Explain the body’s chemical, metabolic, permeability, and vascular changes that occur as a result of trauma.
Explain how different joint structures respond to the inflammatory process.
Summarize the effect that immobilization has on muscle, periarticular connective tissue, articular cartilage, ligaments, and bone.
Describe the sequelae of events that result in synovitis.
Describe the process that can result in arthrofibrosis.
Summarize how muscle, periarticular connective tissue, articular cartilage, ligaments, and bone respond to exercise following a period of immobilization.
Explain the therapeutic benefits of the use of continuous passive motion.
List several ways to help deter the deleterious effects of immobilization on specific body structures.
Describe the mechanism and appropriate use of plasma-rich platelet therapy.
Explain the physiology and rationale for appropriate preparticipation warm-up techniques.
The effects of immobilization on bone and connective tissue have been widely reported in the literature. The evolution from immobilization to implementation of early motion programs has become accepted practice in the orthopedic community. Proper use of specific exercises can accelerate the healing process, whereas lack of exercise during the early stages of rehabilitation can result in long-term functional impairment. Caution must be observed, however, because exercise that is too vigorous can also result in undesired effects on healing tissues. Immobilization initially results in loss of tissue substrate, with subsequent loss of basic tissue components. The reversibility of these changes appears to depend on the length of immobilization.
To understand the body’s response to immobilization and remobilization, its normal reaction to injury must be addressed. The sequence of events that transpire after trauma to a joint can cause cartilage degradation, chronic joint synovitis, and stretching of the joint capsule as a result of increased effusion.
Reaction to injury
Inflammation is the body’s response to injury, and optimally, it results in healing of tissues by replacement of damaged and destroyed tissue, along with associated restoration of function. Repeated injury or microtrauma to a specific region can cause a cumulative effect that results in adverse effects on the joint and its surrounding structures. The inflammatory response is the same, regardless of the location and nature of the injurious agent, and consists of chemical, metabolic, permeability, and vascular changes, followed by some form of repair.
Figure 2-1 illustrates the primary and secondary injuries affiliated with trauma and the associated inflammation and repair processes. Primary injury is the result of trauma that directly injures the cells themselves. Secondary injury (sometimes referred to as secondary hypoxia) is precipitated by the body’s response to trauma. This response includes decreased blood flow to the traumatized region as a result of vasoconstriction, which decreases the amount of oxygen to the injured area. Thus, additional cells die because of secondary hypoxia; these dead cells organize and ultimately develop into a hematoma.
Cell degeneration or cell death perpetuates the release of potent substances that can induce vascular changes. The most common of these substances is histamine, which increases capillary permeability and allows fluid and blood cells to escape into the interstitial spaces. In the noninjured state, plasma and blood proteins escape from capillaries by osmosis and diffusion into the interstitial spaces but are reabsorbed. This homeostasis is maintained by colloids present within the blood system. However, trauma leads to increased capillary permeability as a result of the release of cell enzymes, which allows blood plasma and proteins to escape into surrounding tissues. Concurrently, the concentration of colloids greatly increases in the surrounding tissues, thus reversing the colloidal effect. Rather than the colloids pulling fluid back into the capillaries, the presence of colloids outside the vessels causes additional fluid to be pulled into the interstitial tissues with resultant swelling and edema.
The body’s reaction after injury is to mobilize and transport the defense components of the blood to the injured area. Initially, blood flow is reduced, which allows white blood cells to migrate to the margins of the blood vessels. These cells adhere to the vessel walls and eventually travel into the interstitial tissues. When in the surrounding tissues, the white cells remove irritating material by the process of phagocytosis. Neutrophils are the first white blood cells to arrive, and they normally destroy bacteria. However, because bacteria are not usually associated with athletic injuries, these neutrophils die. Macrophages then appear and phagocytize the dead neutrophils, cellular debris, fibrin, red cells, and other debris that may impede the repair process. Unfortunately, destruction of the neutrophils results in the release of active proteolytic enzymes (i.e., enzymes that hasten the hydrolysis of proteins into simpler substances), which can attack joint tissues, into the surrounding inflammatory fluid. Although this is the natural response of ridding the body of toxic or foreign material, prolongation of this process can damage surrounding joint structures.
After the inflammatory debris has been removed, repair can begin. Cleanup by macrophages and repair often occur simultaneously. However, for repair to occur, enough of the hematoma must be removed to permit ingrowth of new tissue. Thus, the size of the hematoma or the amount of the exudate is directly related to the total healing time. If the size of the hematoma can be minimized, healing can begin earlier and total healing time is reduced.
The primary role of the rehabilitation specialist during the acute phase of injury is to decrease inflammation and prevent damaging secondary effects, such as decreased range of motion (ROM), decreased muscle strength, and prolonged edema. The presence of inflammation must be regarded with caution because too much activity can prolong the inflammation and increase pain. Inflammation is controlled with ice, rest, and electrical stimulation, such as electrical galvanic stimulation or transcutaneous electrical stimulation. Secondary effects are prevented with gentle ROM exercises, isometrics, and avoidance of maladaptive postures or gait patterns.
