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The Natural History and Tailored Treatment of ACL Injury

Nick A. Evans, MD; Hall F. Chew; William D. Stanish, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 29 - NO.9 - SEPTEMBER 2001


In Brief: The fate of the injured anterior cruciate ligament (ACL) is variable. The spectrum of injury ranges from partial sprain (grade 1 or 2) to a complete disruption (grade 3), which may occur in isolation or in combination with injury to other structures in the knee. Postinjury symptoms of knee instability usually depend on the degree of joint laxity and the athletic demands of the individual. If an ACL injury is left untreated, repeated episodes of subluxation can inflict further intraarticular damage, with an increased risk of developing osteoarthritis. Predicting the outcome after ACL injury is difficult, and treatment should be individualized.

Knee injuries that damage the anterior cruciate ligament (ACL) inflict a spectrum of pathology in various patients. Predicting outcomes can be difficult (1-3). However, careful assessment of the injured knee and the patient to whom it belongs will afford the best treatment options. Treatment selection must be individualized, and the tailored treatment plan may include an initial trial of nonoperative measures.

Prevalence, Mechanism, and Classification

The prevalence of ACL injury in the United States is about 1 in 3,000, and approximately 95,000 new injuries occur each year (4). The largest proportion of these injuries occur during sports that involve deceleration, twisting, cutting, or jumping. ACL injury can occur as a result of excessive valgus stress, forced external rotation of the femur on a fixed tibia (with the knee in full extension), or forced hyperextension.

Acute ACL injuries can be classified by the degree of damage to the ACL (partial or complete disruption) and the presence or absence of damage to other structures in the knee (isolated or combined). Injuries can be visualized and assessed with arthroscopy (normal; figure 1A). Fifteen percent of ACL injuries are partial sprains (grade 1 or 2; figure 1B), whereas 85% are complete disruptions (grade 3, figure 1C) (1,5,6). ACL damage occurs as an isolated injury in only 25% of cases. Combined injuries may involve damage to the menisci (60%), articular cartilage (30%), collateral ligaments (30%), joint capsule, or a combination of such injuries (1,5-7). This spectrum of pathology influences healing and functional outcome.

Anatomy, Function, and Healing Potential

The ACL is approximately 3 cm long, has its origin on the lateral femoral condyle within the intercondylar notch, and inserts into the tibial plateau medial to the anterior horn of the lateral meniscus (8). It functions as a knee-joint stabilizer, and in addition to being the primary restraint to anterior tibial translation, it counteracts excessive rotation and valgus stress.

The ligament consists of an anteromedial and a posterolateral band. The anteromedial band is tighter when the knee is flexed, and the posterolateral band is tighter in extension. When the knee is straight, the secondary restraint action of the hamstrings is minimal, and the posterolateral band provides additional stability.

During physical examination, the anterior drawer test (figure 2) is specific for anteromedial band rupture; the Lachman test (figure 3) and pivot shift test (figure 4) are preferential for a disrupted posterolateral band. All three tests are likely to be positive when the ACL is completely torn (2,6,8). A 5-mm side-to-side difference on KT-1000 arthrometry is a strong indicator of complete ACL disruption (1). A positive Lachman or anterior drawer test with a firm end-point suggests a partial (grade 2) ACL sprain, particularly when the pivot-shift is negative.

The ACL is the fulcrum for knee stability, providing the primary restraint to anterior tibial translation on the femur. It is able to resist a tensile force of 2,000 N. The ligament carries only small loads during normal daily function (20% of its failure capacity), with the highest loads being quadriceps-powered knee extension from 40° to full extension (2).

The poor healing potential of the ACL has been attributed to its "harsh" intra-articular environment (9). In general, the localized hematoma that forms after soft-tissue injury provokes an inflammatory response, and repair occurs by the formation of scar tissue. ACL healing may depend on the integrity of its thin synovial envelope. When the synovial lining remains intact, the hematoma is kept in place, providing a fibrin network for subsequent healing. If the synovial lining is torn during injury, blood dissipates within the joint. Without the formation of a blood clot, soft-tissue repair will not initiate (9). Scar formation may occur in partial ACL tears, but very little local healing is detectable at the injury site in complete ACL ruptures. Instead, a layer of synovial tissue forms over the damaged surface, and the ruptured ends contract (10).

Fate of the Injured ACL

The natural history of a torn ACL is variable. Despite the publication of more than 2,000 scientific articles on the ACL during the last 20 years, certain fundamental issues regarding the fate of the injured ACL remain unclear (2,11). Questions about outcome can be divided chronologically into three phases:

  • Early: Will the ACL heal?
  • Delayed: Will the knee become symptomatic?
  • Late: Will the knee deteriorate?

Thus, when considering the injury's natural history, we must first address the fate of the sprained ACL. Then, if the ligament fails to heal, our concern shifts to the development of symptomatic knee instability. At later stages, intra-articular deterioration of the knee with chronic ACL insufficiency becomes an issue.

