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OVERUSE SYNDROMES IN ADULT ATHLETES
MUSCULOSKELETAL MEDICINE
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OVERUSE SYNDROMES IN ADULT ATHLETES N. Nichole Barry, MD, and James L. McGuire, MD
Physicians are now required to view their patients as athletes who have adopted various modes of regular exercise. Rheumatologists, in particular, as specialists in musculoskeletal disorders, are seeing more patients with problems due to their exercise programs and the sports in which they participate. OVERUSE SYNDROMES
Overuse syndromes, including tendonitis, are common in adult athletes. Approximately 50% of all sports participants will be injured at one point, and at least half of those injuries will be attributed to overuse.1hOveruse injuries are generally considered to be due to “overload,” or repetitive microtrauma to the musculoskeletal Microtrauma, produced by tension or shear force, results in damage at both the molecular and microscopic level. Although microtrauma can occur with a single episode of excessive stress, the usual mechanism is repetitive loading forces on the musculotendinous unit at a force well within the physiologic limit. Each of the components of the musculotendinous unit usually adapts to an applied load in a different way. Bone will increase its local mass to withstand increases in loads, muscle becomes hypertrophic, and tendons and ligaments increase both their collagen content and cross-linking to reinforce their tensile strength. These processes will collectively result in an overall increase in the strength and flexibility of the musculotendinous unit over time. Repeated overload to the unit, which does not allow time for repair and adaptation results in disruption and inflammation. Further stress will compound the injury.I6 Many intrinsic and extrinsic factors contribute to overuse syndromes. Intrinsic factors include malalignment and muscle imbalance. For example, pes caws
From the Division of Immunology and Rheumatology, Stanford University Medical Center, Stanford, California
RHEUMATIC DISEASE CLINICS OF NORTH AMERICA VOLUME 22 NUMBER 3 AUGUST 1996
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(excessively high arches of the feet) is commonly associated with Achilles tendonitis and poor tracking of the patella (patello-femoral syndrome). Extrinsic factors, which consist primarily of training errors, account for 60% to 80% of injuries in runners.27Most studies show a consistent relationship between increased training mileage or intensity in runners and subsequent injury.I1 Improper training techniques, even if minor, can lead to muscular imbalance, which results in a strain on other musculotendon units. Furthermore, the diminished contractility of fatigued muscles limit the ability to absorb shock or stressz7 Any component of the musculotendinous unit is susceptible to injury-the muscle belly, tendon, musculotendinous junction, or the bony insertion of the unit itself. Injury generally occurs at the weakest point in the unit, which varies with age. In young athletes, excessive stress most often causes an avulsion fracture. After 25 years of age, the tendon is most susceptible to both traumatic and overuse injury due, at least in part, to the progressive degeneration of the collagen fibers. Muscle injuries and tears tend to be more common in the In addition to age, the dominant motions of the specific sport motions may amplify the already described intrinsic and extrinsic factors of overuse. Epicondylitis, shoulder impingement, patellofemoral syndrome, Achilles tendinitis, and stress fractures emerge as the most common overuse syndromes that athletes encounter. EPlCONDYLlTlS Lateral or medial epicondylitis are the most common overuse injuries that present with elbow pain in athletes involved in throwing and racquet sports. The cause of the tendon inflammation as a result of shearing forces over the epicondyle of the humerus is considered to be multifactorial. This would include the grip size, the weight of the racquet, the extensive range of motion of the entire arm, and the long durations of eccentric muscle contractions around the elbow.Is With racquet sports, microtrauma and overload may also be generated by the energy and vibrations transferred to the arm from the sudden impact between the racquet and high-velocity balls.28These factors all result in stiffness and weakness of the wrist extensors and supinators in lateral epicondylitis, and flexors and pronators in medial epicondylitis. The resultant inflexibility and weaknesses alter the smooth motion required in throwing and racquet strokes. This change in kinematics and lack of muscle tendon pliability contribute to inflammation of the tendons.I8 Lateral epicondylitis occurs in approximately 40% to 50% of all racquet sport athletes at one point in their career, and most are over 30 years of age.28It is characterized by pain on the lateral aspect of the elbow, which occurs with any activity requiring resisted wrist extension, as in a backhand stroke with a racquet. The pain can radiate to the forearm and improves or even resolves with rest, but recurrence on return to the inciting sport activity is usual. Morning stiffness of the elbow with persistent aching may occur if the athlete continues to play despite symptoms? On physical examination, maximal tenderness is present either directly over or somewhat distal to the lateral epicondyle with the elbow in flexion. Pain can be elicited in the same area with resisted wrist extension. Overall, the range of motion of the elbow is full. Swelling or erythema in the area or the forearm is not typical.6 Differentiation from degenerative changes of the radiocapitellar joint is crucial and can be done by applying an axial load on the forearm combined with gentle, passive supination and pronation. This motion com-
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presses the radiocapitellar joint without stressing the surrounding tendons and does not elicit pain in epicondylitis. Radiographs are typically negative, but calcific deposits and degenerative changes can be seen in chronic cases of epicondylitis.6 Medial epicondylitis (also known as golfer's elbow) is characterized by pain and tenderness over the medial epicondyle at the origins of the flexor and pronator tendons. As with lateral epicondylitis, pain is exacerbated by activity and alleviated with rest, and usually persists with chronic use. On physical examination, resisted wrist flexion and pronation will elicit symptoms. Again, a full range of motion of the elbow joint is present. Medial epicondylitis is associated with overhead tennis serves and some golf strokes. The repetitive valgus (outward from the midline) stress on the soft tissues of the medial elbow combined with tension generated by the wrist flexors and pronators during these strokes produces overload. Medial epicondylitis must be differentiated from a medial collateral ligament tear of the elbow. Application of a valgus force to a slightly flexed elbow with the wrist flexed and forearm pronated stresses the medial collateral ligament but should not cause pain in patients with intact ligaments or medial epicondylitis. Of note, medial epicondylitis may also lead to reversible impairment of conduction in the ulnar nerve, or ulnar neurapraxia, and the presentation of medial forearm and hand pain. Approximately 60% of patients undergoing surgery for medial epicondylitis had some signs or symptoms of ulnar nerve involvement.6 Treatment for lateral and medial epicondylitis are similar. Initially, the inciting activity, usually a racquet or throwing sport, should be avoided. Nonsteroidal anti-inflammatory drugs (NSAIDs) are also helpful to reduce pain acutely and should be continued for at least 3 weeks after the pain has resolved. Passive range of motion exercises should be carried out three to six times a day until pain-free motion is obtained. Rehabilitation exercises