All right, now we're moving on to knee ligaments, a far cry from what you just heard. So these are my disclosures. I have no conflict with this presentation. So when we read the journals, go to meetings, and sit in the hallways and talk to our compatriots, we like to talk about what's new and what's controversial, what's innovative. But for the purpose of why you're here today and the purpose of this course, we are going to focus on this area of the knowledge triangle, what's testable, what's well-established, and we're going to avoid the new, the controversial, and the innovative. So these are the topics that we're going to cover here in the next hour. And we're going to focus again on testable information. So some of this presentation may be less than exciting to those of you who do a lot of knee work. So what about the anatomy and biomechanics of the knee? Well the knee is a diarthrodial joint, so they may ask that. It has many coupled motions, it has rotation and translation in all three planes. The mechanical model of the knee joint is a four-bar cross linkage, and the four bars are the cruciates and the bony bridges you can see in this image. It has a roll-glide mechanism. With flexion, the femur rolls posterior but slides anteriorly on the tibia. So the net result is the femur moves posteriorly on the tibia plateau. If it didn't slide anteriorly, the articular surface of the femoral condyles is much greater than that on the top of the tibial plateau, so if it simply rolled, it would roll off the back of the tibia. To prevent it from rolling off the back of the tibia, it actually slides anteriorly. So the net result in flexion, the condyles like to sit on the posterior horns of the menisci. Okay, we can talk about the ACL. The ACL is pretty well established and described as having two bundles. The bundles are named by the tibial attachment. That's different than the PCL. The anterior medial bundle is taught in flexion. It's larger, it's stronger, and it controls AP motion. The posterolateral bundle is taught in extension and has rotational control. And again, you can see in this diagram why they named the bundles off the tibial attachment because the femoral attachments actually reverse their anterior-posterior placement when the knee's extended versus flexed. And this is very testable. The anterior medial bundle controls AP. The posterolateral bundle is for rotational control. So know that. That's very likely to be tested if they're going to ask you questions about the two bundles. The blood supply for the ACL is from the middle geniculate artery, innervations from the tibial nerve, and the ACL has both mechano and pain receptors. So it is innervated. It's 34 millimeters on average in length. It's about 11 millimeters wide. It has a tensile strength between 17 and 2200 newtons. And relatively speaking, the PCL is stronger than the ACL, which is stronger than the MCL, which is stronger than the LCL. So sometimes they ask about relative strength. The femoral attachment is posterior to the lateral intercondylar ridge, often known as the resonance ridge, and the anteromedial and posterolateral bundles on the femur are separated by the lateral bifurcate ridge. I would remember those two terms. Anteromedial intercondylar ridge, it's posterior to that, and the two bundles are separated by the lateral bifurcate ridge. Tibial attachment, it inserts anterior to the intercondylar fossa. It's anterolateral to the medial tibial spine. It can be viewed as a continuation of the anterior horn of the lateral meniscus. The continuation of the anterior horn of the lateral meniscus I think is a good concept. You may be asked what is an anatomic landmark to help guide your tibial attachment site during ACL reconstruction. If they offer you an adjacent to and a continuation of the anterior horn of the lateral meniscus, that's the correct answer. So the function we know, the primary function of the ACL is to prevent anterior translation of the tibia, but be aware of these secondary functions. It helps prevent knee hyperextension. It can resist valgus angulation, particularly if the MCL is injured, and it resists internal tibial rotation near extension. And again, remember we talked about rotation, posterolateral bundle. So the PL bundle helps resist extension. This valgus and internal rotation, those two combinations, those two movements keep popping up when we talk about the ACL. They're going to pop up again a couple more times in this talk. And you can see the mechanism for injuring your ACL probably is related to those secondary functions. So what are the secondary restraints to anterior tibial translation? Number one restraint we said is the ACL. You have static and dynamic secondary restraints. The dynamic ones are the hamstrings. The static ones are the posterior horn of the medial meniscus, the MCL, and the posterior medial capsule. So this medial meniscus, the posterior horn being a secondary restraint to help keep the tibia from moving anteriorly, know that because that's very testable. And that comes to these ramp lesions. A ramp lesion is a tear of the posterior horn of the medial meniscus tearing the meniscal capsular attachment. Ramp lesions, posterior horn medial meniscus lesions, they interact with the ACL. If you're an ACL deficient, you're more likely to have a ramp lesion or posterior horn medial meniscus tear. If you don't have a posterior horn medial meniscus, you have more strains on your ACL. And if you don't have an ACL, you have more clinical instability. So posterior medial meniscus, ACL, they're intimately linked in keeping the tibia from moving anteriorly. ACL injuries, approximately 200,000 a year just in the U.S. Risk factors. Cutting sports, downhill skiing. Females, two to four times increased risk compared to males. There is a genetic predisposition. Many other risk factors have been studied with mixed evaluations. But I think, no question, the two biggest predictors that are well accepted by everyone participating in cutting sports, female gender. Others that are increasingly accepted is the increased tibial slope, neuromuscular control, and notch width. So what's the presentation when someone tears their ACL? It's typically a non-contact deceleration movement. They often describe a pop. They fall to the ground. They're unable to continue to play. And within a couple hours, most of them have some type of effusion. They can also describe a shift or a wobble in the knee. Beware of patellar dislocation. This can mimic this. So in the vignette, be careful of a 16-year-old soccer player who's playing soccer, makes a cut, feels something shift her knees, falls to the ground, unable to continue to play, and has a hemarthrosis. It sounds like an ACL tear. It could be a patellar dislocation, so beware of that. Mechanism of injury, there's a couple that are proposed. There's always axial compression and quad contraction involved for the non-contact. So one of the original descriptions of the mechanism was a quad contraction