Response of Joint Structures to Injury
As a result of the inflammatory process, each joint structure responds differently to injury ( Fig. 2-2 ). The reaction of the synovial membrane to injury involves the proliferation of surface cells, an increase in vascularity, and gradual fibrosis of subsynovial tissue. Posttraumatic synovitis is not uncommon after most injuries. Continued mechanical irritation can produce chronic synovitis, which results in the reversal of normal synovial cell ratios. Changes in synovial fluid occur as a result of alterations in the synovial membrane. Cells are destroyed as a consequence of the synovitis; white blood cells ingest the lysosomes and proteolytic enzymes. This ingestion and the subsequent death of white blood cells in the transudate result in the further release of proteolytic enzymes. The overall consequence is spawning of a vicious inflammatory cycle, which can keep reactive synovitis active for some time, even without further trauma ( Fig. 2-3 ). As chronic posttraumatic effusions occur, changes in the synovial membrane can continue, with progressing sclerotic alterations as a sequela. If conservative treatment consisting of antiinflammatory medications, rest, aspiration, and application of cold does not relieve the symptoms, synovectomy may be necessary.
Articular cartilage lesions within a synovial joint or meniscal lesions within the knee, whether acute or chronic, are invariably accompanied by increased synovial effusion. Surgical correction is often required to prevent secondary damage to other joint structures as a result of prolonged inflammation. After the problem has been corrected, the synovial irritation usually subsides. If, however, the problem is left uncorrected, tissues not injured by the original trauma can be damaged from the prolonged inflammation, thus resulting in progressive degradation of the synovial membrane.
Fortunately, when the inflammation begins to abate, synovial tissue can regenerate remarkably well, an ability that possibly stems from its excellent blood supply and origin. Synovium regenerates completely within several months into tissue that is indistinguishable from normal tissue. Acute and chronic synovitis directly affects the amount and content of synovial fluid produced. Synovitis can result in an increased protein level within the synovial fluid. In addition, chronic synovitis can cause a reduction in the viscosity of synovial fluid and a decrease in the concentration of hyaluronic acid. The concentration of hyaluronic acid is directly related to synovial fluid viscosity. Minor joint trauma results in no change in either the concentration or molecular weight of hyaluronic acid. As the severity of trauma increases, however, the concentration of hyaluronic acid decreases to levels below normal, and when the inflammatory process becomes sufficiently disruptive, joint-lining cells fail not only to maintain the hyaluronic acid concentration but also to maintain normal polymer weight.
Hemarthrosis, or bleeding into a joint, can have an effect on joint structures. When a vascular joint structure is damaged, the synovial fluid has a lower sugar concentration, blood clots can be found in the synovial fluid, and fibrinogen can be detected as a result of bleeding into the joint. Although the average time for natural evacuation of a hemarthrosis is approximately 4 days, it depends on individual factors, such as the magnitude of injury, the nature of the structures injured, and the individual’s activity level after injury. The presence of blood in a joint has a damaging effect on articular cartilage, with a potentially irreversible decrease in proteoglycan synthesis. In addition, younger individuals with hemarthrosis have been shown to have a greater decrease in proteoglycan synthesis and a slower return to normal rates of synthesis.
The absorption rate of solutions from the joint space is inversely proportional to the size of the solutes: the larger the molecules, the slower the clearance. Clinically, absorption from a joint is increased by active or passive ROM, massage, intraarticular injection of hydrocortisone, or acute inflammation, whereas the effect of external compression is variable.
The reaction of the joint capsule to injury is similar to that of the synovial membrane. If the inflammatory process continues, the joint capsule eventually becomes a more fibrous tissue, and effusion into the joint cavity can lead to stretching of the capsule and its associated ligaments. The higher the hydrostatic pressure and volume of effusion, the faster the fluid reaccumulates after aspiration. Conversely, a significant rise in intraarticular hydrostatic pressure contributes to the joint damage by stretching the capsule and associated ligaments.
The load-carrying surfaces of the synovial joint are covered with a thin layer of specialized connective tissue referred to as articular cartilage. The response of articular cartilage to trauma is not unlike that of the other structures within the joint. The mechanical properties of articular cartilage are readily affected by enzymatic degradation of the components of cartilage. This can occur after acute inflammation, synovectomy, immobilization, or other seemingly minor insults. When articular cartilage loses its content of proteoglycan (a protein aggregate that helps establish the resiliency and resistance of articular cartilage to deformation), the physical properties of the cartilage are changed; this renders the collagen fibers susceptible to mechanical damage. The opposite is also true: if a joint loses collagen in the outer layer of the articular surface, the proteoglycans beneath are subject to damage. As a result of either of these two types of degradation, articular cartilage can erode and leave denuded bone, which results in early, irreversible osteoarthritis or degenerative joint disease ( Fig. 2-4 ).
Reduction of posttraumatic joint effusion is paramount in the early rehabilitation process and is important for restoration of joint kinematics. Prolonged effusion, if left unchecked, can result in reactive synovitis, damage to the joint capsule, and degradation of articular cartilage. Early use of mobilization techniques, such as continuous passive motion (CPM) and modalities such as cryotherapy and vasopneumatic compression, can aid in reducing joint effusion.
Effects of immobilization
One of the first and most obvious changes that occur as a result of immobilization is loss of muscle strength. This correlates with a reduction in muscle size and a decrease in tension per unit of muscle cross-sectional area. MacDougall et al reported that 6 weeks of elbow cast immobilization results in greater than a 40% decrease in muscle strength. This deficit in strength is correlated with loss of fiber cross-sectional area and with an associated decrease in muscle mass. The cross-sectional area of the quadriceps muscle may decrease from 21% to 26% with 4 to 6 weeks of immobilization in an individual without a pathologic condition. It is important to note that immobilization atrophy is due to loss of fiber cross-sectional area and not to loss of fibers, as seen in older persons.