that focus on strengthening wrist flexors and extensors can then begin. Athletes can then slowly increase to small weights and rubber band resistance exercises. Counterforce bracing, which puts pressure directly over the involved tendons, has been shown to be useful in the treatment of epicondylitis as well. The nonelastic support acts to constrain extensor muscle expansion, thus decreasing the contractile tension and hopefully distributing forces to surrounding tissues.h In tennis, novice players have been shown to have an increased chance of developing lateral epicondylitis. To minimize recurrence, a review of technique, especially the backhand stroke, is essential prior to return to play. For instance, players using a one-handed backhand are more likely to develop lateral epicondylitis. It is well accepted that the one-handed backhand requires greater strength and coordination than a two-handed stroke. One theory is that the onehanded backhand links five body parts prior to impact (hips to trunk to shoulder to elbow to wrist), then to the racquet itself. With the two-handed backhand, only two body parts are linked prior to impact with the ball (hips to trunk) because the trunk, arms, and racquet move as one. No movement occurs at the elbows or wrists on impact, which helps the entire arm absorb the energy of the impact. It also forces the ball impact to be transmitted through the elbow rather than absorbed by the tissues around the elbow.6 In addition, equipment can play a role. Racquets with a larger head, but not necessarily heavier, can act to decrease vibrations and the number of miss-hits, which diminishes the microtrauma to the soft tissues of the elbow.2x Completing a well-planned rehabilitation program with appropriate strengthening of muscles and correction of poor technique is imperative for recovery and return to prior level of play. Previous injury may play a large role
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in elbow pathology. Incomplete rehabilitation of a previous epicondylitis episode may have a 70% chance of recurrence.'* At least 6 months (preferably 1 year) of rehabilitation should be attempted prior to considering surgery. Local steroid injection may also play a role in the management of chronic epicondylitis and should be coordinated within the rehabilitation plan. The downtime following the injection should be at least 6 weeks. Despite being asymptomatic, the chance of tendon rupture from premature resumption of play remains for at least a month. An intensive rehabilitation process can begin again 6 weeks postinjection. Surgery is a last resort and involves local debridement of abnormal granulation tissue and abrasion at the site of origin of the involved tendons. Here again, a comprehensive postoperative program is also necessary.18 IMPINGEMENT OF THE SHOULDER AND ROTATOR CUFF
Overuse injuries to the shoulder are common in athletes involved in throwing and racquet sports. Impingement of the tendons of the rotator cuff (the teres minor, infraspinatus, supraspinatus, and subscapularis) between the head of the humerus and the acromion may ultimately lead to frank tears of the rotator cuff (Fig. 1). Both overhand throwing and racquet strokes place repetitive, highvelocity stress on the shoulder joint, gradually resulting in subluxation or movement of the humeral head anteriorly. This instability, which is subtle, may then lead to recurrent subluxation and impingement of the rotator cuff.I5 This "cascade" of events, which can ultimately result in a tear of one or more tendons of the rotator cuff, is often referred to as the instability complex.15 Athletes may present with pure and isolated impingement without any instability. This is usually seen in older athletes and is considered secondary to degenerative changes within the joint itself. Impingement may also be associated with instability caused by repetitive microtrauma on the labrum (the ring of fibrocar-
Subscapularis
Figure 1. Superior view of the rotator cuff muscles. (From Hartley A: Practical joint assessment. In Weimer R (ed):A Sports Medicine Manual. St. Louis, Mosby-Year Book, 1991, p 92; with permission.)
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tilage that forms the glenoid cavity of the scapula) and the capsular ligaments. Inherent hyperelasticity can lead to instability and impingement as well. Ultimately, all impingements can progress to rotator cuff tears.Is The glenohumeral joint is considered to be ”inherently unstable.” The stability is provided by the static glenohumeral ligaments and dynamic musculotendinous units of the rotator cuff, which together restrain the limits of motion of the humeral head; however, the position of abduction, coupled with external rotation, applies significant stress to the anterior shoulder. Repetitive motion from this position initially leads to damage of the glenohumeral ligaments, and even vascular compromise due to pressure from the acromion, eventually stretching the joint capsule. Any abnormal capsuloligamentous laxity or muscle weakness then allows greater humeral head motion.’ With injury to the static stabilizers of the joint, the musculotendinous units (the rotator cuff) must act to maintain stability. The eccentric overload (which refers to contraction of muscle fibers as they lengthen) of the rotator cuff will eventually result in fatigue and inflammation of the tendons as well as asymmetric weakness of the muscles. This further compromises stability and allows translation of the head of the humerus. As the humeral head moves further anteriorly and superiorly, with abrasion of the labrum, impingement of the rotator cuff tendons occurs as they approximate against the coracoacromial arch.’, 25 The unusual location of the rotator cuff tendons, confined between the humeral head on one side and the acromion on the other, also contributes to the confinement of the swelling and the chronicity of tendinitis. Ultimately, this degeneration results in attrition of the tendons.’ The muscle-tendon complex of the biceps brachii assists in the maintenance of the anterior stability of the glenohumeral joint. Together with the rotator cuff it controls the deceleration of the arm after striking or throwing the ball and minimizes the stress placed on the inferior glenohumeral ligaments. Irritation and inflammation of the biceps tendon may also occur with impingement. Although biceps tendonitis may be the initial presentation of overuse, the possibility of humeral instability should be considered because a more extensive treatment and rehabilitation would be necessary.’” 25 In the early 1970s, Neer23stated that 95% of rotator cuff tears are associated with impingement (not including those secondary to one-time traumatic events). He described three stages in the development of rotator cuff tears from overuse, which still remains clinically useful. Stage One-Edema and hemorrhage within and around the tendons are the pathologic manifestation of this stage. Clinically, the patients describe a ”toothache-like” pain extending from the shoulder to the mid-upper arm, usually occurring after activities involving flexion and abduction of the arm. On physical examination, point tenderness is present over the greater tuberosity of the humerus.’ A positive impingement sign is demonstrated by pain with forward flexion and internal rotation of the arm, which compresses the supraspinatus tendon of the rotator cuff between the greater tuberosity of the humerus and the anterior-inferior acromial s ~ r f a c e . At ’ ~ this point, no weakness or loss of motion is present. Stage Two-The shoulder pain becomes constant but often worsens at night. Any activity involving overhead movement of the arm will exacerbate the pain. On physical examination, tenderness is more diffuse than in stage one and more intense. The range of motion may be limited by pain, but passive range is usually normal. Involvement of the acromioclavicular joint may also be present.’
