One of the best ways to understand how something, anything, works is to take it apart and put it back together again. For the knee, this is fairly simple. We need a relatively short list of parts: 4 bones, 2 tendons, 4 ligaments, and 2 types of cartilage.
To start, we place the femur, tibia, and fibula bones in their proper positions (Figure 1-1). Next, we need a system of ligaments to hold them together (Figure 1-2) and a coating of articular cartilage on the surface of the femur and tibia, two of the three bones that will articulate against each other (Figure 1-3). Of all the structures used to assemble the knee we are building, this thin layer of glistening articular cartilage tissue is probably the most important and the most interesting (please read the sidebar on articular cartilage). Now we are ready to add the meniscus cartilages, which sit like two rubbery, horseshoe-shaped pads on the surface of the tibia (Figure 1-4). The exact role that the meniscus cartilages play in the function of the knee is poorly understood, but they do not act as a “cushion” between the femur and tibia, as many of us were taught (see sidebar). The last bone we need to add if we are building a knee is the patella. The patella is a link in the chain of structures known as the extensor mechanism (Figure 1-5). These structures—the quadriceps muscle, the quadriceps tendon, the patella, and the patellar tendon—allow us to forcibly straighten (extend) our knees. When it contracts, the quadriceps muscle (via its quadriceps tendon attachment to the patella) pulls the patella proximally. As it is pulled proximally, the patella (via its patella tendon attachment to the tibia) pulls the anterior tibia proximally, which rotates the knee into extension.
THEY ARE NOT CUSHIONS!
I can’t tell you how many times I’ve heard it said that the meniscus cartilages are the “cushions” that reside between the femur and tibia. This isn’t true. They do reside between the tibia and femur bones, and it is true that, if a meniscus cartilage is damaged or surgically removed, the articular surfaces adjacent to it will wear out faster. But, the meniscus cartilages are peripheral to the load-bearing contact surfaces in the knee. This deserves a little further explanation. Illustrations like the drawing in Figure 1-4 are misleading. To enable you to see the meniscus cartilages, I have distracted the femur and tibia apart, opening the joint space much wider than it is anatomically. A more accurate representation would be what is illustrated in Figure 1-A. To better understand the relationship between the meniscus, articular cartilage surfaces, and bones, let’s study a series of cross-sectional lateral views (Figure 1-B). Here, we can see that the dimensions and location of the contact patch between the tibia and femur are not affected by the presence or absence of the meniscus. While the exact function of the meniscus cartilages is not known, they do not function as cushions interposed between the articular surfaces of the tibia and femur. Figure 1-C shows how this same anatomy appears on a sagittal MRI image of the knee.
Figure 1-B.
A cross-sectional lateral view of the knee 1. showing the layer of articular cartilage on the surface of the femur and tibia; 2. showing the anterior and posterior horn of the medial meniscus; 3. after removing the anterior and posterior horns of the meniscus; 4. showing the contact patch between the tibia and the femur and how its dimensions are not changed when the meniscus is removed.
Figure 1-C.
How the anatomy in Figure 1-B appears on a corresponding MRI image (Reproduced with permission from Ross Goldstein, MD).
Having completed the simple “build-a-knee” exercise, it is time to study the different knee conditions seen in a typical outpatient clinic.
Patients with ligament injuries are usually easy to separate from other patients with knee complaints. The role of the knee cruciate and collateral ligaments is to stabilize the joint. These structures connect the bones in a way that allows normal motion (flexion and extension) but resists the forces that create abnormal motion (hyperextension; varus/valgus [see further discussion]; anteroposterior translation and rotation). The knee ligaments of a given patient are about the same length and diameter as that patient’s pinky finger, so they are essentially impossible to tear without substantial trauma. A patient with knee pain but no history of trauma or injury is not likely to have a ligament injury, at least not a recent ligament injury. You will encounter patients who tell you that they had a “knee sprain” years ago that seemed to heal well, but ever since, they’ve had a “trick knee” that will give out on them once or twice a year if they twist just right. These episodes of instability are usually followed by a few days to a week of pain and swelling, then the knee returns to normal. This is a classic history for a patient with a chronic ligament-deficient knee. In these patients, the pain and swelling from the initial injury have resolved, but, because the ligament did not heal, they are prone to intermittent episodes of instability. With very few exceptions, trauma, even remote trauma, is requisite in the history for a patient to have a knee ligament injury.