The rate of loss appears to be most rapid during the initial days of immobilization. Structural and metabolic changes in muscle cells have been documented after as little as 2 hours of immobilization. Lindboe and Platou reported that in humans, muscle fiber size is reduced by 14% to 17% after 72 hours of immobilization. After 5 to 7 days of immobilization, the absolute loss in muscle mass appears to slow considerably. The amount of training before immobilization may dramatically decrease the amount of atrophy during immobilization.
Both type I (slow-twitch) and type II (fast-twitch) muscle fibers atrophy. It is generally accepted that a selective decrease in type I (redundant) fibers occurs. However, conflicting evidence is found in the literature. After immobilization, the contractile ability of type I fibers is more adversely affected than that of type II fibers. The decreased contractile ability of type I fibers, rather than decreased fiber proportion, may be more clinically relevant, which implies that exercises involving decreased intensity and increased frequency should be performed after immobilization. This is particularly relevant in an athlete who is specifically conditioned to aerobic activity because of the more dramatic decrease in the percent area of type I fibers. These studies evaluated the effect of immobilization only on muscle fiber composition, not the combined effect of injury and immobilization. Muscle fiber atrophy after injury or surgery may be different from that occurring when a healthy muscle is immobilized.
The mechanical properties of the myotendinous junction are changed as a result of immobilization. The contact area between the muscle cells and the collagen fibers of the tendon is decreased by 50% ; the glycosaminoglycan (GAG) content of the myotendinous junction is also decreased. These changes can predispose the myotendinous junction to injury after immobilization. A dramatic increase in activity after immobilization may lead to secondary tendinopathy.
In addition to causing changes in muscle size and volume, immobilization also results in histochemical changes. Such changes include a reduction in levels of adenosine triphosphate (ATP), adenosine diphosphate, creatine, creatine phosphate, and glycogen and a greater increase in lactate concentration with work. Furthermore, the rate of protein synthesis decreases within 6 hours of immobilization.
Immobilization also causes an increase in muscle fatigability as a result of decreased oxidative capacity. Reductions occur in maximum oxygen consumption, glycogen levels, and high-energy phosphate levels. Rifenberick and Max reported fewer mitochondria in atrophic muscle and a significant decrease in mitochondrial activity by day 7 after immobilization, which causes a reduction in cell respiration and contributes to decreased muscle endurance ( Box 2-1 ).
Decrease in muscle fiber size
Change in muscle resting length
Decrease in size and number of mitochondria
Decrease in total muscle weight
Increase in muscle contraction time
Decrease in muscle tension produced
Decrease in resting levels of glycogen and adenosine triphosphate (ATP)
More rapid decrease in ATP levels with exercise
Increase in lactate concentration with exercise
Decrease in protein synthesis
It appears that the muscle atrophy that occurs after immobilization is selective. For example, immobilization of the thigh is often associated with selective atrophy of the quadriceps femoris muscle. Although the knee is the area traditionally noted for selective atrophy, this phenomenon can also be observed in the triceps brachii of an immobilized elbow. Clinically, one can observe that atrophy of the quadriceps is greater than that of the hamstrings. This finding is supported by evidence on computed tomography that despite significant loss of quadriceps cross-sectional area, no significant difference in hamstring or adductor muscle cross-sectional area is seen after 5 weeks of immobilization.
The selective atrophy that occurs in the quadriceps femoris and the triceps brachii with immobilization of the knee and elbow, respectively, may be due to their roles as primarily one-joint muscles. Three of the four heads of the quadriceps cross only the knee joint, and two of the three triceps heads cross only the elbow joint. In contrast, all heads of the biceps and the hamstrings cross two joints. The biceps and hamstrings are therefore less immobilized by having all portions contract across one of the two joints that they cross (the hip or the shoulder), which may be the reason that cross-sectional area is preserved in these muscles.
The volume of muscle in the thigh decreases after immobilization, but the volume of subcutaneous adipose tissue does not change. This can mask the amount of quadriceps atrophy and invalidate girth measurements as a tool for measuring atrophy. Girth measurements also do not distinguish between muscle groups and can therefore underestimate the amount of quadriceps atrophy. Girth measurements do not correlate with deficits in strength.
Reflexive inhibition, or arthrogenous muscle wasting, can contribute to selective muscle atrophy, particularly of the quadriceps, after trauma to or surgery on a joint. Pain has traditionally been regarded as the general cause of reflex inhibition. The perception and fear of pain can greatly affect muscular strength. Athletes who fear that muscle contraction will result in pain may be very apprehensive about contracting these particular muscles, but severe inhibition of muscle strength is seen even after the pain subsides. At 1 to 2 hours after arthrotomy and meniscectomy, a 62% decrease in quadriceps electromyographic (EMG) activity occurs. This decrease is due to reflexive inhibition. A significant amount of anesthetic injected into the knee may decrease (but not eliminate) the inhibition temporarily, but the effects are lost after 4 to 5 hours. Ten to 15 days after surgery, quadriceps EMG activity decreases by 35%. Whether this reduced activity is due to reflexive inhibition or disuse atrophy is unclear. Pain has been shown to inhibit strength in patients with preoperative pathologic changes in the shoulder, but postoperative reflex inhibition has not been investigated. In studies investigating arthrogenous muscle wasting, the level of quadriceps activation is typically determined by EMG testing. The degree of unilateral quadriceps inhibition is then judged by the difference in maximum voluntary activation between the two limbs. Because no method is available to directly measure inhibition, it is indirectly quantified by EMG testing. This may not be a valid measure of true reflex inhibition during the first few hours after injury or surgery. After injury, reflex inhibition leads to muscle atrophy. When the inhibition has ceased, muscle weakness from disuse or immobilization atrophy will continue. Caution must be used when one generalizes the findings of studies pertaining to arthrogenous muscle weakness.