with decreased relative hamstring strength because when the knee is extended, when the quad fires, it has an anti-rejective vector, and it's pulling the tibia out from beneath the femur. I think a more common mechanism is the knee is in valgus with internal rotation. You see that? What's the secondary restraint of the ACL? It resists valgus, and it also resists internal rotation. So there again, you see that valgus-internal rotation combination. The rule of 70s, 70% of ACL tears are non-contact, 70% of ACL tears are sport-related, 70% of acute hemarthrosis are ACL tears. So if you have an otherwise healthy knee with no prior history, they have an acute injury and they show up with an acute hemarthrosis from an injury, two-thirds or 70% of those are ACL tears. The next is patellar dislocation, and after that is a peripheral meniscus tear. So acute hemarthrosis, think ACL. 70% of ACL tear patients feel a pop in their knee. The contact injuries are about 25% of injuries result from direct blow to the knee or leg. Very commonly, they have concurrent injuries. So remember that, a lot of concurrent ligament injuries with a contact ACL injury. So what are some of these associated injuries with ACL injury? Meniscus tears, 40% of index ACL injuries have a meniscus tear. The lateral meniscus is more commonly torn at the index injury. The medial is more common with the passage of time. So you remember, the lateral meniscus tear occurs more commonly with acute injury, and the chronic ACL deficiency is more likely to be medial. The rationale for that, I hope you understand that, again, we talked about how the poster horn medial meniscus helps prevent the tibia from going anteriorly, right? So if you don't have an ACL and you're chronically ACL deficient, the odds of you tearing a medial meniscus is quite high because that poster horn is trying to be a bumper to keep the tibia in place, and it tears. Acutely, you have that big lateral pivot shift, right? You have that anterolateral rotary instability, that lateral tibia plateau shifts out abruptly, the ACL tears, and that's when the lateral meniscus tears, when you have that major index injury. But with a minor accumulative microtrauma of living in a daily fashion without the ACL, the medial meniscus tears. The terrible triad, ACL-MCL meniscus tear. If you look at terrible triads, first described by O'Donohue, he talked about ACL-MCL and a medial meniscus tear. The more recent literature talks about the terrible triad being the ACL-MCL and lateral meniscus. What goes there? How do you explain that? Well O'Donohue predated MRI imaging for acute injuries, and he probably saw more chronic injuries. So chronic injuries are more likely to be medial. Acute injuries, you review MRIs of acute injuries, you're more likely to see lateral meniscus. So that explains why historically you may see two different definitions of the terrible triad. So bone bruise pattern. When you see this, I think you guys already know this, that's pathognomonic for an ACL. You have bone bruise at the lateral femoral condyle at the terminal sulcus. You see it in the post-lateral tibial plateau. You can also get bone bruising medially, so don't think it only has to be laterally. But this pattern here is pathognomonic for ACL tear. Also be aware of this depression of lateral terminal sulcus. If it's deep from the impaction, in fact I'll even call it a fracture sometimes on the MR, if it's deeper than two millimeters, that's very suggestive of an ACL tear. So they may show you an x-ray, a lateral femoral condyle, and you have this deep terminal sulcus of greater than two millimeters. They're leading it down the path, and that's probably an ACL tear. So this bone bruise pattern here, you can see why that happens. You can see how gross that, how far the lateral compartment has to move anteriorly in order to put that posterior aspect of the lateral tibial plateau against the terminal sulcus, and that's why you can see where that lateral meniscus will tear. Okay, how about ACL injury prevention? Braces have not been shown to be effective in preventing ACL injuries. Neuromuscular training programs can reduce the need by preventing at-risk positions. There have been several studies that have shown a reduction of ACL injury risk in young female athletes. If they ask you, how do you prevent ACL injury in an at-risk patient, such as a soccer player, braces have not been shown to be effective. That's not the answer. Neuromuscular training is the answer. Physical exam for an ACL injury, Lachman, best exam for an ACL injury, knee has to be flexed 20 to 30, you have to make sure the quadriceps and the hamstring are both relaxed. You're assessing both excursion and the quality of the end point. Beware of poster instability if you have a pseudopositive Lachman, meaning you see, gee, I have a lot of excursion, but I have a crisp end point. If you have that, make sure you're not getting fooled, and it's actually a poster laxity. How about the pivot shift? Well, the pivot shift is done by putting the knee into internal rotation, valgus, and axial load. There again, what do you think? Axial load, internal rotation, valgus, that's the mechanism that you tear the ACL, right? So we're linking internal rotation and valgus with ACL loading and ACL injury. You start an extension after you've put the knee in internal rotation, valgus, and axial load, then you flex the knee. As the IT band passes posterior to the axis of rotation, the tibia reduces, slips back from a subluxed position to its native position. This causes a shift or a clunk or a jerk. So it's going from an anteroly subluxed position to a reduced position in the pivot shift test. They may ask you that. So internal rotation, valgus, axial load, you're starting subluxed, and after you have that little clunk, you're reduced. Bone film, Sagan fracture, pathognomonic for an ACL tear, that's another x-ray find that I may show you. It's a fleck of bone there off the lateral tibial plateau. Make sure it's not an avulsion off the femur head. So it's an avulsion fracture probably from the lateral capsule. A lot of people would say that's from the ALL, the anterolateral ligament, which is a capsular ligament. Another pathognomonic I mentioned earlier, the deepened sulcus terminalis. It's a compression injury from the acute injury, and that sulcus terminalis is more than two millimeters in depth, I think, ACL injury. MRI, most sensitive specific imaging test for ACL, acutely you have a high T2 signal and discontinuity, inability to visualize the remaining fibers in the ACL. So what about ACL deficient gait pattern? The gait pattern most associated with ACL deficiency is quadriceps avoidance pattern. Remember we talked about that one of the first mechanisms describing why ACLs tear in a noncontact injury is that if the knee is between zero and 70 degrees of flexion and you fire your quadriceps the way the mechanics are of the patella tendon, you have an anterally directed vector that pulls the tibia