Biomechanics of rotational instability and anatomic anterior cruciate ligament reconstruction

Biomechanics of Rotational Instability and Anatomic Anterior Cruciate Ligament Reconstruction Andrew A. Amis, DSc (Eng),*,† Anthony M.J. Bull, PhD,‡ and Denny T.T. Lie, FRCS Ed* The anterior cruciate ligament (ACL) is the primary restraint to tibial anterior translation (anterior draw). Tibial anterior draw is normally accompanied by a “coupled” tibial internal rotation. Both internal rotation and anterior translation can be increased by rupture of the ACL, resulting in a large movement of the mobile lateral tibial plateau. Arthroscopic ACL reconstruction adequately restores the anterior draw; however, the peripheral structures that are the primary restraints to tibial rotation often are neglected. Recent work has shown that a residual or “mini” pivot shift can remain after successfully restoring the anterior– posterior laxity of the knee. The search for a better restoration of normal kinematics has reawakened interest in double-bundle reconstructions. Although biomechanical studies have demonstrated that this type of reconstruction may better restore the normal kinematics, there is as yet no clinical evidence. Draw testing should now be superseded by kinematics measures of both rotations and translations of the knee with quantified loads to provide objective measures that better assess the efficacy of new surgical techniques. Oper Tech Orthop 15:29-35 © 2005 Elsevier Inc. All rights reserved. KEYWORDS ACL, rotational laxity, measurement, biomechanics, kinematics

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he anterior cruciate ligament (ACL) is the primary restraint to tibial anterior translation (anterior draw), in which the tibia is displaced anteriorly in response to a force applied at a fixed angle of knee flexion. The lack of congruency of the tibiofemoral joint also allows secondary movements, principally tibial internal– external rotations, in response to relatively low torques applied. In general, the lateral compartment is more mobile than the medial because of the difference in the capsular attachments of their menisci. This tendency is accentuated by weight-bearing activity because the medial tibial plateau is concave, so the joint load stabilizes the medial femoral condyle, whereas the lateral plateau is convex in the sagittal plane and so is inherently less

*Department of Mechanical Engineering, Imperial College London, London, United Kingdom. †Department of Musculoskeletal Surgery, Imperial College London, London, United Kingdom. ‡Department of Bioengineering, Imperial College London, London, United Kingdom. Supported by the Arthritis Research Campaign, a charity based in Chesterfield, UK. Dr. Lie was supported by the Singapore Government. Address reprint requests to Andrew A. Amis, DSc (Eng), Department of Mechanical Engineering, Imperial College London, London SW7 2AZ, United Kingdom. E-mail: [email protected]

1048-6666/05/$-see front matter © 2005 Elsevier Inc. All rights reserved. doi:10.1053/j.oto.2005.10.009

stable. This means that there is more movement of the lateral compartment than of the medial compartment under most loading combinations. The result of this is that tibial anterior draw is normally accompanied by a “coupled” tibial internal rotation (Fig. 1). (A “coupled” movement occurs automatically in response to a load acting in another degree of freedom.) Similarly, a posterior draw force causes both tibial posterior translation, plus a coupled tibial external rotation. Rupture of the ACL allows the proximal tibia visibly to translate anteriorly more than normal in response to an anterior draw test. This movement often is accompanied by increased mobility of the lateral aspect of the tibial plateau, which is an increased coupled tibial internal rotation. This has led to the label “anterolateral rotatory instability” (ALRI).1 This laxity pattern may be because of the fact that the ACL often is injured in combination with other structures. However, a notable evolution has been the introduction of arthroscopic methods for ACL reconstruction: the surgeon now obtains an intimate view of the femoral intercondylar notch, but perhaps at the expense of losing sight of the peripheral structures, and their contribution to controlling knee laxity. Thus, the pioneering efforts to control ALRI by using peripheral procedures2-4 have fallen from favor, leaving the emphasis on endoscopic intraarticular procedures. 29

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Figure 1 Anterior draw produces combined anterior translation plus coupled internal rotation due to more mobile lateral compartment.