The nature of the surgical procedure performed may have an effect on the amount of arthrogenous muscle wasting after surgery. Advances in technology have led to the use of a less invasive arthroscope for many procedures that previously required an arthrotomy. A significant decrease in quadriceps muscle EMG activity is seen after arthrotomy of the knee. Although this decrease in EMG activity is still present after arthroscopy of the knee, the magnitude of the change is much decreased. Two-portal arthroscopy produces a lesser decrease in quadriceps strength after surgery than three-portal arthroscopy does. Clinically, patients undergoing an arthroscopic procedure would be expected to recover at a more rapid rate, but consideration must be given to the specific surgical procedure. In general, patients who have undergone less invasive procedures (arthroscopy) will initially recover faster than those who have undergone more invasive procedures (arthrotomy), but the long-term outcome is usually the same. This has been demonstrated in the knee and shoulder.
Tourniquet-related ischemia has also been thought to contribute to quadriceps shutdown. When a tourniquet is used to provide a relatively bloodless field during surgery, the pressure required to staunch blood flow is also enough to damage the tissues being compressed. Use of a tourniquet, although necessary, leads to postoperative EMG changes and increased quadriceps atrophy. Nonroutine complications from tourniquet use include compression neurapraxia, wound hematoma, tissue necrosis, vascular injury, and compartment syndrome.
Research has shown that distension of a knee with plasma can lead to quadriceps shutdown and subsequent quadriceps weakening in normal individuals, even in the absence of pain. Young et al and others reported that injection of small volumes of fluid (20 to 30 mL) into normal knees results in 60% quadriceps inhibition, with the inhibition increasing as the infusion increases. Spencer et al found the threshold amount of effusion for reflexive shutdown to be between 20 and 30 mL for the vastus medialis and between 50 and 60 mL for the vastus lateralis and rectus femoris. The decreased threshold for the vastus medialis can contribute to patellar tracking problems when the knee is even slightly effused. Inhibition is directly related to the degree of effusion and increases as the amount of effusion increases. With a chronically effused joint, aspiration of the effusion does not result in any difference in quadriceps inhibition. This may be attributed to concomitant disuse atrophy.
Joint angle has also been shown to have an effect on quadriceps inhibition. In normal knees, the highest quadriceps EMG activity is obtained with the knee in the shortened position, or full extension. Stratford reported that effusion inhibits quadriceps contraction less when the knee is in 30° of flexion than when it is fully extended. Similar results have been found even after arthrotomy with meniscectomy, with isometric quadriceps contraction being inhibited less in flexion than in extension. This has been postulated to occur because intraarticular pressure is less when the knee is in 30° of flexion than when in full extension. Despite higher EMG activity being obtained with the knee in flexion, it is not desirable to perform all exercises in the clinic with a flexed knee position. On the contrary, this information emphasizes to the clinician the importance of training the quadriceps in a fully extended position to overcome the biomechanical disadvantage.
The length at which the muscle is immobilized also affects selective atrophy. Tardieu et al suggested that muscle fibers under stretch lengthen by adding sarcomeres in series whereas those immobilized in a shortened position lose sarcomeres. Thus, when a muscle is immobilized in a lengthened position, the length of the muscle fibers increases to accommodate the muscle’s new length, along with other connective tissue changes. A similar adjustment in sarcomere number occurs in muscle that is immobilized in a shortened position; the length of the fibers decreases, and the number of sarcomeres is reduced to achieve the physiologic change. Immobilization of a muscle in a shortened position leads to increased connective tissue and reduced muscle extensibility. Muscle immobilization in a lengthened position maintains muscle weight and fiber cross-sectional area better than does immobilization in a shortened position. This theoretically explains the selective atrophy of the quadriceps when the knee is immobilized in full extension. Because the knee is usually immobilized in an extended or slightly flexed position, the hamstrings are placed in a lengthened position and the quadriceps in a shortened position. These positions help preserve muscle cross-sectional area and strength, but the sarcomeres will no longer be able to shorten enough to achieve maximal extension. Clinically, the position of the joint cannot be the only factor that influences muscle atrophy; for example, in a shoulder that is immobilized in internal rotation, the external rotators (the rotator cuff muscles) still demonstrate marked atrophy.
One of the factors that may also influence reflex inhibition is the muscle spindle. When a muscle is immobilized in a shortened or lengthened position, the spindle will assume a new resting length. A muscle in the shortened position will then have greater resistance to stretch, and a muscle immobilized in the lengthened position will have decreased contractile ability. This is especially true at the shoulder, which is typically immobilized in internal rotation, and at the elbow, which is typically immobilized in flexion. The shortened position facilitates the shortened muscles (elbow flexors and shoulder internal rotators) and may account for the decreased strength of the shoulder external rotators and elbow extensors. Treatment of these joints should include facilitatory techniques for the lengthened muscles and inhibitory techniques for the shortened muscles. The shortened muscles should be stretched often but gently because quick or aggressive stretching can cause a facilitatory response. Isometric contractions can also preserve tension in the muscle spindle while allowing healing of damaged tissues.