ACL healing. The prognosis for a partially torn ACL may be favorable (6,11) if the synovial envelope of the ACL remains intact (9,10). This phenomenon takes place within the early phase (2 to 3 months) following injury.

Although complete ACL ruptures have a less favorable outcome, healing potential does exist, and intra-articular reattachment of the torn ACL can occur. In these cases, the ACL is usually seen scarred onto the posterior cruciate ligament (PCL) (12). However, healing in the form of intra-articular reattachment of the torn ACL does not necessarily ensure knee stability. Adhesions onto the PCL may stretch out with time. Increased stress placed on the secondary restraints causes these structures to lose competence. This temporary apparent stability has been termed the "honeymoon period."

Instability. In the months that follow ACL injury, "functional impairment" becomes the prime concern. The development of symptomatic knee instability after ACL injury is unpredictable; instability rates range from 16% to almost 100% of cases (2). Some patients are disabled for sports, while others appear to have minimal impairment. Such discrepancies may be due to varying degrees of ACL damage, different combinations of knee injury, and the diverse physical demands and expectations of different populations. Functional instability is more likely to occur with combined damage to the meniscus, articular cartilage, and other ligaments.

Deterioration. A knee with ACL laxity is at risk of developing secondary damage and is liable to undergo progressive intra-articular deterioration (1). Approximately half of acute ACL disruptions are associated with meniscus damage. This figure rises to 90% in ACL-deficient knees that are assessed 10 or more years after the initial injury. Acute tears usually involve the lateral meniscus (figure 5), whereas secondary lesions following chronic instability occur more frequently in the medial meniscus. In a similar fashion, the prevalence of articular cartilage lesions (figure 6) rises from 30% in fresh ACL injuries to approximately 70% of ACL-deficient knees at 10 years postinjury (1,5,6,11). Magnetic resonance imaging (MRI) of the acute ACL-injured knee reveals a typical bone bruise pattern in the lateral condyle and tibial plateau. Such lesions are characterized by microfracture of the cancellous bone and fragmentation of the overlying cartilage (13).

Osteoarthritis. The final outcome of such deterioration is joint arthrosis. The prevalence of progression to radiographically detectable osteoarthrosis (OA) in ACL injury ranges from 15% to 65%, and the findings depend somewhat on the length of follow-up (2,5). The reasons for this variability are not fully understood, but mechanical and biochemical changes in the knee are influential. ACL deficiency alters knee biomechanics, and in areas of overload, the articular cartilage may wear down. An alteration in the cytokine profile within the injured knee may facilitate the breakdown of articular cartilage. Additional damage to the meniscus and/or articular cartilage will also worsen the prognosis (14), and one of the goals of treatment is to reduce the risk of secondary damage. ACL reconstruction may protect the integrity of the menisci, but whether it prevents progression to knee OA is unknown (14). Reconstruction of the injured ACL is paramount to the success of surgical repair of associated damage to menisci or other ligaments.

Outcome. Noyes' "rule of thirds" (3) predicts the outcome of symptomatic ACL-deficient knees after a program of rehabilitation, bracing, and activity modification. One third of patients will improve and be capable of recreational activities without symptoms. One third will remain the same, compensating by reducing their activity level. One third will become worse, and probably will require reconstructive surgery. Following rehabilitation, less than 10% of patients return to unrestricted competitive sport. The chance of future episodes of instability and reinjury is 50% or more, but largely depends on the patient's activity level (11). As previously noted, the results of ACL surgical reconstruction are not universally predictable; however, long-term rates of good and excellent results of functional stability, symptom relief, and return to preinjury level of activity are reported to be between 75% and 90% (15).

Selection of Treatment

Without treatment, a complete ACL rupture can result in progressive knee instability, which in turn causes recurrent intra-articular damage and eventual OA (1,5). The fundamental rationale for surgical reconstruction of the disrupted ACL is to prevent this unfavorable cascade (2). However, patient selection for treatment is not straightforward, since not all patients with injured ACLs become symptomatic, and not all knees with chronic ACL insufficiency progress to OA. Thus, not all such injuries warrant surgical reconstruction. Owing to the range of injury severity and the variety of athletic demands encountered, the treatment of ACL injury should be customized to the individual patient. The patient's expectation and treatment preference should also be taken into account.

High-risk factors. Certain characteristics indicate that a patient is at high risk of symptomatic knee instability following ACL injury (1). High-risk patients should be treated with early ligament reconstruction, whereas low-risk patients should be treated with nonsurgical modalities. The patient's risk depends on age, sports activity, and degree of joint instability. High-risk features include:

  • Complete ACL disruption (grade 3 injury),
  • Combined injury: meniscus and/or other ligament tear,
  • High-demand sport: level 1 (jumping, pivoting, and cutting), and
  • Young age of patient.

Treatment plan. Isolated and partial lesions are amenable to conservative treatment, whereas total ruptures, combined with damage to menisci, capsule, or collateral ligaments, are better served by surgical reconstruction. Decision making is based on careful evaluation of the extent of the pathology, with consideration of the patient's level of activity and expectation (figure 7).