Some patients will offer that they felt, or even heard, a “pop” when the ligament was injured. Knee ligaments are very strong structures. They can store a tremendous amount of energy before failing. If the load is big enough to fail the ligament, then the ligament will rupture, and that stored energy is released suddenly, creating what the patient perceives as a pop. Though not pathognomonic, when patients report a “pop,” this important clue strongly suggests a knee ligament injury. An effusion and the timing of its onset can also be important clues, especially when trying to distinguish ligament injuries from meniscal tears. Ligaments are more vascular than meniscal tissue, and patients with ligament injuries tend to develop effusions within an hour of their injury. In patients with meniscus tears, effusions usually develop much more slowly.
The four knee ligaments, the two collaterals and the two cruciates, each provide a unique and specific aspect of knee stability. Think of the knee as a hinge connecting an upper segment (the femur) to a lower segment (the tibia and fibula). The hinge-like knee joint enables us to flex (bend the knee) and extend (straighten the knee). If the lower segment deviates toward the midline, we call that a varus deformity. If the lower segment deviates away from the midline, we call that a valgus deformity (Figure 1-6). The collateral ligaments are designed to prevent the lower segment (the tibia and fibula) from swinging back and forth like a pendulum. The medial collateral ligament (MCL) prevents the lower segment from swinging away from the midline creating a valgus deformity (Figure 1-7A). The lateral collateral ligament (LCL) prevents the lower segment from swinging toward the midline, creating a varus deformity (Figure 1-7B). When the distal segment deviates toward the midline, it is called a varus deformity.
Figure 1-6.
Varus and valgus are terms used in orthopedics to describe angular deformities in the coronal plane. In a varus deformity, the distal segment of the articulation (the tibia and fibula in the case of a knee joint) deviates toward the midline. In valgus deformities, the distal segment deviates away from the midline.
Figure 1-7.
A. The medial collateral ligament (MCL) prevents valgus deformities. B. The lateral collateral ligament prevents varus deformities. C. While the collateral ligaments prevent varus and valgus deformities, the cruciate ligaments prevent anterior and posterior translation of the tibia. The anterior cruciate ligament prevents anterior tibial translation. D. The posterior cruciate ligament prevents posterior tibial translation.
Knowing this, we can easily invent the physical exam tests for the collateral ligaments (Figure 1-8). Both tests are done with the patient lying supine, with muscles relaxed and both knees out in full or near-full extension on the exam table. To test the MCL, place one hand on the lower leg and pull it away from the midline while using the other hand to push the thigh toward the midline. Test the LCL by doing the opposite, using one hand to push the lower leg toward the midline while the other hand is pulling the thigh away from the midline. Try to estimate how many millimeters the joint opens and the quality of the “end point” you feel when the ligament stops the knee from moving (see sidebar). If you want to be fancy, you can use the ligament-grading system described in the sidebar and illustrated in Figure 1-9.
EXAMINING LIGAMENTS
To better understand the knee ligament exam, think of the ligaments as ropes or chains that span the joint like a bridge connecting one bone to the other. The ligaments are positioned not only to allow normal motion but also to resist abnormal motion. When we test a ligament, we apply a force to the knee that attempts to create an abnormal motion and then measure what happens. Specifically, we try to measure two things: the amount of displacement and the quality of the end point. The ligaments are not perfectly rigid; they have a slight amount of elasticity, so they stretch a bit under an applied load. The elasticity of human ligaments varies a great deal from person to person. This helps explain why I have a hard time reaching down to touch my toes, while a contortionist can cross their ankles behind their head. Because of this variability, there is no standard, “normal” amount of displacement to expect when we test a patient’s ligaments. The medial side of one patient’s knee may open 2 mm on the MCL test, while another patient’s might open a centimeter, and both ligaments could be perfectly normal. To know whether the amount of opening we feel on the ligament exam is normal or abnormal, we have to compare our findings on the knee we are examining to the gold standard: the patient’s other, uninjured knee. While there is considerable variability in the elasticity of the ligaments from one person to another, there is little variability when we compare the elasticity of the ligaments of one knee to the other in the same person. A difference of 3 mm or greater between the right and left knees of the same patient suggests a ligament injury.
The “end point” we refer to in the ligament physical exam test is the cessation of motion that occurs during the test when the ligament reaches its elastic limit and displacement stops. In the clinic, I illustrate this to patients by holding my necktie between my two hands. I let it sag a bit, then abruptly tug it tight. The sudden stop that occurs when the tie snaps taut is the end point.