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Stage Three-Although the symptoms of this stage are similar to stage two, athletes usually have had a long history of shoulder problems. Athletes may feel weak secondary to pain or prolonged disuse. The range of motion is decreased, either secondary to disuse or a partial rotator cuff tear. Pathologically, tendon degeneration and attrition are present. Partial thickness tears, the next stage in the continuum of rotator cuff disease, may then easily occur or extend with minor trauma or stress. Rotator cuff tears usually involve the supraspinatus muscle; therefore, subtle changes in strength may reflect partial tears or extensions of tears. Isolation of the supraspinatus muscle can be accomplished by abducting the athlete's outstretched arm to 90 degrees, forward flexing to 30 degrees, and maximally internally rotating it (thumbs down). Strength can then be tested by forced resistance and compared for ~ymmetry.'~ Several signs on physical examination suggest complete tears of the rotator cuff. These include supraspinatus wasting, with or without infraspinatus wasting; a painful arc of motion at 90 degrees of abduction or forward flexion; and greater passive than active range of motion, especially in abduction and external rotation. The inability to slowly lower the arm from 90 degrees of abduction, the "drop arm test," may also be elicited. In addition, weakness in abduction and external rotation may be present.' Radiographs, especially the anterior-posterior view, allow for the visualization of the undersurface of the acromion, the acromioclavicular joint, and the glenohumeral joint. If the distance between the undersurface of the acromion and the superior surface of the humeral head is less than 6 mm, then the possibility of a rotator cuff tear should be considered. In addition, a complete tear is often associated with sclerosis and osteophyte formation along the anterior-inferior acromion and over the greater tuberosity of the humerus.2 Calcification of the tendons composing the rotator cuff may also occur with prolonged inflammation. The differential diagnosis should include subacromial bursitis and acromioclavicular osteoarthritis, both of which can be aggravated by overuse, especially in older adults. Both are usually associated with pain on palpation of the involved structure. Local injection of lidocaine may be used to differentiate the cause of the shoulder pain if necessary. Treatment of stage one overuse involves avoidance of the inciting activity (overhead sports), NSAIDs, and intensive physical therapy to strengthen the muscles involved in internal and external rotation. The strengthening program should use isometric (contraction with both ends of the muscle held fixed), isokinetic (contraction with constant motion), and isotonic (contraction leading to shortening with a constant load) exercises.15Local steroid injections with a low dose of a short-acting glucocorticoid may also be used, but no more than twice and with at least 3 months between injections. Some orthopedic surgeons believe that athletes who require a steroid injection for pain relief should have more aggressive evaluation involving an MRI or arthroscopy. The vast majority of cases of stage one tendinitis is reversible with conservative treatment.' Athletes with stage two impingement have a fibrotic supraspinatus tendon and persistent pain. They should initially receive conservative treatment with intensive physical therapy and NSAIDs. If athletes do not respond within 3 to 6 months, then more aggressive diagnostic and even surgical management should be considered.' Many orthopedic surgeons initially obtain an MR image to evaluate the diagnosis of a cuff tear. Arthroscopy is also a diagnostic alternative because it allows direct inspection of the glenohumeral joint and subacromial
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area as well as the rotator cuff. At the same time, repair of small tears with dbbridement to initiate healing can be carried out. Removal of acromial spurs and subacromial decompression can also be performed, in which the anterior acromion is exposed and shaved at the lateral tip of the acromioclavicular joint. These manipulations are designed to diminish any pathology from the acromion that may be contributing to impingement of the rotator cuff tendons. This allows increased free movement between the humeral head and the undersurface of the acromion. Up to 90% of patients describe dramatic pain relief, and hopefully the future inflammatory response will be minimized.2 Early surgical intervention in the shoulder of patients with impingement unresponsive to conservative treatment or patients with a partial rotator cuff tear results in improved function, pain relief, and most importantly, the prevention of progression to complete tears. In addition, small tears are more easily repaired and have better outcomes.2 Prevention of complete rotator cuff tears also decreases the incidence and severity of secondary arthropathy. By stage three, the rotator cuff deficiency will usually have resulted in some degree of glenohumeral arthritis. Of note, two factors that contribute to a poor prognosis of surgical repair of a rotator cuff tear are the size of the tear and the duration of the restricted motion preoperatively, further supporting the argument for early, aggressive surgical intervention.2 PATELLO-FEMORAL DYSFUNCTION
Anterior knee pain is the most common complaint presenting to sports medicine physicians, and overuse is a major contributing factor, especially in sports involving running, jumping, quick stops, and turns. The most common cause of anterior knee pain is abnormal patellar tracking produced by mechanical overload and excessive lateral vector forces on the joint (patello-femoral dysfunction).z' In fact, patello-femoral dysfunction is often seen in the general population, occurring in up to one in four patients, and is considered to have a higher incidence in athletes.13 The primary function of the patella, a special sesamoid bone, is to increase the "lever arm" of the quadriceps muscle during extension. Throughout the entire range of motion of the knee, the patella has been demonstrated to increase the force of extension by as much as 50Y0.~~ The patella also transmits load from the quadriceps to the trochlear surface of the femur. Biomechanical studies have demonstrated forces on the patello-femoral joint as among the highest per unit area of any joint in the body.I4 The patella also has the thickest cartilage in the body, which enables it to withstand forces that may exceed seven times the body weight during squatting.14 Disturbances of patellar mechanics are due to abnormalities in the position of the patella as it moves through the trochlear groove of the femur. The patella does not articulate with the trochlea until 20 degrees of flexion (full extension is 0 degrees). Disturbances range from an abnormal tilt of the patella to abnormal tracking in the trochlear groove to frank dislocation. Athletes who have shallow trochlear grooves or low lateral walls of the trochlea have an increased risk for patellar malalignment or subluxation. Other risk factors for patellar dysfunction include general ligamentous laxity and abnormal limb alignment (e.g., knee valgus or foot ~ r o n a t i o n ) .Because ~~ the vastus medialis muscle functions throughout the range of motion of the knee to align the patella, this muscle is a factor in patello-femoral malalignment. Focal strengthening of the vastus medialis muscle is a major factor in rehabilitation. Straight-leg raising exercises are
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considered the most effective means of focal strengthening, although they are not uniformly used (Fig. 2).13 One type of malalignment is characterized by a lateral tilt of the patella within the trochlear groove, which leads to an adaptive shortening of the lateral retinaculum, and as a result, the medial retinaculum may stretch or tear? With flexion of the knee, the patella is forcefully drawn into the lateral trochlear groove. Eventually, the cartilage of the undersurface of the patella can be di~rupted.'~ The relationship between abnormal patellar tracking and changes in articular cartilage are often causally liked." An association between changes in articular cartilage and tilt-subluxation patterns of malalignment has been similarly suggested. The incidence of chondromalacia is higher in patients with subluxation (93%)than in those with frank dislocation (62%)of the patella. Any increase in compressive forces that exceed physiologic range, which are normally quite high, may lead to damage of the cartilage or ch~ndromalacia.'~ The historical causal relationship between chondromalacia and patello-femoral pain due to malalignment has recently been reexamined, in part because of the lack of correlation of arthroscopic findings of fibrillation, cartilage softening, or disruption in many patients with the clinical syndrome of patello-femoral
Vastus Lateralis
Rectus Femoris
Vastus Medialis
Patella Lateral Retinacul urn
Medial Retinaculum
Patellar Ligament
Figure 2. The knee, illustrating the medial and lateral retinaculum. ( f r o m Wertheimer C: Patellofemoral mechanics as a cause of anterior knee pain. Your Patient and Fitness 9:21, 1995; with permission.)