Despite the fact that the knee is typically immobilized in extension, patients tend to hold the knee in a slightly flexed position, either sitting with the hips flexed or supine with the pelvis tilted posteriorly, which shortens the hamstrings. Hamstring stretches to increase the resting length of the spindle are an important part of a knee rehabilitation program after immobilization. Increasing the length of the hamstrings will decrease the amount of resistance that the quadriceps must contract against to achieve full knee extension. Stretching of the posterior capsule may also be required if the knee is held in a flexed position.
Despite the increased preservation of quadriceps muscle cross-sectional area and increased EMG activity in flexion, this is not the preferential position for immobilization of the knee after injury or surgery. If the knee is immobilized in flexion, full passive extension must be maintained by passively extending the knee to 0° several times per day (barring medical or surgical precautions.) This ensures that the quadriceps will maintain proper length to allow shortening of the muscle to full knee extension.
Active quadriceps exercises should be done in full extension for several reasons. Full active knee extension is needed for a proper gait pattern during initial contact (heel strike). A quadriceps contraction in full extension allows maximal superior glide of the patella in the trochlear groove, thereby preventing patella infera. If patients do not have full active extension, they must be taught to glide the patella superiorly to preserve length of the patellar tendon. If patients do not have full passive knee extension after immobilization, a motion complication program should be initiated.
Periarticular Connective Tissue
The periarticular connective tissue consists of ligaments, tendons, synovial membrane, fascia, and joint capsule. As a consequence of immobilization, injury, or surgery, biochemical and histologic changes occur in the periarticular tissue around synovial joints and may result in arthrofibrosis. Arthrofibrosis has been referred to as ankylosis, joint stiffness, or joint contracture. It is a term that describes excessive formation of scar tissue around a joint after a surgical procedure or traumatic injury. Its characteristic feature is the formation of scar tissue within the joint capsule, the synovium, or the intraarticular spaces.
The two main components of fibrous connective tissue are the cells and an extracellular matrix. The matrix consists primarily of collagen and elastin fibers and a nonfibrous ground substance. Fibrocytes, located between the collagen fibers in fibrous connective tissue, are the main collagen-producing cells. As collagen fibers mature, intramolecular and intermolecular bonds or cross-links are formed and increase in number, thereby providing tensile strength to the fibers. On the basis of the arrangement of its collagen fibers, connective tissue is commonly classified into two types: irregular and regular. The irregular type of connective tissue is characterized by fibers running in different directions in the same plane. This arrangement is of functional value for capsules, aponeuroses, and sheaths, which are physiologically stressed in many directions. Conversely, in regularly arranged tissues, collagen fibers run more or less in the same plane and in the same linear direction. This arrangement affords great tensile strength to ligaments and tendons, which physiologically undergo primarily unidirectional stress.
The extracellular matrix is often referred to as ground substance and is composed of GAGs and water. To understand the changes that occur with immobilization it is important to be familiar with GAGs and their effect on connective tissue extensibility. Four major GAGs are found in connective tissue: hyaluronic acid, chondroitin 4-sulfate, chondroitin 6-sulfate, and dermatan sulfate. Generally, GAGs are bound to a protein and are collectively referred to as proteoglycans. In connective tissue, proteoglycans combine with water to form a proteoglycan aggregate.
Water constitutes 60% to 70% of the total connective tissue content. GAGs have enormous water-binding capacity and are responsible for this large water content. Together, GAGs and water form a semifluid viscous gel in which collagen and fibrocytes are embedded. Hyaluronic acid with water is thought to serve as a lubricant between the collagen fibers. This lubricant maintains a distance between the fibers, thereby permitting free gliding of the fibers past each other and perhaps preventing excessive cross-linking. Such free gliding is essential for normal connective tissue mobility.
Sliding of collagen fibers across each other, the collagen weave pattern, and their cross-links can all be illustrated by the Chinese finger trap analogy. When tension is applied to the Chinese finger trap, the trap lengthens to a certain point as the straw weave patterns of the trap move across one another ( Fig. 2-5 ). If tension continues to increase when the end point of the trap is reached, the straw fibers will begin to fail. This illustration is not unlike how body connective tissue functions.
Arthrofibrosis is induced primarily by immobilization after trauma to a joint; a significant reduction in GAG content and subsequent water loss take place and contribute to abnormal cross-link formation and joint restriction. In addition, within the joint space and recesses, excessive connective tissue is deposited in the form of fatty fibers, which later mature to form scar tissue that adheres to the intraarticular surfaces and further restricts motion.
The most significant reduction in GAG content occurs within the matrix. Akeson et al reported a 40% decrease in hyaluronic acid and 30% decreases in chondroitin 4-sulfate and chondroitin 6-sulfate; collagen mass decreases by about 10% and collagen turnover increases, with accelerated degradation and synthesis ( Box 2-2 ).
Reduction in water and glycosaminoglycan content, which decreases the extracellular matrix
Reduction in extracellular matrix, which is associated with a decrease in lubrication between fiber cross-links
Reduction in collagen mass
Increase in rates of collagen turnover, degradation, and synthesis
Increase in abnormal collagen fiber cross-links
The pathophysiology of arthrofibrosis appears to be a reduction in the semifluid gel as a result of the loss of GAGs and water, which causes a decrease in the critical fiber distance between collagen fibers. Friction is created between fibers, thus reducing collagen extensibility. It has been suggested that arthrofibrosis may be the result of an increase in the expression of collagen IV, which forms a fibrous network between collagen I and III fibrils. Collagen IV forms irregular cross-links between the collagen fibrils that decrease the ability of the fibrils to slide ( Fig. 2-6 ). Evidence suggests that arthrofibrosis may be the result of an autoimmune reaction.