Based on the amount of displacement and the quality of the end point, we can report the findings of the ligament exam using the orthopedic three-grade classification (see Figure 1-9). A grade I ligament injury is one where the ligament is strained, but there is no macroscopic fiber damage. On physical exam, we won’t detect any increase in displacement compared to the opposite knee, and there will be a normal, firm end point. The only finding that differentiates a grade I injury from a normal knee on exam is that the patient will experience pain when the ligament is stretched during the test. In a grade II injury, there is a partial tear of the ligament, with some fibers torn and some still intact. In this case, the exam will show increased displacement but a firm end point. In a grade III injury, there is complete rupture of all fibers of the ligament. The ligament exam will demonstrate increased displacement and a soft, mushy end point.
The function of the cruciate ligaments is very different from the function of the collateral ligaments. While the collateral ligaments resist varus/valgus angular deformities in the coronal plane (varus/valgus deformities), the cruciate ligaments resist translational motion, specifically anterior and posterior translation of the tibia (Figure 1-7C,D). The examination used to assess the anterior cruciate ligament (ACL) has evolved some in recent years. The anterior drawer test is slowly being replaced by a more accurate test called Lachman’s test. In both tests, the examiner tests the ACL by pulling the tibia anteriorly, which pulls the ACL tight; however, what makes Lachman’s test superior to the anterior drawer test is that the observed changes in displacement are greater (and therefore easier to detect) using Lachman’s test. The reason for the difference is the iliotibial band (ITB), which suppresses anterior tibial translation when the knee is in 90 degrees of flexion (see sidebar).
HOW THE ILIOTIBIAL BAND KILLED THE ANTERIOR DRAWER TEST
The ITB is a long, dense, firm band of connective tissue that runs down the side of the thigh. Technically, it is the tendon that connects the gluteus maximus and tensor fascia lata muscles of the pelvis to the lateral side of the tibia just below the knee (Figure 1-D). In the time-honored anterior drawer test, the knee is placed in 90 degrees of flexion, the examiner sits on the patient’s foot to stabilize it, and then the examiner pulls the tibia anteriorly to apply a load to the ACL (Figure 1-E). In 90 degrees of flexion, the ITB is in a position to resist anterior tibial translation, so the amount of translation isn’t as obvious. Lachman studied ACL-deficient knees in many different flexion angles and found that the best knee flexion angle for optimizing anterior tibial translation is 30 degrees. In 30 degrees of flexion, the ITB is not in a position to mute anterior tibial translation, so there is greater displacement, which is easier to detect (Figure 1-F).
The posterior drawer test is still valid and popular for assessing the posterior cruciate ligament (PCL) because the ITB shortens when the tibia is pushed posteriorly (Figure 1-10).
Note that it can be difficult, even impossible due to pain and swelling of the acutely injured knee joint, to perform a meaningful ligament exam on an acutely injured knee. If the patient is too uncomfortable to relax for the exam, the options are to repeat the exam in 1-2 weeks when the pain has decreased or to obtain a magnetic resonance image (MRI).
If the mechanism of injury is trauma, which it usually is for knee ligament injuries, x-rays are probably warranted to rule out a fracture. This trauma may be contact trauma (i.e., two football players colliding) or noncontact trauma (a soccer player running down the field makes a cutting move and twists his or her knee). Anytime there is a history of significant trauma, an x-ray should be taken to rule out a fracture. Another imaging option is an MRI. An MRI is a very specific and sensitive test for evaluating ligament injuries, and it will pick up fractures as well. For suspected ligament injuries, the MRI can help diagnose patients who are too uncomfortable to be examined acutely or too impatient to be reexamined a week or two later to confirm the diagnosis on physical exam.
The cruciate and collateral ligaments live in very different physical environments. The collateral ligaments are extra-articular. They are surrounded by vascular soft tissue and have blood vessels inserting along their entire length to nourish them. As a result, nearly all collateral ligament injuries, even grade III injuries (complete, full-thickness tears resulting in two, unconnected ligament “stumps”), heal well without surgery. Treatment goals are to optimize patient comfort, minimize atrophy and stiffness, and support the injured ligament as it heals. A brief period (2 weeks) on crutches and in a knee-immobilizing brace (Figure 1-11) followed by motion and strengthening exercises is a typical recommendation. Transition to a hinged brace (Figure 1-12) at 2 weeks may be necessary for high-grade injuries; low-grade injuries can transition from the straight leg brace to no brace at all.
