Nonsurgical Repair versus Surgical Repair

Ligaments can be repaired surgically or allowed to heal conservatively without surgery, depending on the degree of injury and involvement of supporting tissues. Investigators have shown that untreated ligaments heal by way of scar tissue proliferation rather than true ligament regeneration.⁸ Untreated ligament tears are biochemically inferior, possessing a large portion of type III immature collagen, and generally are not healed even at 40 weeks after injury.⁸

The following is a list of grades of injury occurring to ligament tissue. They are graded by severity:

Grade I and II ligament sprains are most common, with only 15% of all knee sprains classified as grade III.³ Generally, grade I and II ligament sprains can be treated with protective bracing and comprehensive and progressive rehabilitation with appropriate strengthening to provide dynamic muscular support. With grade I and II ligament sprains of the knee (ACL, MCL, posterior cruciate ligament [PCL], and lateral collateral ligament [LCL]), good to excellent results can be anticipated in 90% of those cases treated nonsurgically.²

Surgical repair of a grade III sprain frequently involves repair of associated tissues. Cartilage (menisci) and MCL-, LCL-, or PCL-related injury often is seen with primary ACL grade III injury.

Repair versus Nonrepair

The decision to surgically repair a torn ligament is based on several intrinsic and extrinsic factors. The most clinically relevant example is to contrast the differences between tears of extraarticular MCLs with those of intraarticular ACL tears. Not only must the severity of injury (grade) be considered, but also the anatomic location (biomechanical influences) and vascular supply.

By virtue of its extracapsular anatomy, the MCL provides for a greater periarticular vascular response and the ability to protect the ligament from unwanted forces (e.g., varus, valgus, and internal and external rotation), and allows for an appropriate environment to stimulate healing and propagation of motion, collagen synthesis organization and orientation, proteoglycan concentration, and joint function. Therefore all three distinct grades (grades I, II, and III) of isolated MCL tears appear to heal uneventfully without surgical repair. Even though a fibrous repair gap may exist between torn ends of the ligament, resulting in inferior mechanical resistance to tensile loads, the greater cross-sectional area of the healed ligament provides for biochemical properties (e.g., ultimate tensile load to failure) that more closely resemble an uninjured ligament.²⁴

Conversely, the relative pristine environment of the ACL is not conducive to intrinsic repair. In addition, the difficulty of protecting the injured ACL from unwanted deforming forces by using commercial or custom braces contributes to and maintains a high-stress force environment of the ACL that limits healing.

Effects of Immobilization

Immobilization, surgery, injury, and rehabilitation of ligaments must take into consideration not only the healing response of the ligament itself, but also that of the ligament–bone interface. Stress deprivation of the ligament and ligament–bone complexes resulting from prolonged immobilization after injury or surgery can have significant and profound negative effects. Joint stiffness after immobilization is related to adhesion formation, active shortening of dense connective tissue (ligament),and decreases in water content.² Studies show a gradual deterioration in ligament strength, loss of bone, weakening of cartilage and tendons, significant muscle atrophy, and negative effects on joint mechanics after periods of immobilization (Box 8-1).¹ Immobilization also affects ligament–bone complexes. Studies report that loss of bone directly beneath the junction of ligament and bone reduces the strength of both the insertion site and entire ligament–bone complex.¹⁵

Rigidly immobilized joints produce chemical and morphologic changes in ligaments 2 and 4 weeks following injury, respectively.⁹ After 8 weeks of immobilization, ligaments lose 20% of their weight; significant atrophy results, and marked infiltration of periarticular connective tissue is observed surrounding the ligament.⁹ Although immobilization may be needed to promote healing of damaged tissues, the extended use of rigid immobilization should be limited. As an alternative, limited range of motion braces (Fig. 8-1) can be used to protect healing structures and decrease unwanted external forces, as well as allow for progressive motion of involved joints to minimize the negative effects of immobilization.

The biochemical, histochemical, and morphologic changes that occur in ligament and dense connective tissue in response to immobilization are related to the length of time tissues are immobilized. In addition, both structure and mechanical function of ligament substance, as well as ligament–bone insertion complexes (direct insertion and indirect periosteal insertion with Sharpey’s perforating fibers), are significantly affected in response to the quality and duration of immobilization.