Currently, arthrofibrosis most commonly affects the knee joint, particularly as a complication after anterior cruciate ligament (ACL) reconstructive surgery in which the operative knee develops a thicker joint capsule and a secondary flexion contracture. Arthrofibrosis of the knee joint is characterized by a lack of flexion, as well as extension (the most commonly involved motion is extension). Prolonged joint immobilization is the most recognized risk factor for the development of arthrofibrosis. Microscopic examination of a knee with arthrofibrosis shows a proliferation of fibroblasts and an associated accumulation of extracellular matrix. The principal component of the matrix is type I collagen, which is specifically found as an unorganized network of fibers. Although these findings are well recognized, the cause underlying formation of the exuberant scar tissue is less clear.
With a lack of experimental studies and suitable animal models, the pathophysiology of arthrofibrosis remains poorly understood. However, several theories have been proposed to explain and prevent this condition. Several authors have recommended delaying reconstructive surgery on an acutely injured ACL until the knee joint recovers from the initial trauma. It is theorized that the synovitis that occurs after the initial injury, which is then compounded by the synovitis developing after surgical reconstruction, may predispose the joint to arthrofibrosis. The authors suggest that surgery be delayed until the hemarthrosis and synovitis have decreased, ROM is restored, and the patient has active control of the quadriceps. ACL reconstruction is not an emergency surgical procedure, and better outcomes are seen after preoperative rehabilitation to decrease the initial response to injury.
Fibrosis results from increased numbers of collagen-synthesizing cells (from proliferation and recruitment), increased synthesis by existing cells, or deficient collagen degradation with continued collagen synthesis. Injury-induced inflammation precedes the repair process; therefore, precise regulation and control of the inflammatory response will have a direct impact on the timing and amount of fibrosis developing during healing. It has been suggested that an immune response is the cause of the capsulitis that leads to excessive connective tissue proliferation. This supports the theory that the excessive intraarticular deposition of connective tissue is a result of consecutive inflammatory phases after trauma to the joint. This has clinical implications; if the rehabilitation is overly aggressive, it can cause increased inflammation and potentially worsen this process. Long-duration, low-load techniques should be used to increase ROM and decrease the potential for an inflammatory response. The location of the fibrous lesions has a relationship to the amount of motion lost in terms of knee flexion. The presence of fibrous connective tissue bands in the suprapatellar pouch is the primary reason for limitation of flexion. Flexion can also be limited by patella infera or by shortening of the patellar tendon. This complication can be prevented by superior mobilization of the patella on a daily basis. Extension of the knee is limited by shortening of the posterior capsule.
It has been shown that arthrofibrotic tissue matures over time and that maturation is complete by approximately 6 months after onset. However, although the tissue matures over time, progressive loss of ROM has not been seen. Attempts to lengthen the tissues will be less successful as time passes because of maturation and decreased remodeling capability of the tissues. Efforts to treat arthrofibrosis conservatively are likely to fail after 6 months has passed. Figure 2-7 illustrates the sequelae leading to arthrofibrosis or return to sport.
Early recognition of arthrofibrosis is important, and its prevention is paramount. Arthrofibrosis has been associated with Dupuytren disease and diabetes. Patients with these conditions, as well as patients who appear to have an excessive amount of fibrous tissue at other joints, should be viewed as being at risk for the development of arthrofibrosis. It is a useful clinical test to examine joint play at another synovial joint, such as a metacarpophalangeal joint, to determine whether the patient is systemically hypermobile or hypomobile. Clinically, arthrofibrosis is rarely found to develop in hypermobile individuals.
Joint motion is essential for the prevention of contractures and formation of adhesions within joints. Physical forces and motion modulate the synthesis of proteoglycans and collagen in normal joints. Stress and motion also influence the deposition of newly synthesized collagen fibers by allowing proper orientation of collagen to resist tensile stress. Motion appears to inhibit periarticular tissue contractures by the following mechanisms :
Stimulating proteoglycan synthesis, thereby lubricating and maintaining a critical distance between existing fibers
Ordering (rather than randomizing) the disposition of new collagen fibers to resist tensile stress
Preventing the formation of anomalous cross-links in the matrix by preventing a stationary fiber-fiber attitude at intercept points
The matrix changes associated with immobilization (noted earlier) are relatively uniform in ligaments, capsules, tendons, and fasciae. These changes involve loss of extracellular water and depletion of GAGs, along with changes in collagen cross-linkage.
Articular cartilage is a thin covering on the ends of bones that creates the moving surfaces of synovial joints. It varies from 1 to 7 mm in thickness, with the cartilage covering larger weight-bearing joints (e.g., hip and knee joints) being thicker than that covering smaller, non–weight-bearing joints. Articular cartilage consists of fibers, ground substance, and cells. The fibers are composed primarily of type II collagen and make up 57% to 75% of the dry weight of cartilage. Collagen provides the tensile strength of articular cartilage and aids in the gliding of opposing articular surfaces. The ground substance is similar to that of periarticular tissue and consists of water (70% to 80%) and proteoglycans (15% to 30%). Proteoglycans have a unique bond with water that allows articular cartilage to resist and distribute compressive forces. The quantity of proteoglycans in articular cartilage depends on joint location, with weight-bearing joints having a higher proteoglycan content than non–weight-bearing joints. Both collagen and proteoglycans are produced by chondrocytes, the cells residing in articular cartilage.