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pain. This does not mean that cartilage degeneration will not cause pain when bone is exposed, but rather that other factors related to patellar malalignment, such as chronic strain on the retinaculum (which is richly innervated), may also result in similar pain. It is now generally agreed that chondromalacia is most likely caused by chronic patello-femoral dysf~nction.~, ’. l7 Chondromalacia is considered a gross pathologic diagnosis and is reserved for findings from arthroscopy or s ~ r g e r yThe . ~ relationship to osteoarthritis is still debated. The diagnosis of patello-femoral dysfunction may be somewhat difficult. Athletes complain of gradual onset of a dull ache in the peri- or retro-patellar region. In milder cases, symptoms are initiated by activities involving running (especially long distance) as well as jumping and quick stops and starts. Pain initially resolves if the inciting activity is discontinued; however, as the condition worsens, pain may become constant. Classic activities that exacerbate pain include squatting, walking up or down stairs, and prolonged sitting. Some athletes will describe a popping, grinding, or a catching sensation under the patella. Continued aggravation of the patello-femoral joint dysfunction will lead to constant pain and the sensation of weakness in the quadriceps.’? On physical examination, atrophy of the vastus medialis may be present. Tight hamstring muscles (the muscles of the posterior thigh, which include the semimembranosus, semitendinosus, gracilis, sartorius, and biceps femoris) may be noted. Tight hamstrings are thought to lead to increased knee flexion during running, which in turn increases the patello-femoral joint forces.I3Patellar stability should be evaluated by having the athlete flex the knee to 20 degrees over a pillow, which engages the patella into the trochlear groove. The patella should then be manually pushed medially and laterally to determine the percentage of its total width that can be forced out of the trochlear groove. Displacement to the side by more than 75% of its total width suggests an increased risk for subluxation. If the patella can barely be pushed out of the groove medially, a tight lateral retinaculum is present and suggests the possibility of patellar tilt. Both are indicative of patello-femoral malalignment /dysfunction.?? The amount of patellar tilt can also be evaluated by having the athlete relax the knee in extension (the patella will not be in the trochlear groove). The patella is then grasped between the examiner’s thumb and index finger and the lateral edge is pulled straight upward and tilted. A normal patella will only tilt approximately 20 degrees above horizontal. Any tilt greater than 20 degrees is abnormal. Again, inability to pull the patella to or above the horizontal plane is strongly suggestive of a tight lateral r e t i n a c ~ l u m . ~ ~ A positive apprehension sign, occurring when the knee is flexed to 30 degrees and lateral pressure is placed against the medial aspect of the patella, is suspicious for recurrent subluxation. Patellas at higher risk for subluxation are those which are ”high-riding” or have a lateral rotation over the trochleas on inspection. Lastly, patellar cartilage or bone may be assessed by compressing the patella against the trochlea while the knee is passively moved from full extension to partial flexion. Pain and crepitus elicited with compression suggests cartilage degeneration or exposure of bone, which may accompany long-term patellar rnalaligr~ment.~~ Differentiation between a plica and patello-femoral malalignment in the affected knee is important because some symptoms are similar. A synovial plica is a redundant fold in the synovial lining of the knee, which is present in 60% of the population. It is usually crescent shaped, extending from the infrapatellar fat pad medially, looping around the femoral condyle, crossing under the suprapatellar tendon, and then passing laterally over the lateral femoral condyle to
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the lateral retinaculum. When chronically inflamed and fibrotic from overuse and stress, anterior knee pain results (Fig. ,).I4 Common complaints of an inflamed plica include gradual onset of pain over the anterior knee, which increases when sitting with the knee in flexion for a prolonged period of time. More severe pain then occurs upon rising, but diminishes after 8 to 10 steps. This occurs because the plica is trapped over the femoral condyles in flexion. With extension of the knee, the articularis genus muscle acts to extract it to prevent impingement in the patello-femoral joint; however, sufficient elevation of the plica may require 8 to 10 steps. If the plica does become entrapped as the quadriceps contract, the athlete will feel pain and the sensation that the knee may give out or b~ck1e.I~ On physical examination, palpation of the fibrotic and inflamed plica along the anterior femoral condyle may elicit pain. Otherwise, examination of the knee and patella will be normal and no effusion is noted. Treatment includes rest, ice, stretching of hamstrings, and strengthening of the quadriceps. If symptoms become chronic, surgical intervention may be necessary and is usually curative.13 In regard to patello-femoral malalignment and dysfunction, radiographs may be helpful. Lateral views provide information as to patellar thickness and height. The presence of a patella alta (a high-riding patella) can be determined by comparing the length of the patella to the length of the inferior patellar tendon (distance from the inferior pole to the tibia1 tubercle). If the tendon length is greater than 1.2 times the length of the patella, then patella alta is present and the risk for subluxation is higher.33An infrapatellar, or sunrise view, allows for evaluation of patello-femoral articulation. A lateral tilt of the patella may be appreciated on this view as well. Low femoral condyles or a shallow groove provide less of a sulcus for tracking and suggest poor patellar stability and malalignment.14 Treatment of patello-femoral dysfunction should initially include an aggres-
Figure 3. The knee, demonstrating the anatomy and location of the suprapatellar plica. Note also the articularis genu muscle, which inserts on the superior portion of the plica. (Adapted from Jacobson K, Flandry F: Diagnosis of anterior knee pain. Clin Sports Med
8:88,1989.)