Cruciate ligaments live in an environment that is very different from that of the collateral ligaments. They have a relatively poor blood supply, spanning the joint space with no blood vessels inserting along their length. For this reason, complete, full-thickness cruciate ligament injuries do not heal. The fate of partial cruciate ligament tears depends on how much ligament tissue is still intact. For example, those with more than 90% still intact do well, those with less than 10% intact are likely to fail at some point in active patients. While it is possible to differentiate partial (grade II) tears from complete (grade III) tears on the physical exam (see the sidebar in this chapter on examining ligaments), it is impossible to use the physical exam to determine exactly how much of the ligament remains intact in partial tears. Some have advocated obtaining an MRI on suspected partial tears so that those with high-grade partial tears can be identified and considered for surgical treatment.
Grade III (complete) cruciate ligament injuries (and the rare grade III collateral ligament injuries that don’t heal) result in ligament-deficient knees. In general, ligament-deficient knees are not well tolerated by patients and require surgical reconstruction. As mentioned, collateral ligament injuries, even complete tears, typically heal without surgery. The few torn collateral ligaments that don’t heal can often be successfully repaired (their torn ends sutured back together) or reconstructed with a graft. Because of their poor blood supply, torn cruciate ligaments will not heal with suture repair and have to be replaced with a graft. Grafts can be either from the patient’s own tissue (autograft) or from cadaveric donors (allograft). Artificial (synthetic) grafts and grafts from nonhuman animals have been tried and have not worked well.
Recovery after ACL surgery is long, 6-12 months, but results are generally very good, with high rates of return to sports and strenuous activities. Keep in mind that not all ligament-deficient knees require surgery. The goals of ligament reconstruction surgery are a) to eliminate symptoms of joint instability and b) to help prevent the pattern of arthritis that these patients typically experience years or decades after their injury. Rarely, patients with ligament-deficient knees do not have instability (see sidebar). Patients who don’t have instability do not need surgical reconstruction to stabilize their knees … or do they? This is somewhat controversial. There is a body of evidence that suggests that some of these patients who have no subjective sense of instability have a pattern of “micromotion” instability that, over the course of decades, results in destructive arthritis. If this is true, then the only ACL-deficient patients who should be treated nonoperatively are those who both (a) have no instability symptoms and (b) are old enough that, for these patients, the development of arthritis 20 or 30 years down the road is inconsequential.
THE THEORY OF “THE NEUROMUSCULARLY ELITE”
The dogma as it relates to ligament-deficient knees, specifically ACL-deficient knees, is that ligament deficiency results in arthritis. While this is true in many, perhaps even most, patients, it is not true for all patients. An ACL-deficient knee will usually have a specific pattern of instability: In certain sports or activities, the knee will experience a force that tries to drive the tibia anteriorly with respect to the femur above it. Without an ACL to counteract this force, the tibia slides farther forward than it should, allowing the condyles of the femur to strike the posterior horns of the meniscus cartilages. This results in meniscus tears, and meniscus tears accelerate the rate of wear of the knee’s articular surfaces, which in turn results in arthritis. But, patients who are sedentary are unlikely to apply the knee stresses necessary to create instability. A simple and brief course of muscle strengthening in physical therapy can give them the stability they require for the modest demands of daily activities. These patients can do well treated nonoperatively. What’s interesting is that there are a few humans out there who aren’t sedentary, who can still be quite active on their ligament-deficient knees without experiencing any instability! (Figure 1-G) Although it is controversial, one explanation is that these patients have a better proprioceptive system than the rest of us, and, when the tibia starts to translate too far anteriorly, they fire a compensatory hamstring muscle contraction that arrests the pathologic motion of the tibia. Best estimates are that these individuals account for less than 5% of the population, and, as of right now, we don’t have any reliable way to test for this gift. For now, the consensus recommendation favors ACL reconstruction in active patients because 95% of them will experience a pattern of instability that eventually results in arthritis.
Figure 1-G.
The relationships between ACL deficiency and the development of arthritis. The accepted fact is that ACL tears result in arthritis. This is because, in most patients, ACL tear result in a pattern of instability that creates meniscus tears, which leads to arthritis. For some patients, ACL tears do not result in instability, so they don’t get arthritis.