As a result of immobilization, articular cartilage undergoes structural, biochemical, and physiologic changes at the cellular and ultrastructural levels. Consistently reported changes include the following: fibrillation, fraying, cyst formation, varying degrees of chondrocyte degeneration, atrophy in weight-bearing areas, sclerosis, and resorption of cartilage. The proteoglycan GAG content is also decreased, which reduces the ability of cartilage to resist compressive forces. These changes are generally permanent, but the length of immobilization is important in determining whether the articular changes are irreversible.
Articular cartilage is avascular, with its nutritional requirements being met by diffusion and osmosis. Diffusion occurs through a hydraulic pressure gradient, and this pressure is increased by weight bearing or joint movement. Low hydraulic pressure has no effect, whereas constant pressure interferes with nutrition. High intermittent pressure loading does not contribute much to the diffusion rate. Joint motion, however, increases the diffusion rate to three to four times the static level. This implies that in the absence of weight bearing, motion must be present to preserve the integrity of articular cartilage. The opposite (weight bearing without ROM) is not desirable, however, because compressive forces on only the weight-bearing aspects of the immobilized joint can cause severe articular damage.
The effects of immobilization depend on the position in which the joint is immobilized. A flexed knee position produces greater chondrocyte necrosis and degeneration of the articular cartilage than does an extended position. This result may be due to the increased compression and intraarticular pressure in the fully flexed position. The position of immobilization is not as critical in the upper extremities because they contain primarily non–weight-bearing joints.
The effects of immobilization on articular cartilage can be separated into contact and noncontact effects. In contact areas, the seriousness of the changes depends mainly on the degree of compression. In noncontact areas, it depends on the ingrowth of connective tissue into the articular surface. Constant compression of articular cartilage decreases the diffusion rate of synovial fluid and leads to pressure necrosis and chondrocyte death. Whether the lesions are reversible depends directly on the duration of continuous compression. In addition, loss of contact between opposed articular surfaces in weight-bearing and non–weight-bearing joints appears to lead to degenerative changes, thus suggesting a functional relationship between joint motion and normal articular cartilage surface contact ( Box 2-3 ).
Decrease in chondrocyte size
Decrease in capability of chondrocytes to synthesize proteoglycan
Softening of articular cartilage
Decrease in articular cartilage thickness
Adherence of fibrofatty connective tissue to cartilage surfaces
Pressure necrosis at points of cartilage-cartilage contact
Intermittent joint loading appears to have a critical role in maintaining healthy articular cartilage. The formation and circulation of synovial and interstitial fluids are stimulated by intermittent joint loading and retarded in its absence. Because synovial fluid is important for nourishment and lubrication of cartilage, intermittent pressure can facilitate chondrocyte nourishment and is vital for cell function. Conversely, joint immobilization in which the joint is constantly loaded or unloaded can compromise the metabolic exchange necessary for proper structure and function and eventually result in cartilage degradation and eburnation. Immobilization of the knees in extension leads to irreversible and progressive osteoarthritis. The compression between articular surfaces increases in an immobilized knee and, after 4 weeks of immobilization, reaches a level that is three times greater than the initial level.
Roth et al found that prolonged knee immobilization after ACL reconstruction leads to significant patellofemoral chondromalacia and that immediate mobilization prevents patellofemoral degeneration. It may be assumed that immobilization after other types of surgery leads to articular changes as well. Although it is important to begin motion and gentle strengthening exercises after surgery, it is essential for the clinician to remember that excessive activity has the potential to compromise the articular surfaces. Moderate activity after immobilization has been shown to stimulate regeneration of the articular surface, but strenuous activity can reduce the proteoglycan content of articular cartilage. Do not “overrehabilitate” the articular surfaces with too much activity too soon.
Ligaments undergo the same changes in structure as do other elements in periarticular tissue. However, because of the function of ligaments and because of the bone-ligament interface, additional factors must be considered to understand the response of ligaments to immobilization.
Like bone, a ligament appears to remodel in response to the mechanical demands placed on it. Stress results in a stiffer, stronger ligament, whereas inactivity yields a weaker, more compliant structure. These structural changes appear to be caused more by an alteration in the mechanical properties of ligaments and by subperiosteal resorption at the bone-ligament junction than by actual ligament atrophy. With immobilization, the bone-ligament junction rather than the midsubstance of the ligament is at increased risk for injury. The alterations in ligament collagen lead to a decrease in tensile strength of the ligament and thus reduce the ability of ligaments to provide joint stability ( Box 2-4 ).
Significant decrease in linear stress, maximum stress, and stiffness
Decrease in cross-sectional area of the ligament fibril, which results in a reduction in fibril size and density
Increased synthesis and degradation of collagen, which results in an increased turnover rate
Disruption of the parallel arrangement of collagen
Reduction in load and the energy-absorbing capability of the bone-ligament complex
Decrease in glycosaminoglycan level
Increase in osteoclastic activity at the bone-ligament junction, which causes an increase in bone resorption in that area
Immobilization of the ligaments of the knee has been widely studied. It is well established in the literature that the amount of time that the ligament is immobilized is much shorter than the amount of remobilization time necessary for the ligament to reach its preimmobilization strength. The reconditioning process must provide progressive stress that overloads the ligament enough to stimulate regeneration, but the stress must be controlled to prevent cumulative microtrauma. The effects of immobilization on ligament structure and function may be specific to each particular ligament.