anteriorly. So if you don't have an ACL and your tibia wants to slide anteriorly, your body instinctively avoids the quadriceps to avoid trying to sublux the tibia. So you need to know that, quadriceps avoidance pattern, ACL deficient knee, that's the gait pattern. So quad contraction between zero and 60 results in that anterior vector. So question, 22-year-old basketball player with ill-defined deep pain but no locking in his knee, his MRI is below, what's his diagnosis? This is the one we're looking at here. This is a cruciate cyst. A cyst can occur in either of the cruciates, it's more common in males and you treat it with arthroscopic excision. A Sagan fracture, path of the mnemonic for an ACL injury is a result of avulsion by what structure? We talked about the ALL, the anterolateral ligament. Or you might want to say the lateral capsule. The ALL is a capsular ligament and there's a lot of debate about the ALL. So what are the concerns of ACL deficient? You have three concerns, functional instability, further injury to the knee, i.e. meniscus tears and long-term osteoarthritis. What are your treatment options, non-operative treatment or reconstruction? If you see repair and there's a lot of talk about repair, repair is not an answer for the purpose of this exam. So non-operative management, the indications for treating an ACL injury non-operative, you have an older patient, a low demand activity level patient, they have no instability with activities daily living and they're able to avoid re-injury episodes. They don't have any buckling or shifting in their knee. So the treatment, the non-operative treatment is neuromuscular training, physical therapy, activity modification. If there's things that do tend to make the knee have a re-injury, avoid those. And you may or may not put them to a brace. Again, a brace can help an ACL deficient knee be more functional, but it will not protect an intact or reconstructed ACL. All right, so it can help deficiency, but not prevention. Surgical management, indications, younger patient. We know the younger the patient, the less well they do long-term. If they're ACL deficient, they're more likely to have meniscus, subsequent damage. If they have a repairable meniscus, saving the meniscus is highly desirable. If the athlete, if the patient desires to return to cutting sport or if they have instability with daily activities. So doing an ACL reconstruction in a 55-year-old is very reasonable if they've failed non-operative treatment and they continue to have instability with ADLs. Stabilizing that knee is a reasonable thing to do. So surgical management is reconstruction. Repair is being, again, investigated, but it's out for this exam. It's not the right answer. Timing, you want to do it in a subacute state. You don't want to do it in the acute state. You want to have minimal effusion, full range of motion, good quad control, and a normal gait. Statistically, 95% of the patients who tear their ACL can achieve that by three weeks. So they ask for an actual time, say three weeks or more. But you also want to achieve minimal effusion, good motion, good quad, you know, normal gait patterns. By achieving these four characteristics, you can decrease the risk of post-operative arthrofibrosis. Again, three weeks is kind of the magic number. Surgical concepts, you want to use a strong graft. You want to anti-acute place it. You want to make sure it's rigidly fixed. If you do those three things, you can start early motion. Early motion is key. And to me, those four concepts are what kind of entered us into the modern era of ACL reconstructions. So what about graft choices? Allograft advantages, no harvest morbidity, shorter OR time, faster early recovery, they have less pain, and you have repeat availability. Disadvantages of allograft, risk of transmission of HIV, hepatitis. They may ask you for a number. It's like roughly 1 in 1.6 million risk. Three megarads are needed to kill the HIV virus, but the more you radiate the graft to kill the virus, the more you weaken the graft. Allografts have a higher retail rate in young active patients. It's been shown in animal models that allografts have a longer time to bioincorporate into the knee. It's more expensive. You can have a low-grade immune response. And if you are going to use an allograft, you should know that the less processed the graft, the better the graft appears to be. So if you're going to use an allograft, a fresh frozen is better than one that's been highly processed. So know this higher retail rate in young active patients and this fact that the more you radiate it to sterilize it, the more you weaken the graft. What about the autografts? Well, BTBs, they're more stiff and they can have increased kneeling pain long-term. That's well established. That's testable. Hamstrings have higher ultimate strength, but they consistently can have a small, like 1 millimeter, increased laxity. They have similar clinical results, meaning the patient satisfaction and how happy the patient is is equal between a hamstring and patella tendon. But more recently, it's been shown that hamstrings can have a higher retail rate in young cutting sport athletes. So what's the difference between a patella tendon and a hamstring graft? Patient satisfaction is the same. Patella tendons have increased kneeling pain, but the hamstrings may have a small but real increased retail rate in the young cutting sport athlete. And a quad tendon is an acceptable option. It's been less well studied, but it's widely accepted. What about a patella tendon graft complications? Patella fracture, catastrophic. Numbness lateral to the incision by damage or transection of the infrapatellar branch of the saphenous nerve. The nerve, as you know, runs medial to lateral. You have numbness laterally, and they can have kneeling pain. So those are all well established complications of using a patella tendon. Hamstring, you can have a saphenous nerve injury in the harvesting. You can have some weakness of terminal flexion. You can have premature amputation during the harvest. If you don't cut the indirect attachments of semiteninosis, and then more recently, as I just said, you may have an increased retail rate in young cutting sport athletes. What about double bundle ACLs? You heard a lot about that the last 15 years. The basic science studies show that double bundle does indeed give you increased rotational control of the knee, and it more closely replicates normal key kinematics. That's in the lab. Clinical studies in real patients show maybe they have better pivot shift results, maybe, a lot of studies don't show it, but the bottom line is no difference in patient-reported outcomes. The patients are not more happy or less happy. They don't return to sport any faster whether it's a single bundle or double bundle. So I would say the bottom line is other than being tested in the lab where they have better rotational control and more normal kinematics, for the clinical evaluation, there's no difference. There's