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sive physical therapy program that involves stretching of the iliotibial band and the hamstring muscles as well as the lateral retinaculum if it is tight. Strengthening of the vastus medialis muscle should also be included to help provide dynamic medial stabilization of the ~atel1a.I~ Taping of the patella (McConnell method), which supposedly facilitates proper tracking, may decrease or eliminate pain and allow muscle strengthening.l3Patellar stabilization braces (usually neoprene with a hole for the patella), which can be obtained off the shelf in many sports stores, may also be of use. The best approach is to diminish symptoms as much as possible during the athletic activity. To allow continued participation in the activity while undergoing physical therapy,I3 it is important to remind the athlete that it may take several months of continuous exercise to achieve the increased strength and flexibility necessary to resolve the pain. At least 8 to 9 months of conservative management should be attempted before considering surgery. Realignment of the patello-femoral joint is generally considered a major surgical procedure. Clear-cut evidence of poor tracking of the patella, with or without subluxation, should be present either radiographically or arthroscopically before considering corrective surgery, which is usually done by arthroscope as well.R The lateral release of the patella is an appropriate procedure for correction of mild malalignment, without history of subluxation, as well as denervation of the painful, tight lateral retinaculum, which also serves to reduce the pathologically tilted r at el la.^ This procedure limits articular cartilage contact under stress with the associated decrease in soft-tissue strain. Athletes with more advanced malalignment do not do as well with a lateral release procedure alone.KAdditional surgical techniques that serve to change the position and dynamics of the patella, such as patellar realignment and tibia1 tubercle anteromedialization, may be required if the athlete has recurrent patellar subluxation or considerable patellar tilting and degenerati~n.~
ACHILLES TENDINITIS
Achilles tendinitis i s another common overuse injury seen among recreational athletes. It most typically affects adult male athletes involved in sports requiring constant running and repetitive jumping3' Epidemiologic studies have shown that Achilles tendinitis accounts for 15%of all running injuries.?' The Achilles tendon is the strongest and largest tendon in the body. It arises from both the medial and lateral heads of the gastrocnemius muscle as well as the deeper layers of the soleus. These layers join together to form the oblongshaped Achilles tendon, which inserts on the proximal aspect of the calcaneal t~berosity.~ The Achilles tendon is subjected to the highest forces in the body, able to withstand tensile loads of up to eight times the body's weight during running. Blood supply may also have a role in the development of tendinitis. A watershed area exists 2 to 6 cm above the calcaneal insertion, which coincides with the location of most noninsertional Achilles tendon overuse injuries.3" Overuse injuries have been described in the Achilles tendon as a progression through stages defined by the site of involvement.2hInitially, the sheath surrounding the tendon (paratendon) becomes inflamed and then thickened and edematous. If the inciting activity is continued, the paratendinitis spreads to the tendon itself. Tendinosis occurs when the inflammation leads to focal, poorly organized scar tissue and degeneration, all of which tend to weaken the tensile strength of the tendon. Tendon rupture is considered the most serious Achilles
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tendon overuse injury and usually occurs as a result of eccentric contraction leading to tensile overload at the site of tendinosis. The rupture can be partial or complete. All of these stages can be differentiated histologically, but this differentiation can be clinically difficult despite its vital importance in defining therapeutic option^.^, l9 The cause of Achilles tendinitis is usually multifactorial. It is considered a combination of poor body mechanics, training errors, and environmental factors that can relate to malalignment of the hip, knee, ankle, or foot. Extrinsic factors, such as athletic shoes that do not stabilize the hindfoot sufficiently to prevent excessive varus/valgus rotation or do not contain maximal shock absorbing material, can also contribute to increased stress on the Achilles tendon. Even the type of exercise surface, especially firm or banked, can also be associated with tendinitis in recreational runners or aerobic exercisers.'" As with all overuse injuries, poor warm-up or abrupt increases in intensity, duration, or frequency of training can be seen as contributing factors to this tendiniti~.~' Clinically, in the early phase, athletes complain of pain primarily after strenuous activity. If the athlete continues to exercise, pain occurs with activity, usually running or repetitive jumping.'" The pain is localized to the inferior aspect of the posterior calf. The athlete may also note weakness during activity.31 Morning stiffness may be present in more chronic cases.'" Physical examination varies depending on the degree of tendon involvement. Decreased ankle dorsiflexion and tight hamstring muscles are common. Tenderness to palpation is usually present 2 to 6 cm above the insertion of the tendon on the calcaneus. Paratendinitis usually has a fixed point of tenderness and swelling near the malleolus as the ankle moves from dorsiflexion to plantar flexion. A thickened, possibly nodular area of tenderness on the Achilles tendon that moves as the ankle flexes is characteristic of involvement of the tendon itself? Paratendinitis and tendinosis may occur together. A retrocalcaneal bursitis can result from impingement between the inflamed Achilles tendon and the prominent superior angle of the calcaneus.'" Both ultrasound and MR imaging are useful in the evaluation of the extent of Achilles tendon injuries. Ultrasound can fairly reliably help to determine the extent of paratendon thickening and degeneration. MR imaging more effectively illustrates the degree of tendon injury, including partial or complete rupture, and also provides detailed information regarding the surrounding tissue.'" Although response to conservative management seems to be controversial and most likely related to part of tendon involvement as well as the chronicity of symptoms, noninvasive treatment is always advocated initially. The mainstay of conservative treatment is abstinence from the inciting activity together with physical therapy that emphasizes stretching and progressive resistance strengthening of the calf muscles.'o Correction of limb malalignment and the use of orthotics may be helpful. Heel wedges of 3/8 inches can help to diminish symptoms during daily activities; however, close monitoring to avoid further tendon contracture must be employed. Heel pads have not been demonstrated to be of help in the treatment of Achilles tendinitis.'" Because it is difficult to confine steroid injections to the paratendon (because a true sheath is not present), their use is not advocated because of their potential risk of causing intratendinous injury and subsequent rupture. Athletes are then usually instructed to gradually return to their previous activities once pain and tenderness have resolved and flexibility and strength are restored. For athletes who remain unresponsive to conservative management, surgery is an option, although the period of time to allow for noninvasive treatment is also controversial, ranging between 2 to 6 months.'", 31 Chronic fibrotic paraten-