Clinical reviews have found that failure of ACL reconstruction is caused most commonly by malplacement of the tunnels for the grafts. This led to studies of ACL fiber length changes and, hence, to the concept of “isometry.” If a reconstruction is isometric, that means that the distance between the attachment points of the graft to the femur and tibia remains constant when the knee is moved in flexion-extension. Isometricity is only a theoretical concept because the compliance (ie, low stiffness) of soft tissue means that isometry will be lost with any small change of loading on the knee. However, the attraction of this simple concept led to the widespread adoption of “isometric” graft tunnel placement. The corollary of this has been a neglect of the natural anatomy and physiology of the complex structure of the ACL. Thus, it should not be a surprise to find that endoscopic ACL reconstructions do not restore normal anatomical knee behavior. This article is concerned primarily with rotational stability of the knee and the role of “anatomic” ACL reconstructions. These attempt to reproduce the macroscopic arrangement of ACL fibers more closely than does a simple patellar tendon or hamstrings tendons graft, and thus is going back to the anatomical basics. The aim of this work is to address some of the limitations of the conventional single-bundle endoscopic reconstructions that have come to light recently, particularly relating to residual tibial rotational laxity.

Tibiofemoral Laxity in the Intact and Ligament-Damaged Knee Although the knee has six degrees-of-freedom of movement, this article is concerned primarily with normal and abnormal movement of the tibia beneath the femur, which disturbs the tibiofemoral joint articulation, and so the situation is simplified to consideration of just two of these: anterior–posterior (AP) translation plus internal– external rotation. These occur in the transverse plane, corresponding to the tibial plateau. The other possible degree-of-freedom in this plane is mediallateral translation, but that is of minor clinical importance even after major knee injury. The diagnosis of ligament damage follows from identification of increased laxity in a vector that is controlled by that specific ligament. The ACL is known to be the primary restraint to tibial anterior translation, resisting approximately 85% of the force applied across the arc of knee flexion.5

A.A. Amis, A.M.J. Bull, and D.T.T. Lie Therefore, measurement of AP translation has been the principal objective method to quantify tibiofemoral laxity and the pathological increase after ACL injury or reduction after reconstruction. The translation (mm) must be reported at a known anterior draw force (N), because of the low stiffness of the soft tissues that resist. Much data have been published arising from cadaveric and clinical work.5-7 This led to widespread adoption of devices such as the KT1000. Because there is a range of natural laxity in the population, with some intact knees having greater AP laxity than others with ACL deficiency,8 it is not appropriate simply to quote a laxity measurement in isolation: the side-to-side difference is more informative and a difference greater than 3 mm is often taken to be diagnostic of ACL damage.6 If the tibia is free to rotate when it is drawn anteriorly, there is a “coupled” tibial internal rotation and vice versa with posterior draw. This coupled tibial internal rotation has been reported to range from a mean of 3° with 220 N draw force at 20° flexion9 to 10° with 150 N at 90° flexion.10 If the tibia is not free to rotate, but held in neutral rotation, the anterior translation laxity is reduced approximately 30%.5,11 Clinical studies of knee laxity relating to the ACL have not often reported on the rotational mobility of the tibia, but this might change in the light of the recent increase in appreciation of rotational aspects of functional instability. Tibial anterior translation is reduced significantly if the tibia is held in fixed internal or external rotation.5,10,12 This reduction is because of tightness in the peripheral structures, so that they can share the load with the ACL. Tibial external rotation moves the tibial attachment of the medial collateral ligament complex anteriorly; this both tightens and aligns these structures to restrain tibial anterior translation. Similarly, the iliotibial tract and lateral collateral ligament act in tibial internal rotation.5,9 Although it is accepted universally that an isolated ACL rupture allows significantly greater tibial anterior translation,6 the effect on tibial rotation is more controversial. For the intact knee, most studies have reported that rotation laxity is least in the extended knee and increases as the knee flexes.13 The amount of rotation depends on the torque applied. Andersen and coworkers13 found a total range of rotation laxity varying from 28° at 10° knee flexion to 42° at 90° flexion, in response to ⫾6 Nm. Very similar results were demonstrated by Lane and Daniel.14 The tightening in extension occurs because all capsular and ligamentous structures attaching to the femur posterior to the epicondyles are nonisometric and tighten in knee extension,15 especially the posteromedial capsule with its oblique fibers,16 the posterior capsule, and the arcuate ligament complex. There have been differing reports about the effect of isolated ACL damage on tibial rotational laxity. That is partly because ‘damage’ might mean an isolated transection in an experiment, or a traumatic rupture, that is accompanied by stretching or rupture of other structures. A large increase in tibial rotation laxity followed an experimental ACL rupture caused by anterior draw at 90° flexion: from 31° to 44°, in response to ⫾3 Nm torque at 90° knee flexion.10 Andersen and Dyhre-Poulsen13 found a small but statistically signifi-