no benefit. All right. Evidence for ACL reconstruction, why we do them. ACL reconstructions, there's good evidence that ACL reconstructions do increase stability of the knee. There's evidence that it decreases the incidence of subsequent meniscus tears. So two of those three problems we talked about, reconstructions can help, but there is not evidence that we can decrease the long-term osteoarthritis in the knee by doing ACL reconstruction. So if they say ACL reconstructions prevent long-term OA, that's not right. We can't show that. What about complications after ACL reconstruction? Loss of motion was very common in the 90s and early 2000s and much less common now because of early aggressive motion and aggressive rehab. But if you still have loss of motion despite adequate physical therapy by 6 to 12 weeks, you should really seriously consider doing an MUA. So earlier than later. You don't wait until 6, 9 months to do an MUA. You can have a cyclops lesion, a fibrous mass at the base of the ACL graft. You can have clicking within out pain at terminal extension. It's, if you look for it, you'll see it and it's easily treated by excision with arthroscopy, a time of arthroscopy. So what about re-tears of the graft? That's the biggest complication of ACL reconstructions. The reason for re-tear can be a technical issue at time of reconstruction, lack of biologic healing by the graft, or traumatic re-injury. For the purpose of this test, the number one reason I'll still be asked on the exam of why a graft re-tore, they're going to say a technical problem at the time of the reconstruction. The overall re-tear rate is somewhere around 6 to 8%, but it varies widely. If I had an ACL re-construction done, my risk for re-tear is under 1%. A 14-year-old female soccer player, it could be as high as 16 to 18, even 20%. Allografts have an increased re-tear rate, especially in young active patients. The contralateral knee in someone who has a non-contact ACL re-construction is at equal or even greater risk for subsequent ACL injury. So if you have another ACL injury after a successful ACL reconstruction, the ipsilateral graft re-tears occur early, within the first year or two. The contralateral tears tend to occur later. So if you see a paper or a study of someone who says, gee, we have a higher rate of re-tears of the graft as opposed to contralateral, if you look at the length of the follow-up for that particular study, it was probably short. If they start going out four, five, six, eight, ten years, you're going to see the lateral contralateral side have more tears. What are the risk factors in a well-done ACL reconstruction? You need to know these. Allograft use in a young patient, just being young. Any graft has a higher re-tear rate the younger the patient. And use is probably a proxy for activity, because high-demand cutting activities, the more active you are, is also a risk factor. Having recurvotum, hyperlaxia of the knee, having an increased posterior tibial slope, and poor rehabilitation. These are relatively... These bottom three are now widely accepted. I think they could be on the test, but they're relatively new as far as the science having evidence behind them. Recurvotum, increased tibial slope, and poor rehabilitation. So graft re-tears. If your slope is greater than 10 to 12 degrees, similar to that, you have a significant increased risk of re-tear. So you may ask, what about a slope-decreasing osteotomy? It may be considered revision cases. You're starting to hear more about them being done. The concern is you can also increase your recurvotum, which in of itself is a risk factor. So I don't think they're going to ask you about decreasing tibial slope, but I think what you may need... What they might ask you on is, what's the amount of posterior tibial slope that puts the patient at risk? And the answer is 10 or 12 degrees, if they're greater than that. What about lateral-sided tenodesis to augment your ACL reconstruction? There's recently some increasing evidence of this, some interest in it, but it's still very controversial. I'd be very hesitant to say that's a correct answer for the purpose of this test. You may consider augmenting a revision. If you have a high-risk patient that has a recurvotum with generalized laxity, you may augment your revision reconstruction with a lateral tenodesis, but again, this is something new. It's controversial. I'd be very hesitant to check that box. What about female gender? It's well-established that females have an increased risk to tear their native ACL. They also have an increased risk to tear the contralateral native ACL, but there's no clear evidence that they have an increased risk of tearing their graft. So that's a slippery point you may get caught up on. There's no clear evidence that they have an increased risk of re-tearing their graft compared to males. How about infection? You know these three things clearly and that's been shown. Smoking, diabetes, and using a hamstring graft have an increased risk of infection. The number one, far and away, is diabetes. What about technical errors? Again, this is what will probably be on the exam. The most common technical error is tunnel placement. The most common tunnel placement issue is placing the femoral tunnel to anterior. If the femoral tunnel is too anterior, your knee will be tight in flexion. If your femoral tunnel is too posterior, you can be tight in extension. A vertical tunnel is less anatomic and you have less rotational control, but a vertical tunnel does not correlate with increased re-tear or patient satisfaction. All right. So the landmarks on a lateral plain film for appropriate tibial tunnel placement in the ACL reconstruction, you should know this because they may show this x-ray. The line of the tibial tunnel should be posterior to Blumenstadt's line in full extension. So they may show you a lateral x-ray of a graft that failed and they may ask, why did this fail? And they're going to show... Let's see if my mouse shows here... That this will be anterior and the tibial tunnel will not be behind Blumenstadt's line. So be aware of that. Question. A vertical ACL graft on x-ray implies... We just talked about it. Less rotational control. Repatient reported outcomes, clinical stability, re-tear risk are not affected by a vertical graft. How about ACL reconstruction rehabilitation? You should avoid open chain quad work, 0 to 45 degrees in the early post-op phase. I think it's pretty widely accepted. You need to pursue early motion, widely accepted. Early weight bearing is encouraged and has been shown to decrease patellofemal pain. There's no evidence that a CPM or bracing provides you a long-term benefit. CPM may help in the first couple of weeks, but long-term, no evidence that CPM or post-operative brace is any benefit. What gait pattern is associated with ACL deficiency? We talked about how the quadriceps between 0 and 60 creates an anterior tibial vector, quadriceps avoidance pattern. Again, the quadriceps