The effects of immobilization on dense connective tissue have been described by Cummings and Reynolds⁵ as follows: Following only 2 weeks of immobilization, animal studies revealed increased GAG synthesis and concentration, decreased water content, thickening of the joint capsule and ligaments, adaptive muscle shortening and adhesion formation of unopposed articular surfaces. After 4 weeks of immobilization, the biochemical and morphologic changes become more pronounced, with a reduction of GAGs, fissures in articular cartilage, increased ligament stiffness, and decreased capsular remodeling. After 6 weeks of immobilization, joint mobility becomes significantly limited, with thickening noted in the joint capsule, ligaments, and cartilage and decreased ligamentous compliance. In summary, joint immobilization causes a progression of dense connective tissue remodeling, resulting in joint stiffness.

During the first 2 weeks, adaptive muscle shortening appears to be the primary limiting factor in joint mobility. As immobilization extends to 4 weeks, changes in GAG synthesis and water concentration become more pronounced, resulting in a loss of normal fiber lubrication, spacing, and connective tissue disorganization. As the immobilization period approaches 6 weeks, morphologic and biochemical changes become more evident as the dense connective tissue remodels in a shortened position.²⁴

Specifically, immobilization causes more pronounced mechanical and biochemical changes in ligament–bone complex insertion sites compared with ligament substance alone. Generally the area of bone directly beneath the ligament–bone insertion site becomes osteoporotic with osteoclastic activity, resulting in pronounced bone resorption, loss of cortex, and reduced strength of the entire ligament–bone insertion complex.²⁴

Exercise

As stated, stress deprivation of ligaments, because of immobilization, results in atrophy.8,9,16,18,25 Conversely, motion, stress, and general physical activity prescribed for healing ligaments produce hypertrophy and increased tensile strength.^2,9 Research shows that ligament and ligament–bone complex strength is related to the mode and duration of exercise used during rehabilitation.² Tipton²³ has shown that endurance types of exercise are more effective in producing larger diameter collagen than nonendurance types of exercise. In addition, the long-term detrimental effects of prolonged immobilization on ligament–bone insertion sites are reversible.² In fact, the effects of mobilization and exercise are seen 4 months to 1 year after immobilization.²

Continuous Passive Motion

Motion, exercise, and protected progressive stress can influence and determine the degree and type of healing that occur after trauma and subsequent immobilization.¹⁷ Studies have demonstrated that healing is dramatically different in immobilized joints compared with those moved passively through limited motion.¹⁰ Gelberman and colleagues¹⁰ have shown that joints moved passively have well-organized, longitudinally oriented collagen fibers in which no adhesions are present. Conversely, joints that were immobilized demonstrated scar tissue and adhesions.

The concept of early protected motion applied to healing soft tissues has resulted in the development of a technique termed continuous passive motion (CPM) (Fig. 8-2). CPM is used in the treatment of the following: knee joint contractures; postoperative ACL reconstructions; joint effusions; knee, elbow, and ankle fractures (after immobilization); joint arthrosis; and total knee arthroplasty.¹⁴ Early motion after surgery or immobilization acts to enhance and facilitate connective tissue strength, size, and shape; evacuate joint hemarthrosis (bloody effusion within the joint space); improve joint nutrition; inhibit adhesions; initiate normal joint kinematics; reduce articular surface changes; and minimize other deleterious effects of prolonged immobilization.¹⁴ With postoperative ACL reconstruction, no stretching out of the graft occurs when CPM is used.^4,6,17,20 CPM can be used postoperatively; applied in the operating room; or be done a few days after surgery, immediately upon cast removal, or during the early phases of rehabilitation.

CPM devices have been designed for use on many body parts.¹⁴ The knee is the most common, with the ankle, shoulder, elbow, wrist, hand, and hip joints also benefiting from CPM. The CPM machine is calibrated in cycles per minute and degrees of motion. Progressive increases in the cycle mode and degrees of motion are made gradually so as not to initiate pain or increase the time necessary for healing.