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dinitis is considered a definite indication for surgery because the symptoms always recur with activity because of tightness of the paratendon.” For chronic tendinosis, surgery involves release of the posterior fascia and debridement of the focal areas of degenerated tendon.’(’Many athletes who have been diagnosed with chronic tendinosis are found to have partial tears upon exploration that were not detected by MR image. In these cases, the necrotic areas are then excised and the tendon is reinforced and r e ~ a i r e d Surgery .~ has actually been shown to allow 75% of athletes to return to high performance sport activity and 90% of recreational athletes to return to full previous a ~ t i v i t y . ~ Achilles tendon ruptures, partial and complete, may occur as the result of overuse and chronic tendinosis. Complete ruptures are most common in middleaged men involved in recreational athletics. Partial ruptures tend to occur in athletes between 20 and 40 years of age who perform at a more elite athletic level.”, 31 Ruptures usually result from rapid, eccentric loading of the Achilles tendon with the knee extended and the ankle flexed. The athlete often experiences a sensation of a ”pop” in the calf, and although the pain may not be disabling, the athlete will be unable to continue the activity because of weakness and acute swelling from edema and hem~rrhage.~’ Initially, a palpable gap in the tendon at the rupture site may be present acutely; however, over the ensuing hours a hematoma may fill the defect.‘ Athletes are unable to perform a single toe raise, indicating significant strength loss. It is important to be aware that active plantar flexion is possible in some cases of complete rupture of the Achilles tendon because of intact tibialis posterior, peroneals, and long-toe flexor muscles. Complete rupture of the tendon is most reliably indicated on physical examination by squeezing the posterior calf while the athlete is in the prone position with the feet off the edge of the table. An absence of plantar flexion represents discontinuity between the calf muscles and the foot, known as a positive Thompson‘s test.31 MR imaging and ultrasound are both useful adjuncts to confirm the diagnosis, especially in cases of partial ruptures. Many recent reports indicate that early surgery is the treatment of choice for ruptures.” Nonoperative management has been shown to carry a higher rate of re-rupture and a lower level of subsequent performance.” Although a fibrous scar band forms without surgery, only 10% to 30% of athletes return to preinjury activity level whereas approximately 75% of elite athletes and 90% of recreational athletes are able to return to pre-injury level with surgery.lY STRESSFRACTURES
A stress fracture is considered the ultimate overuse injury. It is defined as a partial or complete fracture of bone that occurs when the rate of microfractures in trabecular bone (the result of nonviolent, repetitive stress) surpasses the rate of repair.zyStress fractures can occur in any bone, but usually are seen in the lower extremities and are associated with running. It should be considered as a diagnosis in any athlete with continuous and unrelenting pain.21 Two theories exist to explain the occurrence of stress fractures in athletes; both involve muscle function in a key role. The most widely accepted theory is that muscles normally act to absorb energy when loaded and then gradually transmit this energy into the bone, functioning like a shock absorber. During prolonged exercise, muscle fatigues, and its capacity to absorb energy decreases, resulting in the transmission of undampened forces directly to bone. This redistribution of force to the bone increases stress at focal points causing microfrac-
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tures, which, if not allowed to repair, may lead to a stress fracture.22According to the second theory, which is less accepted, muscles act to dynamically cause stress fractures. It is proposed that the pull of the contracting muscle on bone produces sufficient repetitive force to create microfractures. The occurrence of stress fractures in non-weight-bearing bones supports this concept.20, 22 Several extrinsic factors are believed to be associated with the occurrence of stress fractures as well; the most important is the training regimen. A rapid increase in the running mileage or the intensity of workouts per unit of time have been found to be directly related to the incidence of stress f r a c t u r e ~ . ~ ~ Malalignment of lower extremities and alterations in the type of running surface and shoe type are also risk factors.29Stress fractures have an incidence up to 12 times higher in female athletes than in males under similar training conditions. Possible explanations include gait, diminished cortical bone thickness, and altered biomechanics secondary to a wider pelvis.29The high incidence of amenorrhea (especially in distance runners), which leads to some level of osteoporosis, most likely plays a contributing role as well. Therefore, the diagnosis of a stress fracture should also signal the need for an evaluation of training habits, athletic technique, and, if female, menstrual function.2 The diagnosis of a stress fracture may be difficult, which is why the clinician’s index of suspicion must always be high. Athletes characteristically describe localized pain with an insidious onset. Initially, the pain occurs after the activity (often running), but with continued training the pain will occur during exercise and soon limit activity.12Physical examination may reveal localized tenderness and swelling.12 Imaging of the involved bone is often not particularly helpful. Approximately two thirds of radiographs are normal early in the course of the condition, and only one half of these ever develop any radiographic evidence of a stress fracture. The characteristic radiographic findings include periosteal new bone formation, endosteal thickening, and a radiolucent line.2 Radionucleotide imaging is considered more sensitive than x-rays, especially early in the condition. Bone scans are able to detect small areas of new bone formation and therefore reflect the early accelerated remodeling that occurs in response to the microfractures. The bone scan also helps to determine the age of the stress fracture. Diffuse uptake in the early stages of the stress reaction is demonstrated, then a sharply marginated, fusiform uptake is present in the more advanced stages of the fracture.I2 Differentiation from other common soft-tissue abnormalities is another important use of the bone scan. The triple-phase bone scan has become particularly useful. It has three phases, including an angiogram, blood pool, and delayed image phase. In shin splints, which are a common cause of anterior shin pain, the angiogram and blood pool phases are negative, but are positive in the delayed image phase. Other soft-tissue disorders, such as plantar fasciitis and retrocalcaneal bursitis, also have characteristic patterns on bone scan, allowing differentiation from stress fractures.12 The incidence and location of the stress fracture vary depending on the sport. One study of 320 athletes with stress fractures confirmed by bone scan found the distribution to be 69% runners, 8% aerobic dancers, 5% racquet sport players, and 4% basketball players.1zThe majority of stress fractures involve the lower extremities. The head of the femur is one of the most serious locations for a stress fracture. Clinically, the athlete complains of groin pain and demonstrates a painful range of motion. The fracture occurs perpendicular to the lines of stress, and due to tension forces, displacement is a common complication. Ultimately, avascular necrosis, nonunion, or malunion can occur if the diagnosis