contraction between 0... The closer you are to 0, the stronger the anterior vector. Another question. In an ACL-deficient knee, what structure provides significant restraint to anterior tibial translation? I can hit you pretty hard with that, but it's a... It enters into so many different vignettes they could test you on. It's this interrelationship between the poster horn medial meniscus and the ACL. If either one of those is injured or insufficient, it places an increased load on the other. So poster horn medial meniscus, this may explain increased risk of medial meniscus tears, ACL-deficient knees, and this whole concept of ramp lesions. Pediatric considerations. Young patients are more likely to do poorly long-term if ACL-deficient. The risk of them tearing an ACL... I'm sorry, meniscus subsequently is very, very high. Obviously, you have to consider the fiseal injury during ACL reconstruction, worried about growth arrest. There's a high rate of meniscus tears in young patients with ACL deficiencies. Tibial eminence avulsion factors. You can attempt to reduce them in full extension. That's an acceptable answer. Most of the time, you're going to end up doing an ORF. You can use either suture or screw. Either one is reasonable. You need to avoid or at least take into consideration fiseal damage. You should also know that it's been shown that in these tibial eminence avulsion fractures, the ACL collagen has been damaged as well. So those are four concepts that have been widely accepted and are clearly testable. So pediatric ACL. If the fysis is closing, which means a TANR-4, which is the vast majority of these, all right? That's that 12, 13, 14-year-old female or male up to even 16 or 17. If the fysis is wide open... So if it's a TANR-4, you can do the adult operation. Don't worry about it. It's closing. The fysis is closing. Do the adult operation. No problem. If the fysis is wide open, a TANR-1, 2, it's safest to avoid crossing the fysis. You may want to do an all intraepiphyseal or an extraepiphyseal over-the-top type reconstruction. You may consider... Some people would recommend non-op treatment, a TANR-1 or 2. They're usually trying to buy time. But be aware that if you have a TANR-1 or 2 ACL deficient and you're trying to let them mature a little bit before you do reconstruction, it's been well shown and well recognized that they have a high risk for subsequent meniscus tear. And a lot of people think the risk to the damage to the subsequent meniscus tear and its consequences are much greater than the risk of having a fyseal closure. So here's an example of fyseal sparing. These are intraepiphyseal fyseal sparing ACL reconstruction. This is the extraepiphyseal all over the top, both in the femur and on the tibia. So if you do an ACL reconstruction in a skeletally immature patient, here's some concepts that are testable. You want to drill the smallest possible tunnel across the fyses. You probably want to make your tunnels a little more vertical so you cross the fyses more perpendicularly and that way you'll have a smaller area of injury to the fyses. You want to fill that tunnel where you cross the fyses with soft tissue. Clearly you don't want to cross the fyses with a metal or plastic screw or some type of implant or bone. Do not cross the fyses with a fixation device or a bone plug. If you do an ACL reconstruction crossing the fyses in someone who's a 10 or 3 or higher, the risk of growth abnormality is actually very, very low. Most of the growth abnormalities done by ACL reconstructions across the fyses had a technical problem. They placed a staple implant or a bone plug across the fyses. All right, ACL bracing. May be effective in facilitating function in an ACL deficiency. That is true for ACL braces. There's no proven benefit of wearing a brace after an ACL reconstruction. No proven ability to prevent tears of either native ACL or reconstructed ACL. So when you talk about parent, if the vignette says the parents come to you and they want their daughters to not have an ACL injury, they're going to play soccer, and one of the options is to give them a brace, that's not the correct answer. It's going to be neuromuscular training program. Question. 31-year-old athlete has continued instability two years after an ACL reconstruction. The most likely cause is, again we talked about it, tunnel malposition. This is an anteriorly placed tunnel, you know, on the femur. Question. 14-year-old cyclist has injured his knee. Exam compromised secondary swelling and pain. So you can see the MRI. Next best step. So you have to be able to recognize what we're seeing here and here. So this is a tibial spinal fulcrum fracture. You want to do an arthroscopic open reductional internal fixation. All right, let's shift to the PCL, anatomy and biomechanics. The PCL is intraarticular, but actually extrasynovial. Its origins are lateral border of the medial femoral condyle and it starts about one and a half centimeters below the joint line in the posterior tibia. Its average length is 38 millimeters. Its average width is 13 millimeters and it's stronger than the ACL. It too has two bundles and here's where it's different. The PCL's two bundles are named by their origin on the femur as an anterolateral bundle and a posterior medial bundle. The anterolateral bundle is stronger twice across sectional strength area of the PM bundle. The blood splatter PCL is also from the middle genicular artery. It's more generous than the ACL. It has an improved capacity to heal. It has this more dense synovial sheath, has better vascularity. It does have some capacity to heal within that sheath. Its innervation is by the posterior tibial nerve, so its blood supply and innervation are very similar to the ACL. What about the meniscal femoral ligaments? They go from the medial femoral condyle to the posterior horn lateral meniscus. Ligament of Humphreys is anterior to the PCL. Ligament of Risberg is posterior to the PCL. They act as secondary restraints. They help posterior... prevent posterior translation. They can be anywhere from 5 to 20 percent the strength of the native PCL. Their occurrence is variable. You may only have one, or you can have the other, or you can have both, but most people have at least one. The naming, Humphreys and Risberg, I remember they're alphabetical, front to back. So whether it's spelled Risberg with a W or an R, it's still posterior to Humphreys. So PCL is a primary restraint to posterior tibial translations, roughly 95 percent when flexed between 30 and 90 degrees. It's a secondary restraint to external tibial rotation, the posterior lateral corner wrist. Now you can see right now from the pattern here, you can see that the posterior lateral corner and the PCL are kind of linked, right? Because if the posterior lateral corner's not working well, now it puts more strain on the PCL. And you can see when the posterior lateral corner's not working well, there's more pressure on the... load on the PCL. So the AL bundles tighten flexion, the