a bony reaction from a proximal MCL injury. It's chronic. So bony reaction from an old MCL injury. Question, 19-year-old quarterback has knee dislocation. The emergency room physician feels decreased pulses and reduces the knee. The pulses return. You are consulted. He has gross anterior, posterior medial laxity. The skin's intact. The pulses are present. Neurologically, he's intact. What's your best recommendation? Immediate MRI, low extremity venography, compartment pressure measurements, knee mobilization to follow up in 48 hours, admission for serial ABIs. The answer always is monitor and evaluate neurovascular status. The answer is E. Question, 24-year-old, unable to fully extend the knee after an ACLR, range of motion is 5 to 140, negative lockman, negative pivot shift, but lacks five degrees of full extension. And here's his MRI. Can't get full extension. So you're looking right in here, some anterior impingement. Your best treatment, to breathe the pouch, to breathe the gutters, to breathe the notch, reconstruction of the ACL or PCL. You're gonna breathe the notch. He's got a cyclops lesion sitting right here. It's pinching, blocking him from full extension. All right, some tips. Dashboard, you see the word dashboard? Think PCL injury. Fall on a flexed knee, think PCL injury. Fall on a flexed knee with dorsiflexed foot, think patella. The anteromedia of the ACL, the anterolateral of the PCL are the number one most important bundles. They both start with A. So when they talk about what's the most important bundle for the ACL, PCL, it's the bundle that starts with A. Little trick. Interference screw divergence greater than 15 degrees can result in decreased fixation strength. So you gotta make sure your interference screw is relatively parallel. The PCL does have some healing potential, unlike the ACL. A chronic PCL can't appear normal in an MRI. It can heal in length and position. An ACL repair is not the correct answer. A PRP injection in the knee is not the correct answer. ACLs are increased in skiers, but decreased in snowboarders. Snowboarders have a decreased risk of knee injuries compared to skiers. Pivot shift is not present if the MCL is torn. Synthetic graft is not a correct answer. Thermal shrink of any type is not a correct answer. An ALL, anterolateral ligament reconstruction is not the correct answer. I know people are talking about doing it, but for this exam, it's not a correct answer. Stem cell injections is not a correct answer. So again, some tips for the exam. So when you review knee ligament exam questions, pay attention to the discussion section in your self-assessment exams, and pay attention to why the wrong answers are wrong. You can learn as much from that, preparing for the test, is why the right answer is right. See some sources for your self-assessment exams, the OKU. Focus on what's known and accepted. Don't get into the weeds with something that's controversial, new, poorly-established concepts. Good luck. Thanks. Thank you.

knee anatomy

biomechanics

ACL ligament

PCL ligament

testable information

knee joint function

knee stability

common knee injuries

treatment options