With immobilization, the medial collateral ligament (MCL) decreases in cross-sectional area and ultimate stress load. These effects are assumed to depend on the exact position of the knee joint. The MCL is taut in full extension, so the assumption is that if the knee is immobilized with the MCL in a shortened position, a tighter ligament would be provided. Research has shown that a reconstructed MCL has increased creep, or lengthening per unit stress, with immobilization rather than with full motion. This has implications for rehabilitation after MCL injury or reconstruction. After MCL injury or reconstruction, the knee should be placed in a position of slight flexion so that extension is preserved but the ligament is not under stress. Progressive motion should be allowed several times per day, however, to prevent creep and loss of cross-sectional area. Although this research involves only the MCL, it is likely that the same biomechanical principles may be applied to the lateral collateral ligament.
The effects of immobilization on the ACL have been widely studied. The specific effects are difficult to measure consistently because of the complex fiber orientation of the ligament. For the rehabilitation specialist, it is enough to note that the ACL is at increased risk for damage after immobilization and that the amount of reconditioning necessary to restore the ligament is much greater than the duration of the immobilization. A discussion of the effects of immobilization after reconstruction is not warranted because of the widespread use of early aggressive ROM exercises and rehabilitation after reconstruction.
The menisci also undergo degenerative changes with immobilization, and this degeneration is directly related to the amount of time that the joint was immobilized. In an animal model, blood flow to the menisci after injury was increased fivefold. However, there was no increase in blood flow when the joint was immobilized. Currently, healing is thought to depend on an adequate blood supply, and immobilization may therefore delay healing of the meniscus. Knee joint immobilization decreases the proteoglycan and water content of the meniscus, which changes its ability to distribute compressive force. In the absence of weight bearing, active joint motion has been shown to decrease the loss of ligament and meniscal mass.
When ligament reconstruction (not a primary repair) is performed, the graft undergoes neovascularization and ligamentization. This process begins at approximately 3 to 7 weeks postoperatively for a patellar tendon autograft. This is the time when the graft is the weakest, and the rehabilitation specialist must take care to not overstress the graft during this period. Bone-to-bone healing occurs faster than bone-to-tendon healing, which implies that rehabilitation should be less aggressive after ACL reconstruction with a hamstring autograft than with a patellar tendon autograft. At 6 months postoperatively the patellar tendon autograft is indistinguishable from a normal ACL, and the mechanical properties are not different. These findings imply that return to sport may occur at this time, but other factors, such as strength, dynamic control, balance, and psychologic readiness, must be considered.
The effects of immobilization on bone are similar to those on other connective tissues. A consistent finding in response to diminished weight bearing and muscle contraction is bone loss. Changes in bone can be detected as early as 2 weeks after immobilization. Although the pathogenesis of immobilization-associated osteoporosis is unclear, animal studies have shown decreased bone formation and increased bone resorption.
Bone hardness decreases steadily with the duration of immobilization, with hardness dropping to 55% to 60% of normal by 12 weeks. A decline in elastic resistance also occurs—the bone becomes more brittle and thus more susceptible to fracture.
It appears that mechanical strain influences osteoblastic and osteoclastic activity on the bone surface. Bone loss from disuse atrophy occurs at a rate 5 to 20 times greater than that resulting from metabolic disorders affecting bone. The primary cause of this immobilization osteoporosis appears to be mechanical unloading, which may be responsible for the inhibition of bone formation during immobilization. Therefore, non–weight-bearing immobilization of an extremity should be limited to as short a period as possible.
Continuous passive motion
In 1970, Salter originated the biologic concept of CPM of synovial joints to stimulate healing, regenerate articular tissue, and avoid the harmful effects of immobilization. In 1978, Salter and Saringer (who was an engineer) collaborated to develop the first CPM device for humans. A CPM machine is an electrical, motor-driven device that helps support the injured limb. It is used to move a joint at variable rates through progressively increasing ROM; no muscular exertion is required of the patient.
Salter et al provided the first histologic evidence in support of CPM. They reported that CPM significantly stimulates healing of articular tissues, including cartilage, tendons, and ligaments; prevents adhesions and joint stiffness; does not interfere with healing of incisions over the moving joint; and influences the regeneration of articular cartilage through neochondrogenesis.
When compared with immobilization of tendons, CPM has proved effective in increasing linear and maximum stress, linear load, and ultimate strength in tendons. Salter and Minster reported the preliminary results of semitendinous tenodesis for MCL reconstruction in experimental animals, in which increased strength was reported after the use of CPM. The application of early tensile force appears to facilitate proper alignment of collagen fibers during the initial healing process. In addition, decreases in medication requests and in wound edema and effusion in operative knees were reported in patients undergoing CPM. The greatest benefit of CPM appears to be the prevention of articular cartilage degradation. Salter reported that healing of cartilage defects in rabbits appears to be more rapid and complete when CPM is used. More recently, a 2007 study reported that the use of CPM stimulates chondrocyte PRG4 metabolism, which benefits cartilage and joint health.
CPM has received widespread attention for use in treating pathologic conditions of the knee. However, CPM machines have been developed for the shoulder as well. Raab et al found increased ROM and decreased pain with the use of CPM after rotator cuff repair, although no difference in combined outcome measures was seen 3 months postoperatively. Lastayo et al found no difference in outcomes between subjects who used a CPM machine and those who had a friend or relative perform manual ROM exercises, thus indicating that the presence of passive motion is more important than the mode of delivery.
It is well established in the literature that the use of CPM is not associated with a significant difference in outcome measures at approximately 4 weeks postoperatively. However, when the short-term effects of CPM are examined, subjects undergoing CPM regain their motion faster and with less pain than do those who are not undergoing CPM. Although there may be no long-term difference, CPM appears to be beneficial to patients in the short term ( Box 2-5 ).