posterior medial bundles tighten extension, and there's reciprocating tension during flexion and extension. Mechanism of injury, high velocity. So when they mention a flexed knee hitting a dashboard in a motor vehicle accident, immediately think PCL, PCL, PCL. It can also be low velocity, it can be contact or non-contact, it can be a posterior directed blow to the proximal anterior tibia in a flexed knee. Also could be injured in hyperflexion or hyperextension. So the posterior drawer test, the physical exam of choice, you want to assess the medial tibial shelf. You can see the normal shelf on the left and you can see how the shelf disappears on the right. The posterior's most accurate exam, you normally have about a 10 millimeter step off the medial tibial plateau, medial formal condyle. A grade one, that tibial plateau remains anterior to the medial formal condyle. A grade two is that when you push, the plateau becomes somewhat flush, it feels like the step kind of disappears, so it's about 10 millimeter laxity. A grade three is when the plateau tends to disappear under the condyle and you have... you almost have a hard time feeling an end point. A grade three PCL is very likely to involve the post lateral corner. So again, post PCL, PLC, they're related. Posterior sag sign, ski slope sign, they may refer to those signs, you can see what they are. Quad active test, we don't hear quite about that so much, but in the case of PCL injury, it can help differentiate posterior from anterior laxity, that's one reason it was developed by Dr. Daniels. You put the knee in about 80 degrees of flexion, the foot is fixed, held to the floor, and the patient actually attempts to extend the knee against resistance and it's positive if the tibia moves anteriorly, again, the quadriceps creating that anterior vector. The MRI is gold standard imaging for acute PCL injuries, and notice I said acute, you use it to assess the tear location and associated injuries. Chronic PCL tears may look relatively normal on the MRI because again, the PCL does have some healing capacity, much better than the ACL. So you can have someone who on exam has a grade 2 posterior laxity chronic for years and depending on who reads your MRI, they may actually read the MR as being unremarkable. So what are the problems if you have chronic PCL laxity? Well one, you get chondral erosions and this is very testable. The articular cartilage that is damaged in a chronic PCL deficient knee is the medial femoral condyle and the patella femoral joint. The pain tends to be vague, poorly localized, and the patients will complain about instability or lack of confidence classically with going downstairs or down a decline. If you think about it, when you're going downstairs down a decline, your femur wants to go off the front of the tibia or conversely, your tibia wants to go behind the femur. So you need a PCL to keep your tibia under the femur. Again, chondral erosions, medial femoral condyle, patella femoral joint, very testable. What's the treatment for an isolated PCL injury? A grade 1 or 2, you do 4 to 6 weeks of relative rest. You want to avoid replicating the mechanism of injury, so you don't take a partial to a complete. If you have a grade 3 PCL, get to it acutely. You can hold the knee in full extension. When the knee is taken to extension, isolated PCL will reduce. So hopefully you get some scarring or healing of the PCL, then you start physical therapy. You could do surgery in acute grade 3 in a young athlete or if you have a tibial avulsion. What about a chronic isolated PCL? Grade 1 or 2, quadriceps rehab, strengthening, activity modification at grade 3. Again, quad rehab and activity modification and if that doesn't do the trick, surgery if the symptoms persist and the surgery is reconstruction. There are two indications for repairing a PCL injury and that's one, you can do a primary suture repair if it's evulsed off the femur and you get to it acutely within the first three weeks. Use non-absorbable suture through the evulsed ligament, pass the suture through bone tunnels, tie over a bony bridge or a button. Attempting a repair is unsatisfactory, it doesn't work in chronic or mid-substance. Those need to have reconstruction. So it's pretty rare, but if it's nice and fresh right off the femoral condyle, you could try a repair. And then you can do an RAF of that bony avulsion off the posterior tibia. So there are two indications acutely to repair a PCL injury. If you're going to do a PCL reconstruction, you have two technique decisions. One is trans-tibia versus tibial inlay and you're going to do a single bundle or double bundle. The post-op protocol, regardless of the technique you use, is to keep the knee in extension to help maintain reduction, really push early quad rehabilitation and strengthening and delay any kind of active resistive hamstring exercises for several months. There's no clear advantage to either one of these, trans-tibial or inlay, single or double bundle. All right, what about trans-tibial or tibial inlay? Trans-tibial inlay, I think it's kind of come and gone, but it's the way these tests kind of delay current knowledge, it may be still tested. If you're going trans-tibial on your PCL reconstruction, you have to be aware of neurovascular structures when drilling. That'll be one of the concerns about trans-tibial. And you have what's called the killer corner, we're going to see here in a minute. The posterior inlay, you have posterior exposure, you got to pull the medial gastroc laterally to protect neurovascular structure, and you have to reposition intraoperatively. So pull the medial gastroc to protect the neurovascular structures and you have that posterior incision. Now, you can see here, you do trans-tibial, you can have this, what some people would call the killer corner, where you can have fraying and stretching of your graft with repetitive loading, where the tibial inlay is designed to minimize that phenomenon. Now, the tibial inlay is done less and less because it's shown that it did not long-term provide any clinical benefit. So again, trans-tibial, tibial inlay, equivalent results. How about single bundle versus double bundle? If you do a double bundle, you tension the AL bundle at 90 degrees, the PM bundle at 30 degrees. The basic science studies show some improvement in restoring normal biomechanics with a double bundle, but just like the ACL double bundle, patient reported outcomes, there's no difference between single or double bundle PCL reconstructions clinically. It's only in the lab that that advantage is seen. So some miscellaneous comments about PCL, meniscus tears and bone bruises are seen much less commonly with PCL tears than with ACL tears. Pathologic posterior tibial translation unloads the posterior horns of the mio-meniscus, that's the opposite of the ACL, ACL deficiency puts the menisci at risk. Combined PCL and PLC injuries are more common than initially believed, so always keep your eyes open. The more serious the PCL