CPM usually is used in conjunction with other agents to reduce swelling and pain. Among these are ice packs, oral or intravenous analgesics, antiinflammatory medications, transcutaneous electrical nerve stimulation (TENS), and joint compression bandages.

Although CPM may be helpful to decrease postoperative pain following ACL reconstruction, systematic reviews suggest that there is no substantial advantage to using CPM, and no difference in long-term outcomes. It is recommend as an adjunct rather than a replacement for a postoperative exercise program.21,27

Practical Considerations

The time constraints and healing mechanics of ligaments are well documented.2,3,8,13,15,16,22,25,28 Careful consideration must be given to the progression of therapeutic exercises and functional activities for patients with ligament injuries. Usually the absence of pain and swelling is an exceedingly poor indicator of healing tissue. With an ACL reconstruction, pain and swelling normally subside within a few weeks, but return of functional joint motion requires a couple of months. Strength values gradually increase, with muscle hypertrophy following slowly.

As the outward clinical signs point to healing, the ligament, being a dynamic tissue, continues to remodel and mature for up to 1 year. Protection of the joint is critical during healing. Functional knee braces with range-limiting devices can have a protective effect for MCL injuries, however no evidence exists that supports the routine use of functional bracing following ACL reconstruction.26,27 Initiating progressive resistance exercises after knee ligament injury or surgery, while maintaining joint protection, can be challenging. Placing the resistance (weight) above the joint line during straight leg raises (Fig. 8-3) after ACL surgery can be the first phase of progressive resistance while protecting the healing ligament and retraining quadriceps activation.

To strengthen hip adduction with an MCL sprain, resistance initially is applied above the knee joint line so as not to overstress the healing MCL (Fig. 8-4). As the time constraints of healing allow, progressive strengthening of the adductors can involve loading the joint more distally, if joint protection is applied. Awareness of the time necessary for healing and duration of immobilization after trauma, weight bearing status, and degree of injury guide the physical therapist assistant (PTA) in making clinical recommendations about the progression of exercise and the placement of force during rehabilitation.

Developing a progressive therapeutic exercise and functional activities program with ankle sprains is similarly challenging. Generally, a grade II anterior talofibular (ATF) ligament sprain does not produce significant pain or functional limitations after a few weeks of conservative treatment involving splinting, crutch walking (non–weight bearing progressing to full weight bearing), ice, compression, and elevation. The PTA should protect the ligament for many weeks after injury because the process of ligament healing occurs slowly (Fig. 8-5).

Encouraging weight bearing as soon as tolerated, while protecting the joint, helps to establish normal joint kinematics and gait. Protecting the ligaments from further stress not only involves external bracing, but more importantly, includes avoidance of motions that place unwanted force on the healing ligaments. For example, the ATF ligament of the ankle is stressed with plantar flexion and inversion. To protect the ligaments, these two motions should be avoided during the early (postacute) and middle phases of rehabilitation.

Early protected motion is encouraged after ligament injury, repair, or immobilization, but caution should be taken to avoid overstressing the ligament or duplicating motions that place unwanted strain too soon after injury. The acute and postacute phases of rehabilitation after ligament injury or repair usually involve pain management techniques, swelling reduction, muscle reeducation (isometric muscle contraction and functional muscle stimulation), CPM, active range of motion, ligament protection devices via range-adjustable bracing, and weight bearing gait maneuvers with crutches as needed. During this early phase of recovery, it is particularly important to avoid excessive motions that may disrupt the intentional scar formation needed for joint stability. The degree of motion, direction of forces, and velocity of joint movement applied during this early postacute phase must be joint specific, functional, and protected. For example, with a cruciate ligament sprain, movements that are allowed include knee flexion and extension but no rotary or torque-producing motions. After an MCL sprain, knee flexion and extension motion can be initiated in the postacute phase (within limits); however, no valgus stress should be applied. As stated, the reason for ligament protection, maintenance of joint stability, and improved motion is that collagen fiber growth and parallel alignment are stimulated by early tensile loading within the normal physiologic range of the healing ligament.

Table 8-1 outlines the stages of ligament healing and subsequent therapeutic interventions that enhance the healing of ligament tissues.