Biomechanics of rotational instability and anatomic ACL reconstruction cant increase in rotational laxity after isolated ACL transection at 10° knee flexion: from 28° to 31°, but no measurable difference beyond 30° knee flexion. Conversely, Lane and Daniel14 found that cutting the ACL had no significant effect on either internal or external tibial rotation laxity; therefore, they concluded that rotational instability is not a major factor after isolated ACL rupture. Although it is easy to produce an isolated ACL rupture in vitro by means of an anterior draw of the flexed knee (rupture at a mean of 673 N at 15 mm anterior translation),10 that is not a typical real-life injury mechanism. The self-releasing design of ski bindings reflects the rotational component of many real ACL injuries; it is hard to imagine the ACL being stretched to failure in this mode without also affecting the peripheral structures. The extraarticular structures are the primary restraints to tibial rotation laxity,17,18 and so they are usually involved in ACL injuries.19 The lateral compartment is most important in tibial rotation laxity: it is more mobile than the medial, and the ACL attaches here. Lipke20 found that isolated cutting of the ACL led to a significant increase in tibial internal rotation; if he then also cut the lateral collateral ligament and/or the posterolateral capsular structures, there was a further significant increase in internal rotation. Conversely, cutting the posterolateral structures first, with the ACL intact, there was not a significant increase in internal rotation. Interestingly, complete transection of the anterolateral capsule, as far back as the lateral collateral ligament, had no effect on either internal or external rotation laxity. Thus, Lipke20 concluded that, for a pathological increase of tibial internal rotation, the ACL must be ruptured. In contrast to the findings of Lipke, Wroble et al21 found that cutting the anterolateral structures, including the iliotibial tract, led to a significant increase in tibial internal rotation in the ACL-deficient knee. Different findings have been published about coupled tibial rotation after ACL rupture: Amis and Scammell10 found that coupled tibial internal rotation increased from 10° intact to 13° after injury; conversely, Fukubayashi and coworkers11 found that coupled internal tibial rotation disappeared after cutting the ACL. This difference may reflect the consequences of an ACL rupture versus an isolated transection. The literature reviewed above suggested that tibial rotational laxity is not increased greatly by ACL deficiency; this conflicts with the widely-held impression that this injury leads to rotatory instability, with the lateral aspect of the tibia moving anteriorly much more than normal. This divergence may be explained by reference to the mechanics of tibial rotation. In the intact knee, the axis of tibial internal-external rotation crosses the joint space approximately at the center of the tibial plateau: Kaneda and coworkers22 located it at the medial tibial spine, whereas Wang and Walker23 reported that it was at the lateral tibial spine. Because it is close to the center of the tibial plateau, tibial internal rotation will cause the lateral aspect of the tibial plateau to move anteriorly, and the medial aspect to move posteriorly, by a similar distance (Fig. 2A). After ACL injury, the axis of rotation passes across the joint approximately 12 mm medial to the normal position, through the center of the medial plateau.24 This means

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Figure 2 Axis of rotation of the tibial plateau. (A) Intact ACL. The axis of rotation is central and therefore internal rotation causes the lateral tibial plateau to move anteriorly and the medial tibial plateau to move posteriorly by similar amounts. (B) Deficient ACL. The pathological axis of rotation is medial; therefore, tibial internal rotation causes a coupled anterior translation and magnifies the movement of the lateral compartment.