Figure 1-4 shows what the meniscus cartilages look like as they sit on the articular surface of the tibia in the knee joint. These thin, rubbery tissues can tear, and when they do, they can be a source of knee pain. Figure 1-13 shows what a typical meniscus tear looks like when we view the meniscus cartilages from above. The history that patients with meniscus tears give is unique in that their chief complaint is pain at the joint line, medially or laterally. In young patients, the meniscus is tough and durable, and it is hard for a person under the age of 25 to tear their meniscus without some element of knee trauma. Usually, this is a weight-bearing, twisting injury. As we age, the meniscus cartilage becomes more fragile. In patients over age 50, it is possible to tear the meniscus cartilage by simply squatting. In the squatting position, the prominent posterior part of the femoral condyle (see discussion that follows) bears down hard and pinches the meniscus between the femur and tibia. Add a little twist, and you might just end up with a torn meniscus. Some patients with meniscus tears will experience catching or locking or other mechanical symptoms as the piece of torn meniscus flips intermittently in and out of the joint.
The three best tests for detecting a meniscus tear are joint line tenderness, pain at the joint line with deep flexion, and McMurray’s test. To test for joint line tenderness, we must first identify the location of the joint line. To find the joint line, have the patient lie supine on the exam table with their knee flexed 90 degrees. Find the patella anteriorly. On either side of the very inferior part of the patella, there is a soft spot. This soft spot is the anterior joint line (it opens when the knee is flexed). Follow the joint line around medially and laterally all the way back to the back of the knee. Most meniscus tears are in the posterior part of the meniscus, so don’t forget to go all the way back posteriorly. Tenderness to palpation at the joint line medially or laterally may indicate that your patient has a meniscus tear.
The deep flexion test takes advantage of the fact that the end of the femur isn’t round; it is oblong, or “cam” shaped, with an extra lobe of bone protruding posteriorly (Figure 1-14). This extra lobe of posterior femur bone bears down on the meniscus in deep flexion. If the meniscus is torn, pinching it like this between the femur and tibia in the deep flexed position is likely to re-create the patient’s pain (the deep flexion test).
McMurray’s test is very hard to describe without physically demonstrating it on a knee or knee model. The maneuver is a combination of knee flexion, rotation, and angular (varus/valgus) stress. To test the medial meniscus, have the patient lie supine with the lower extremity to be tested flexed 90 degrees at the hip and knee (Figure 1-15). Grasp the patient’s foot with one hand and their knee with the other. Externally rotate the hip joint as far as it will go (this will bring the foot and leg across the midline). Note: do not perform this test on patients with a hip replacement. It can cause dislocation. Now, rotate the tibia by rotating the foot while flexing and extending the knee. The first step (hip rotation) closes the medial joint and pinches the medial meniscus between the tibia and femur. The second step (rotation/flexion-extension) “grinds” the meniscus between the two bones, which will cause medial joint line pain in most patients with a medial meniscus tear. McMurray’s test for a lateral meniscus tear is the same, only the hip is rotated into maximal internal rotation.
If the patient is over 40 years old, I recommend obtaining the series of x-rays used to detect arthritis (described on pages 21 through 26). Why? Consider this example: If the patient has medial bone-on-bone arthritis, they will offer a history of medial joint line pain, and all three of their meniscal tests (medial joint line tenderness, medial pain with deep flexion, and pain with McMurray’s test at the medial joint line) will be positive. Based on the history and physical exam alone, we might incorrectly diagnose this patient with bone-on-bone arthritis as having a medial meniscus tear.
HOW TO SEE A MENISCUS TEAR ON AN MRI SCAN
If you look at one of the meniscus cartilages from above, it looks like a horseshoe, or a “half moon” (see Figure 1-13). In fact, another name for the meniscus is the “semilunar cartilage.” Let’s look at the meniscus on the MRI scan. I recommend looking at the T2-weighted sagittal images; they are the easiest to interpret. These are the dark images that present a cross-sectional lateral view of the knee. This view looks a lot like the views of the knee you see in Figure 1-B. When the meniscus is sectioned the way that it is on these MRI images, the meniscus looks like two triangles facing each other (Figure 1-H). Because meniscus tissue is dark black on a T2-weighted study, the anterior and posterior “horn” of a normal meniscus will each appear as a solid black triangle. The joint fluid appears bright white on the T2 image of an MRI, and, if the meniscus is torn, you will see that bright white fluid in the tear creating a white stripe that penetrates into the solid black meniscus. Just to complicate matters, Mother Nature has thrown in a third type of meniscus image. As we age, it is normal for the meniscus to accumulate fluid in its center. This degenerative finding, also known as myxoid degenerative change, does not indicate that the meniscus is torn. We do not consider the meniscus to be torn unless the white signal in the meniscus tissue actually penetrates through the surface of the meniscus cartilage (Figure 1-I).
Figure 1-H.
The anterior and posterior horns of a meniscus cut in cross-section look like two triangles facing each other.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