Assessment begins by taking a detailed history and performing a careful physical examination. MRI is helpful in confirming the diagnosis and in identifying associated injuries, including bone bruises, torn menisci, collateral ligament injury, and capsular damage. In high-risk patients, we perform knee arthroscopy and examination under anesthesia when full range of knee motion has been restored. If the injury is confirmed as a complete ACL tear, we proceed to ACL reconstruction.

If, on the other hand, a partial ACL injury is found, conservative treatment is chosen. This group of patients is prescribed a specific program of rehabilitation that includes muscle strengthening, proprioceptive training, and protective bracing. Following this program, patients who experience persistent symptoms of knee instability may require ACL reconstruction (1).

The Ideal Natural History Study

The fate of the ACL-injured knee treated without surgery requires further investigation to clarify current uncertainties. The ideal natural history study would follow patients with ACL injury prospectively over a long period without intervention, then finally and definitely assess the patients' status objectively, subjectively, and functionally (1,8). Unfortunately, such a study may never be ethically possible in North America.

References

  1. Daniel DM: Selecting patients for ACL surgery, in Jackson DW (ed): The Anterior Cruciate Ligament: Current and Future Concepts. New York City, Raven Press, 1993, pp 251-258
  2. Frank CB, Jackson DW: The science of reconstruction of the anterior cruciate ligament. J Bone Joint Surg Am 1997;79(10):1556-1576
  3. Noyes FR, Matthews DS, Mooar PA, et al: The symptomatic anterior cruciate-deficient knee, part 2: the results of rehabilitation, activity modification, and counseling on functional disability. J Bone Joint Surg Am 1983;65(2):163-174
  4. Miyasaka KC, Daniel DM, Stone ML, et al: The incidence of knee ligament injuries in the general population. Am J Knee Surg 1991;4(1):3-8
  5. Daniel DM, Stone ML, Dobson BE, et al: Fate of the ACL-injured patient: a prospective outcome study. Am J Sports Med 1994; 22(5):632-644
  6. Jackson RW: The torn ACL: natural history of untreated lesions and rationale for selective treatment, in Feagin JA (ed): The Crucial Ligaments: Diagnosis and Treatment of Ligamentous Injuries About the Knee, ed 2. New York City, Churchill Livingstone, 1994, pp 485-493
  7. Casteleyn PP, Handelberg F: Non-operative management of anterior cruciate ligament injuries in the general population. J Bone Joint Surg Br 1996;78(3):446-451
  8. Stanish WD: Knee ligament sprains: acute and chronic, in Harries M, Williams C, Stanish WD, et al (eds): Oxford Textbook of Sports Medicine, ed 2. New York City, Oxford University Press, 1998, pp 420-440
  9. Fu FH, Bennett CH, Lattermann C, et al: Current trends in anterior cruciate ligament reconstruction, part 1: biology and biomechanics of reconstruction. Am J Sports Med 1999;27(6):821-830
  10. Murray MM, Martin SD, Martin TL, et al: Histological changes in the human anterior cruciate ligament after rupture. J Bone Joint Surg Am 2000;82(10):1387-1397
  11. Hirshman HP, Daniel DM, Miyasaka K: The fate of unoperated knee ligament injuries, in Daniel D, Akeson W, O'Connor J (eds): Knee Ligaments: Structure, Function, Injury, and Repair. New York City, Raven Press, 1990, pp 481-503
  12. Lo IK, de Maat GH, Valk JW, et al: The gross morphology of torn human anterior cruciate ligaments in unstable knees. Arthroscopy 1999;15(3):301-306
  13. Faber KJ, Dill JR, Amendola A, et al: Occult osteochondral lesions after anterior cruciate ligament rupture: six-year magnetic resonance imaging followup study. Am J Sports Med 1999;27(4):489-494
  14. Shelbourne KD, Gray T: Results of anterior cruciate ligament reconstruction based on meniscus and articular cartilage status at the time of surgery: five to fifteen-year evaluations. Am J Sports Med 2000;28(4):446-452
  15. Harner CD, Giffin JR, Dunteman RC, et al: Evaluation and treatment of recurrent instability after anterior cruciate ligament reconstruction. Instr Course Lect 2001;50:463-474

Dr Evans is an orthopedic sports medicine fellow in the division of orthopedic surgery at Dalhousie University and a staff physician at the Orthopaedic and Sport Medicine Clinic of Nova Scotia, both in Halifax. Mr Chew is a research student in the faculty of medicine at Dalhousie University. Dr Stanish is a professor of surgery in the division of orthopedic surgery at Dalhousie University and director of the Orthopaedic and Sport Medicine Clinic of Nova Scotia. Address correspondence to William D. Stanish, MD, Orthopaedic and Sport Medicine Clinic of Nova Scotia, 5595 Fenwick St, Suite 311, Halifax, Nova Scotia, Canada B3H 4M2; e-mail to [email protected].


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