that the lateral aspect is further from the axis, so the same angle of tibial rotation will cause the lateral aspect to move further anteriorly (Fig. 2B). When this is added to the increased tibial anterior translation that follows ACL injury, possibly with some increase in the coupled rotation too, there is a significantly greater anterior movement of the lateral tibia than normal. A similar effect is caused by combined rupture of the ACL with the medial collateral ligament: the medial tibial compartment is freed, so the axis of tibial rotation then shifts laterally, leading to anteromedial rotatory instability.12 Because the axis of tibial rotation is close to the center of the tibial plateau, it is also close to the line of action of tension in the ACL. Therefore, the ACL is at a mechanical disadvantage for controlling tibial rotation and is only a secondary restraint, whereas the peripheral structures are well-placed and are the primary restraints.23,25 Wang and Walker23 also reported that tibial rotation laxity was reduced 80% after imposing a tibiofemoral joint load of 1 kN (approximately 1.3 body weight).

“Dynamic” Knee Stability Testing: The Pivot-Shift Although instruments such as the KT-1000 have been used to provide objective measurements of tibial anterior translation laxity, they do not provide information about rotational

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Figure 3 Reduction of the lateral tibial plateau during the pivot shift. Flexion of the tibia allows the iliotibial band to externally rotate and posteriorly reduce the lateral tibial plateau.

laxity. Furthermore, it is accepted that these laxity measurements do not correlate with the patients’ functional symptoms of instability, or “giving-way.” The most widely used “dynamic” test is the pivot-shift test, which correlates with instability symptoms,26 reduced sports activity,27 articular cartilage damage, and meniscal damage.28 The pivot-shift is fundamentally a sudden movement of the proximal tibia from one state of equilibrium to another in a bi-stable situation: it may be stable while subluxed or reduced.29 When the knee is tested by flexing from an extended posture, with a valgus moment applied simultaneously, the lateral tibial plateau gradually subluxes anteriorly and then suddenly reduces.30 If the knee is tested by extending it from a flexed starting posture, the lateral tibial plateau remains in the correct anatomical articulation until it suddenly subluxes anteriorly, when the knee is approaching extension.31 The sudden movement of the lateral tibial plateau is caused by the changing direction of the tensions in the iliotibial tract:32 when the knee is flexed to the point of reduction, this tension has a posteriorly-acting component, that is an external rotation effect, sufficient to pull the convex lateral tibial plateau under the convexity of the femoral condyle to its reduced position (Fig. 3). Because the lateral compartment usually moves more than the medial during the pivot-shift test, the movement normally occurs around a medial axis. It has been reported that injury to the medial collateral ligament makes it more difficult to elicit the pivot-shift.32 A major problem with the pivot-shift is that it is extremely variable, both between examiners and between individual knees. Clinical observation shows that there are differing

A.A. Amis, A.M.J. Bull, and D.T.T. Lie strategies used to elicit the sudden shift of the tibia, with various levels of speed and loading. This was shown clearly by repeated examinations of a single cadaveric knee by the members of the International Knee Documentation Committee (IKDC).33 It can be speculated that the examiners were continuously adjusting the loads imposed while the knee was moving, using tactile feedback, to precipitate the sudden shift. The extreme sensitivity to loading has been demonstrated experimentally.34 Variations also occur between knees: Bull and coworkers35 showed a series of measurements performed under anesthesia, by a single surgeon, before and after ACL reconstruction. This showed (Fig. 4) that some knees had pivot-shifted around a medial axis, as described above, but some moved primarily in posterior translation, as the tibia reduced, and others moved by rotation without significant translation. So far, nobody has measured the forces during clinical pivot-shifts, and there is no way to standardize this test in the clinic. The best approach so far has been a subjective grading system.36 It is clearly desirable to develop a standardized method for imposing a pivot-shift and a clinically appropriate method for measuring the kinematics, so that results may be compared objectively between reconstruction methods, between centers and between surgeons.