is injured, the more you have to look at that post-lateral corner. Failure to address a post-lateral corner injury contributes to increased PCL graft tension and ultimate failure. Same concept that we saw between the posterior horn of the mio-meniscus and the ACL, you're seeing between the PCL and the post-lateral corner. Question, posterior instability is diagnosed by the quad active test with tibial translation anteriorly between 70 and 90 degrees. That anterior vector again, pulling the tibia anteriorly. How about tibial slope and the cruciate ligaments? If you have a higher posterior tibial slope, the tibia tends to want to slide forward. That's good for the PCL, bad for the ACL. So you may want to understand this concept of tibial slope and how it affects the two cruciates. A decreased posterior tibial slope means the tibia tends to want to slide posteriorly, bad for the PCL, but good for the ACL. So you should know the, shifting on to the MCL, you should know the three layers of the MCL. Primary restraint to valgus throughout the arc of motion, isolated injury usually from a blow to lateral knee with the foot planted. You want to evaluate the integrity of the MCL by looking for valgus laxity of knee held at 30, because when you flex the knee to 30, you isolate the MCL from the cruciates and the posterior capsule, all right? So now when you try to take that knee to valgus, you've taken the cruciates and capsule out, minimized their contribution. At full extension, you also test for valgus, and if your knee is lax and valgus, not only are you worried about a MCL injury, but now you're worried about the posterior capsule is torn and you need to really look at your cruciates, because they have some injury as well. So if you have grade three laxity at 30 degrees of the knee, you need to test in full extension. If you're lax in full extension, your posterior capsule is injured and you need to take a close look at your cruciates. Any grade three MCL injury is commonly associated with other ligament injuries. So injury location, it can, you know, it can be diffuse, it can be femoral side or predominantly on the tibial side. This is, I think, also potentially testable. An MCL injury on the femoral side, it heals better, but you can have more stiffness and even a little bit of this pain syndrome. On the tibial side, they heal less readily, they're less likely to have stiffness or pain, but you can also have some chronic laxity. Treatment non-op, non-operative indications for MCL are any kind of truly isolated injury and if they're stable in extension. If they're stable in extension, it makes you more comfortable and it's isolated. Physical indications for an MCL injury, if you have any kind of combined third degree MCL injury. So third degree MCL with any other ligament, now you start thinking about maybe you want to do something to stabilize and address surgery of the medial side. If you have chronic laxity, you can consider a surgical intervention. Surgical technique acutely, you can do a repair. Chronically you have to do a reconstruction. Pediatric considerations. This is a... I almost guarantee it's likely to show up in a test. Beware of valgus laxity and knee with open physis. They love this. You may have a distal femoral physis injury that tend to be proximal to the femoral attachment. You can have a normal x-ray. You must get an MRI or do stress x-rays. If you see any type of medial sided injury in someone with open physis, you have to get an x-ray or MRI or stress x-rays. So watch out for an adolescent with an MCL injury scenario. They're going to lead you down the path of missing the fact that it's a physio injury. What about the LCL in the post-lateral corner? So the papateus, just be aware, it inserts on the femur distal and anterior to the LCL. About 13 to 16 millimeters. Distal and anterior to the LCL. LCL. Isolated LCL injury, much less common than an MCL injury. It's a varus contact injury. If the physes are open, beware of a physio injury. Get an MRI or stress films. I'm sorry. Test for laxity at 30 and full degrees... 30 degrees and full extension. If it's lax... If it's lax at full extension, you have post-lateral corner injury and evaluate for associated cruciate. So you can see these concepts here for the LCL are very similar to what we just talked about for the MCL. Treatment for an LCL. Isolated injuries, non-operative. Combined injury, do surgery. An acute, you can do repair plus mass augmentation. A chronic LCL needs to have a reconstruction. How about the post-lateral corner? Know your anatomy. What's key for those you're not familiar with knee? The popliteal-fibrillar ligament is key when they talk about post-lateral corner anatomy and function. So mechanism can be a bloated anteromedial knee producing a hyperextension, various deformity. It's post-lateral corner injuries are commonly associated with LCL, posterior cruciate injuries. This dial test is important. So your patient is prone. The feet are externally rotated at 30 and 90 degrees of knee flexion and the foot-thigh angle is measured. If you have 10 to 15 degrees of increased rotation, external rotation than the opposite side, this is pathologic. So if you have increased rotation at 30 degrees, your post-lateral corner is injured. If you're lax at both 30 and 90, your post-lateral corner and your PCL are injured, all right? This you need to know. They would love to put that in an exam question. So what's the treatment for post-lateral corner? Isolated post-lateral corners are very rare and they can be treated non-operatively. A combined injury, acutely repair and augment with a graft. This has been shown to be better than a repair alone. A chronic post-lateral corner, you need to reconstruct the popliteal-fibular ligament and this reconstruction of the associated injury, usually it's an LCL and or the PCL. Chronic lateral sided injuries, you must obtain a long leg alignment film. So if you're worried about chronic varus laxity of the knee, chronic LCL laxity or post-lateral corner laxity, if you're mechanical varus and varus, you need to strongly consider an osteotomy. So lateral sided chronic laxity and if you have varus mechanical alignment, osteotomy. Because if you're a varus knee, doing a soft tissue procedure on the lateral side of the knee, it's likely to stretch out and fail. So that's a great test question. Question, flag football player presents three days after injury to his knee. He has a symmetric Lachman, varus stress at 30 is asymmetric but he has a good end point. His dial test has some increased excursion at 30 but he's negative at 90. What's the best management? So we know he has a partial LCL, maybe a little partial post-lateral corner, PCL is intact. He can treat this, incomplete injury, acute. He can try non-op treatment initially, brace and physical therapy. How about multi-ligament injuries? Two or more knee ligaments are injured, classified production of tibial displacement. Anterior dislocation is the most common, tibial