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is not made. Often, internal fixation with multiple threaded pins is the preferred treatment whether or not displacement has occurred.lz Runners tend to have stress fractures involving the tibia, fibula, and metatarsals. The shaft of the tibia is the most common site, accounting for approximately half of all stress fractures.1ZMost tibial stress fractures involve the proximal one third of the shaft and heal well with treatment. Stress fractures of the anterior midshaft of the tibia are not as common and are associated with jumping sports, such as basketball and ballet. They also have the potential to develop into a serious problem. These fractures often continue to delayed union and may fracture completely. The pathogenesis is not clear, but may involve the poor vascularity of the tibial cortex; they may eventually require bone grafting to heal completely.12 Another uncommon site for stress fractures is the tarsal navicular bone, occurring most often in basketball players. Clinicians must be aware of it as a diagnosis because early recognition is crucial for appropriate treatment to avoid chronic complications. The tarsal navicular bone is at high risk for this complication because of the relative avascularity of the central core of the bone. The discomfort may be mild but is usually located over the tarsal navicular bone or along the medial longitudinal arch. Limited dorsiflexion or subtalar motion is sometimes present. Immediate cast immobilization with non-weight-bearing for 6 to 8 weeks is recommended.z2A Jones’ fracture, which occurs at the metaphyseal-diaphyseal junction of the fifth metatarsal, typically occurs in basketball and football players. Poor local blood supply may contribute to its pathogenesis. Early bone scanning of any athlete with pain and tenderness in this area is advocated. Prolonged immobilization to try to avoid nonunion is recommended, but is not always successful. A high incidence of refracture after nonoperative treatment has been shown as well.zz The location, duration of symptoms, and the associated activities are all crucial factors in the management of stress fractures. In the majority of patients who receive prompt diagnosis, conservative management is most effective. A two-stage treatment program is often employed.’ Stage one involves use of NSAIDs and local physical therapy that emphasizes stretching and flexibility. The athlete is also restricted to a modified rest program, including normal weight bearing as tolerated during daily activities, but no sport activity. Once the athlete is free of pain at rest, which usually occurs in 2 to 3 weeks, the second stage is instituted. The inciting activity is gradually re-introduced, initially every other day with rest periods between as needed. Pain is used as the guideline for assessment of progress and when to advance or rest during rehabilitati~n.’~ If compliance is a problem, immobilization in a cast may be necessary. In general, exercise to maintain cardiac conditioning should be encouraged, such as bicycling and swimming. References 1. Beach W, Caspari R Arthroscopic management of rotator cuff disease. Orthopedics 16:1007, 1993 2. Bonutti P, Hawkins R Rotator cuff disorders. Baillieres Clin Rheumatol 3:535, 1989 3. Clement DB: Tibia1 stress syndrome in athletes. J Sports Med 2:81, 1974 4. DeMaio M, Paine R, Drez D Achilles tendonitis. Orthopedics 18:195, 1995 5. Ficat P, Hungerford D Disorders of the Patello-Femoral Joint. Baltimore, Williams and Wilkins, 1977 6. Field L, Altcheck D: Elbow injuries. Clin Sports Med 14:59, 1995
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7. Fulkerson J: Evaluation of peripatellar soft tissue and retinaculum in patients with patello-femoral pain. Clin Sports Med 8:197, 1989 8. Fulkerson J, Schutzer S After failure of conservative treatment for painful patellofemoral malalignment: Lateral release or realignment? Orthop Clin North Am 17283, 1986 9. Galea A, Albers J: Patello-femoral pain. Physician and Sports Medicine 22:48, 1994 10. Galloway M, Jokl P, Dayton 0 Achilles tendon overuse injuries. Clin Sports Med 11:771, 1992 11. Hart L: Exercise and soft tissue injury. Baillieres Clin Rheumatol 8:137, 1994 12. Hershman EB, Mailly T Stress fractures. Clin Sports Med 9:183, 1990 13. Host J, Craig R, Lehman R Patello-femoral dysfunction in tennis players. Clin Sports Med 14177, 1995 14. Jacobson K, Flandry F: Diagnosis of anterior knee pain. Clin Sports Med 8:179, 1989 15. Jobe F, Bradley J: The diagnosis of non-operative treatment of shoulder injuries in the athlete. Clin Sports Med 8:419, 1989 16. Keifhaber T, Stem P: Upper extremity tendonitis and overuse syndromes in the athlete. Clin Sports Med 11:39, 1992 17. Kelly M, Insall J: Historical perspectives of chondromalacia patellae. Orthop Clin North Am 23:517, 1992 18. Kibler W: Pathophysiology of overload injury around the elbow. Sports Med 14:447, 1995 19. Kvist M: Achilles tendon injuries in athletes. Sports Med 18:173, 1994 20. Matheson GO, et al: Stress fractures in athletes. Am J Sports Med 15:46, 1987 21. Mattalino A, Deese J, Campbell E: Office evaluation and treatment of lower extremities in the runner. Clin Sports Med 8:461, 1989 22. Meyer SA, et al: Stress fractures of the foot and leg. Clin Sports Med 12:395, 1993 23. Neer C: Anterior acromioplasty for chronic impingement syndrome in the shoulder. J Bone Joint Surg 54A:4, 1972 24. Paty J: Diagnosis and treatment of musculoskeletal running injuries. Semin Arthritis Rheum 18:48, 1988 25. Plancher K, Litchfield R, Hawkins R Rehabilitation of the shoulder in tennis players. Clin Sports Med 14:111, 1995 26. Puddu G, Ippolito E, Postacchini F: A classification of Achilles tendon disease. Am J Sports Med 4:145, 1976 27. Renstrom P, Johnson R Overuse injuries in sports. Sports Med 2:316, 1985 28. Roetert E, Brody H, Dillman C: The biomechanics of tennis elbow: An integrated approach. Clin Sports Med 1447, 1995 29. Sallis RE, Jones K: Stress fractures in athletes. Postgrad Med 89:185, 1991 30. Scioli M: Achilles tendonitis. Orthop Clin North Am 25:177, 1994 31. Soma C, Mandelbaum 8: Achilles tendon disorders. Clin Sports Med 13:811,1994 32. Steindler A: Kinesiology of the Human Body. Springfield, Illinois, Charles C Thomas, 1955 33. Wertheimer C: Patello-femoral mechanics as a cause of anterior knee pain. Your Patient and Fitness 9:19, 1995 34. Williams J: Achilles tendon lesions in sport. Sports Med 3:114, 1986
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OVERUSE SYNDROMES IN ADULT ATHLETES N. Nichole Barry, MD, and James L. McGuire, MD
Physicians are now required to view their patients as athletes who have adopted various modes of regular exercise. Rheumatologists, in particular, as specialists in musculoskeletal disorders, are seeing more patients with problems due to their exercise programs and the sports in which they participate. OVERUSE SYNDROMES
Overuse syndromes, including tendonitis, are common in adult athletes. Approximately 50% of all sports participants will be injured at one point, and at least half of those injuries will be attributed to overuse.1hOveruse injuries are generally considered to be due to “overload,” or repetitive microtrauma to the musculoskeletal Microtrauma, produced by tension or shear force, results in damage at both the molecular and microscopic level. Although microtrauma can occur with a single episode of excessive stress, the usual mechanism is repetitive loading forces on the musculotendinous unit at a force well within the physiologic limit. Each of the components of the musculotendinous unit usually adapts to an applied load in a different way. Bone will increase its local mass to withstand increases in loads, muscle becomes hypertrophic, and tendons and ligaments increase both their collagen content and cross-linking to reinforce their tensile strength. These processes will collectively result in an overall increase in the strength and flexibility of the musculotendinous unit over time. Repeated overload to the unit, which does not allow time for repair and adaptation results in disruption and inflammation. Further stress will compound the injury.I6 Many intrinsic and extrinsic factors contribute to overuse syndromes. Intrinsic factors include malalignment and muscle imbalance. For example, pes caws
From the Division of Immunology and Rheumatology, Stanford University Medical Center, Stanford, California