Rotational Laxity and ACL Reconstruction When the kinematic data relating to the nine reconstructed knees in Figure 4 was analyzed further, it was found that 6 had some remaining trace of a pivot-shift, at the arc of knee flexion where it had occurred presurgery: 2 had traces of rotation, 2 of posterior translation, and 2 had traces of both components. This remaining “mini-pivot,” shown in Figure 5, often is felt by examining surgeons (sometimes calling it a “pivot-glide”) but has not been documented before. Nordt and coworkers9 noted that this combination of residual translation and rotation laxities may represent a pathologic condition for the knee, even in the presence of gross stability. Recent work by the authors in vitro has found that a conventional endoscopic ACL reconstruction, using a single patellar tendon graft, often left a residual rotational laxity: increasing the graft tension would abolish any difference in anterior translation laxity, but the rotation would not return exactly to normal. When the same cadaveric knees were subjected to a pivot-shift test, there would be a “mini-pivot,” with transient rotation and translation of the tibial plateau. This also showed up clearly by producing simultaneously a sudden increase in the graft tension recording. Awareness of this deficiency of conventional ACL reconstruction methods has led to a search for better methods. The search for isometry led surgeons to place the ACL graft high in the femoral intercondylar notch, perhaps at the 11 o’clock position in a right knee.37 This is not anatomical, the ACL being attached primarily to the sidewall of the notch. Simply moving the graft tunnel to a more oblique position has led to improved restoration of internal rotation laxity.38 However,

Biomechanics of rotational instability and anatomic ACL reconstruction

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Figure 4 Different pivot shifts—single experienced examiner, 9 knees. Top, left: translation without rotation; top, right: rotation without translation; others: combined components.

the search for better restoration of normal kinematics has reawakened interest in double-bundle reconstructions. The double-bundle reconstruction is intended to provide a closer return to the normal structure and function of the ACL. The ACL is often described as having anteromedial and posterolateral fiber bundles. These are not real anatomical structures, but can be created by splitting the ACL into 2 regions of interest. It can then be shown that they have different functions. Thus, although isometric reconstructions have recreated the anteromedial bundle, it has been shown39 that it is the posterolateral bundle that is the primary restraint to anterior draw force when the knee is close to extension (that is the functional posture), whereas the anteromedial bundle is the primary restraint in the flexed knee. Different procedures have used either 140 or 2 tibial tunnels, with double strands passing to 2 femoral tunnels, or to

1 tunnel plus one bundle passing “over the top” of the lateral femoral condyle.41 The double-bundle reconstruction was shown to restore tibial anterior translation laxity better across the range of knee flexion than did either of the single-bundle reconstructions, that were either over the top or at the center of the femoral ACL attachment. More recently, it has been shown that the tensions in each of the bundles of a doublebundle ACL reconstruction reflect the contributions of the natural ACL bundles to resisting anterior draw shown above, and that the double-bundle graft may restore rotational laxity better than does a single-bundle reconstruction.42

Future Developments At the time of this writing, there is intense interest in the double-bundle ACL reconstruction. However, there is no

Figure 5 Residual pivot shift after ACL reconstruction: the “shift” is a sudden posterior reduction with simultaneous external rotation. A normal knee does not show this characteristic.

A.A. Amis, A.M.J. Bull, and D.T.T. Lie

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Figure 6 System for measurement of the envelope of laxity of the knee. 14. 15.

clinical data yet to suggest that the double-bundle yields better knee function than does conventional single-bundle surgery.43 Some basic knowledge is still needed, including the best locations for the graft tunnels and the best tensioning protocols. The double-bundle ACL reconstruction appears to be an ideal use for orthopaedic robotic surgery, which can give greater accuracy for drilling position than hand tools. Better methods are needed to evaluate knee laxity, ideally leading to objective and reproducible pivot-shift testing, with controlled loads and motions. Although this is difficult, it is known that the pivot-shift involves simultaneous tibial translation and rotation, and the authors are developing a system that can apply both an anterior-posterior draw force and an internal-external tibial rotation torque simultaneously to the moving knee (Fig. 6). This leads to “envelopes of laxity” across the range of knee flexion, with combined loading such as anterior draw plus internal rotation, attempting to elicit the movement associated with ALRI and the subluxed position in the pivot-shift test. It is only with more sophisticated clinical evaluation tools that the surgeon will be able to explore the more subtle aspects now needed to tackle the weaknesses of conventional ACL reconstruction, that have themselves come to light from the use of more advanced multi degree-of-freedom instrumentation.

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