hyperextension mechanism. Posterior has the highest risk for vascular injury, lateral knee dislocation, highest risk for peroneal nerve injury. Associated injuries, popularity about a third of the time, peroneal nerve 20 to 30% and some type of tibial plateau fracture can occur as high as 60% of the time. You can see your classification here. You guys can study that. I don't have to walk you through it. The modifiers at the bottom, heading of vascular injury or nerve injury. Papageal artery injury, need to know this. Eight hours of ischemia likely result in amputation. So that magic window of trying to get them within six hours, if you get out to eight, that's the, they may ask you when do you have that risk for amputation. You must repeatedly check pulses. Your ankle brachial index, you want it to be .9. And you also want to keep checking your leg compartments. You should admit them for monitoring of these vascular situations. Have a very low threshold up in an arteriogram and a vascular consultation if you suspect any type of articular, I'm sorry, arterial injury in a dislocated knee. So a multi-leg injury treatment, assess nerve vascular status pre and post reduction. Do a timely reduction. Get AP and lateral films pre and post reduction. Obtain an MRI and admit for monitoring of vascular status and compartment syndrome. Acute surgery for multi-ligament injured knee with the indications of vascular injury, an open dislocation, a compartment syndrome, or an irreducible dislocation. So those are the four indications for acute surgery on a multi-ligament injured knee. And you notice both of these, vascular status is the number one priority. That's the number one thing, number one concept I'm going to test you on is vascular status. So treatment of ligaments. If you have an active individual who's a good surgical candidate, you should acutely repair the medial side. Repair and augment the lateral side and the post-lateral corner acutely. Reconstruct the cruciates either early or late. And then reconstruct the sides, medial and lateral if it's a chronic condition. And a poor surgical candidate, maintain the reduction. Very often you have to use an external fixator. Allow scar to form. Delay it with protected motion. Use a hinge brace and progress protected weight-bearing. What about lateral avulsion fractures of the knee? The biceps and the LCL can avulse from the fibular head. The poppiteus can avulse from the femoral groove. And the ALL can avulse from the tibia, the sagon fracture. And we're familiar with the Pellegrini-Stega lesion. It's a bony reaction from a proximal MCL injury. Question, 19-0 quarterback has knee dislocation. The ER doctor feels decreased pulses and reduces the knee and the pulses return. You're consulted. There's gross anterior, posterior and medial laxity. The skin's intact. Pulses are present. Neuro exam is normal. What's your best recommendation? Immediate MRI, low extremity venography, compartment pressure measurements, knee mobilization, follow-up 48 hours, admission for serial ABIs. For the purpose of this test, it's going to be check vascular, check vascular, check vascular. If they give the option to admit and observe and do repeated valves for vascular assessment, they may make it look like the patient is very benign, very stable, looking good, and you're going to be tempted to follow up in the office in a couple days. The answer is admit and observe. Question, 24-year-old unable to fully extend the knee after an ACL reconstruction. His motion is 5 to 140. Has a negative Lachman, positive pivot shift. So he's lacking 5 degrees of full extension. Take a look at the MRI. What they're getting you to look at is cyclops lesion. He has anterior impingement. You need to breathe a notch arthroscopically. So what are the tips? If you see the word dashboard in the vignette, think PCL. Dashboard equals PCL injury. Fall on a knee with plantar flexed foot, think PCL. Fall on a knee with dorsiflexed foot, think patella. This will help keep it straight. The anteromedial of the ACL and the anterolateral of the PCL are the primarily most important bundles. So it's the A. So anteromedial, anterolateral, ACL, PCL, A. When they ask which is the larger bundle, what's the more important bundle, what's the key bundle, it's the A bundle. Interference screw divergence of over 15 degrees can decrease fixation strength. But if you're less than 15 degrees, your interference screw may be fine. The PCL does have some healing potential. A chronic PCL can or may appear relatively normal on the MRI. But it does heal in length of position. ACL repair is not the correct answer for the purpose of this test. PRP injection for knee ligament is not correct. A knee injection or PRP for OA might be correct. There's more evidence, clinical evidence for that. But using PRP for a ligament about the knee is not correct. ACL tears are increased in skiers but actually decreased in snowboarders. The pivot shift may not be present if the MCL is laxed. So don't get fooled if they have a, they tell you on the vignette the MCL is a grade 3 but you don't get a pivot shift. Synthetic graft is not a correct answer. Thermal shrink is not a correct answer. ALL reconstruction currently, I would say, is not going to be the correct answer. Stem cell injections to augment your ligament work is not a correct answer. ACL reconstruction with a stent is not a correct answer. ACL reconstruction with stem cells is not a correct answer. No fixation technique from the ACL has been shown to be superior to another. So whether you use a metal screw, a reservable screw, cortical suspension. Look for the bone bruise pattern in a re-injury. So you may have an ACL reconstruction. They did fine for three years. They have some re-injury and then they show you the MR. And maybe the MR doesn't quite get into the notch. But they're showing you the bone bruise pattern again that helps you make the diagnosis that true indeed had a re-tear of the graft because that's the only way that that amount of displacement lateral side would happen. Think PCL injury in a lock mitt with increased excursion but a firm end point. All right, so the knee ligament exam questions. If you go through the study questions, pay attention to the discussion section. The discussion section should be telling you why the wrong answers are wrong because that's important. You're going to learn a lot from that. So sourcing of these study questions and discussion references. AOSSM has multiple self-assessment exams. I think the last four or five years are actually, you can download online. The academy has some SAE exam as well. You can do the OKUs. The key is as you get ready for this exam, focus on what is known and accepted. It's interesting and you're kind of enticed to look at the controversial, the new, and the poorly established concepts. But avoid all that. That's a waste of your time. And you'll do well. Good luck. Thanks.

knee ligaments

anatomy

biomechanics

ACL

PCL

MCL

LCL

injuries

surgical techniques