CHAPTER 20 Anterior Cruciate Ligament Repair

Anterior cruciate ligament (ACL) repair is not a new idea, having first been reported by the Mayo Robinson in 1885.¹ Prior to 1970, little emphasis was given to repairing the ACL. Most techniques centered on repairing extra-articular structures with the idea that a competent ACL was not required for normal knee function. Conservative treatment of ACL tears resulted in poor healing rates and a high incidence of instability.²^,³ Primary repair alone did not improve results.⁴^–⁶ Reasons for this lack of healing potential were thought to be lack of blood clot formation, insufficient blood supply, differences in intrinsic cell migration, impaired growth factor ability, and the effect of synovial fluid on cell morphology.⁷^,⁸

In the 1970s, Marshall and colleagues ⁹ increased interest in repairing ACL tears; their technique used primary suture repair. Good results with the repair of proximal tears were obtained. Two randomized studies²^,³ have shown no difference in functional outcomes between repair and conservative treatment with about one third in each group having residual instability. Subsequent focus centered on reconstruction of the torn ACL rather than repair.¹⁰ With better understanding of ACL anatomy, including ligamentous function and insertion footprint anatomy, interest in repair of the ACL has resurfaced. Recent basic science research¹¹^–¹⁵ looking at growth factors, gene therapy, and tissue-friendly scaffolds has shown promise for future progress in ACL repair.

ANATOMY

The ACL has been described anatomically in two bundles, one anterior medial (AM) and one posterior lateral (PL; Fig. 20-1). Whereas the primary function of the larger anterior medial bundle is to resist anterior translation of the tibia on the femur, the posterior lateral bundle also resists abnormal anterior lateral rotation of the tibia on the femur.

FIGURE 20-1 The two bundles of the ACL, one anterior medial and one posterior lateral.

The ACL is actually made up of many ligamentous fibers, each attaching a specific point on the tibia to a specific point on the femur. As the knee moves back and forth from flexion to extension, there is a cascade of tightening and loosening of these fibers. The anterior medial bundle fibers become tight toward higher degrees of flexion and the posterior lateral fibers become more taught in extension.

This attention to multiple ligamentous fiber attachment sites has led to the concept of ACL femoral and tibial footprints (Fig. 20-2). A goal of preserving or reconstructing attachment sites corresponding to the footprints should more closely restore the natural function of the ACL.

FIGURE 20-2 ACL tibial footprint.

(Courtesy of Dr. Nick Sgaglione.)

The ACL arises from a fossa in front of and lateral to the anterior spine in a footprint that averages 11 mm medial to lateral and 17 mm front to back.¹⁶ Its average length is 38 mm, with a width of 10 mm in its midpoint. It inserts on the posterior medial surface of the lateral femoral condyle. Its blood supply is via the middle geniculate artery and it is innervated by branches of the tibial nerve.

Ruptures of the ACL can be complete or partial. Complete ruptures produce patholaxity, with excessive anterior tibial translation and anterior lateral rotation. The latter produces the common pivot shift of the knee on examination. Partial ruptures can be of the anterior medial or posterior lateral bundles. Anterior medial bundle ruptures allow excessive anterior tibial translation but the pivot shift may be minimal or negative when the posterior lateral bundle is intact. Conversely, ruptures of the posterior lateral bundle may allow excessive anterior lateral rotation and a positive pivot shift while anterior translation remains minimal, with an end point that can be felt on Lachman testing. Careful attention to detail during physical examination is necessary to discern the exact injury.

PATIENT EVALUATION

History and Physical Examination

The history of an acute ACL tear usually involves buckling of the knee with hyperextension, a rapid change in direction, or a direct blow. Often, an audible pop can be heard. Rapid onset of acute pain and swelling occurs, but in partial or incomplete tears swelling may be minimal and pain may subside to the point that the athlete tries to resume play.

Patient relaxation and confidence in the examiner are important for performing a good examination. Pain and muscle spasm are most often present in the acute examination and careful explanation of the process to the patient is vital.

Have the patient lie supine, close to the edge of the examination table. Rest the heel of the patient’s injured extremity just off the edge of the table, with the calf fully supported on the table (Fig. 20-3A). This position will allow about 10 degrees of knee flexion and usually the thigh muscles will relax. Accessing the presence of even a small effusion is easy by gently pushing side to side on each side of the patella. Performing a Lachman test is also enhanced by this position, along with medial and lateral stability (see Fig. 20-3B).