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(excessively high arches of the feet) is commonly associated with Achilles tendonitis and poor tracking of the patella (patello-femoral syndrome). Extrinsic factors, which consist primarily of training errors, account for 60% to 80% of injuries in runners.27Most studies show a consistent relationship between increased training mileage or intensity in runners and subsequent injury.I1 Improper training techniques, even if minor, can lead to muscular imbalance, which results in a strain on other musculotendon units. Furthermore, the diminished contractility of fatigued muscles limit the ability to absorb shock or stressz7 Any component of the musculotendinous unit is susceptible to injury-the muscle belly, tendon, musculotendinous junction, or the bony insertion of the unit itself. Injury generally occurs at the weakest point in the unit, which varies with age. In young athletes, excessive stress most often causes an avulsion fracture. After 25 years of age, the tendon is most susceptible to both traumatic and overuse injury due, at least in part, to the progressive degeneration of the collagen fibers. Muscle injuries and tears tend to be more common in the In addition to age, the dominant motions of the specific sport motions may amplify the already described intrinsic and extrinsic factors of overuse. Epicondylitis, shoulder impingement, patellofemoral syndrome, Achilles tendinitis, and stress fractures emerge as the most common overuse syndromes that athletes encounter. EPlCONDYLlTlS Lateral or medial epicondylitis are the most common overuse injuries that present with elbow pain in athletes involved in throwing and racquet sports. The cause of the tendon inflammation as a result of shearing forces over the epicondyle of the humerus is considered to be multifactorial. This would include the grip size, the weight of the racquet, the extensive range of motion of the entire arm, and the long durations of eccentric muscle contractions around the elbow.Is With racquet sports, microtrauma and overload may also be generated by the energy and vibrations transferred to the arm from the sudden impact between the racquet and high-velocity balls.28These factors all result in stiffness and weakness of the wrist extensors and supinators in lateral epicondylitis, and flexors and pronators in medial epicondylitis. The resultant inflexibility and weaknesses alter the smooth motion required in throwing and racquet strokes. This change in kinematics and lack of muscle tendon pliability contribute to inflammation of the tendons.I8 Lateral epicondylitis occurs in approximately 40% to 50% of all racquet sport athletes at one point in their career, and most are over 30 years of age.28It is characterized by pain on the lateral aspect of the elbow, which occurs with any activity requiring resisted wrist extension, as in a backhand stroke with a racquet. The pain can radiate to the forearm and improves or even resolves with rest, but recurrence on return to the inciting sport activity is usual. Morning stiffness of the elbow with persistent aching may occur if the athlete continues to play despite symptoms? On physical examination, maximal tenderness is present either directly over or somewhat distal to the lateral epicondyle with the elbow in flexion. Pain can be elicited in the same area with resisted wrist extension. Overall, the range of motion of the elbow is full. Swelling or erythema in the area or the forearm is not typical.6 Differentiation from degenerative changes of the radiocapitellar joint is crucial and can be done by applying an axial load on the forearm combined with gentle, passive supination and pronation. This motion com-
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presses the radiocapitellar joint without stressing the surrounding tendons and does not elicit pain in epicondylitis. Radiographs are typically negative, but calcific deposits and degenerative changes can be seen in chronic cases of epicondylitis.6 Medial epicondylitis (also known as golfer's elbow) is characterized by pain and tenderness over the medial epicondyle at the origins of the flexor and pronator tendons. As with lateral epicondylitis, pain is exacerbated by activity and alleviated with rest, and usually persists with chronic use. On physical examination, resisted wrist flexion and pronation will elicit symptoms. Again, a full range of motion of the elbow joint is present. Medial epicondylitis is associated with overhead tennis serves and some golf strokes. The repetitive valgus (outward from the midline) stress on the soft tissues of the medial elbow combined with tension generated by the wrist flexors and pronators during these strokes produces overload. Medial epicondylitis must be differentiated from a medial collateral ligament tear of the elbow. Application of a valgus force to a slightly flexed elbow with the wrist flexed and forearm pronated stresses the medial collateral ligament but should not cause pain in patients with intact ligaments or medial epicondylitis. Of note, medial epicondylitis may also lead to reversible impairment of conduction in the ulnar nerve, or ulnar neurapraxia, and the presentation of medial forearm and hand pain. Approximately 60% of patients undergoing surgery for medial epicondylitis had some signs or symptoms of ulnar nerve involvement.6 Treatment for lateral and medial epicondylitis are similar. Initially, the inciting activity, usually a racquet or throwing sport, should be avoided. Nonsteroidal anti-inflammatory drugs (NSAIDs) are also helpful to reduce pain acutely and should be continued for at least 3 weeks after the pain has resolved. Passive range of motion exercises should be carried out three to six times a day until pain-free motion is obtained. Rehabilitation exercises that focus on strengthening wrist flexors and extensors can then begin. Athletes can then slowly increase to small weights and rubber band resistance exercises. Counterforce bracing, which puts pressure directly over the involved tendons, has been shown to be useful in the treatment of epicondylitis as well. The nonelastic support acts to constrain extensor muscle expansion, thus decreasing the contractile tension and hopefully distributing forces to surrounding tissues.h In tennis, novice players have been shown to have an increased chance of developing lateral epicondylitis. To minimize recurrence, a review of technique, especially the backhand stroke, is essential prior to return to play. For instance, players using a one-handed backhand are more likely to develop lateral epicondylitis. It is well accepted that the one-handed backhand requires greater strength and coordination than a two-handed stroke. One theory is that the onehanded backhand links five body parts prior to impact (hips to trunk to shoulder to elbow to wrist), then to the racquet itself. With the two-handed backhand, only two body parts are linked prior to impact with the ball (hips to trunk) because the trunk, arms, and racquet move as one. No movement occurs at the elbows or wrists on impact, which helps the entire arm absorb the energy of the impact. It also forces the ball impact to be transmitted through the elbow rather than absorbed by the tissues around the elbow.6 In addition, equipment can play a role. Racquets with a larger head, but not necessarily heavier, can act to decrease vibrations and the number of miss-hits, which diminishes the microtrauma to the soft tissues of the elbow.2x Completing a well-planned rehabilitation program with appropriate strengthening of muscles and correction of poor technique is imperative for recovery and return to prior level of play. Previous injury may play a large role
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in elbow pathology. Incomplete rehabilitation of a previous epicondylitis episode may have a 70% chance of recurrence.'* At least 6 months (preferably 1 year) of rehabilitation should be attempted prior to considering surgery. Local steroid injection may also play a role in the management of chronic epicondylitis and should be coordinated within the rehabilitation plan. The downtime following the injection should be at least 6 weeks. Despite being asymptomatic, the chance of tendon rupture from premature resumption of play remains for at least a month. An intensive rehabilitation process can begin again 6 weeks postinjection. Surgery is a last resort and involves local debridement of abnormal granulation tissue and abrasion at the site of origin of the involved tendons. Here again, a comprehensive postoperative program is also necessary.18 IMPINGEMENT OF THE SHOULDER AND ROTATOR CUFF
Overuse injuries to the shoulder are common in athletes involved in throwing and racquet sports. Impingement of the tendons of the rotator cuff (the teres minor, infraspinatus, supraspinatus, and subscapularis) between the head of the humerus and the acromion may ultimately lead to frank tears of the rotator cuff (Fig. 1). Both overhand throwing and racquet strokes place repetitive, highvelocity stress on the shoulder joint, gradually resulting in subluxation or movement of the humeral head anteriorly. This instability, which is subtle, may then lead to recurrent subluxation and impingement of the rotator cuff.I5 This "cascade" of events, which can ultimately result in a tear of one or more tendons of the rotator cuff, is often referred to as the instability complex.15 Athletes may present with pure and isolated impingement without any instability. This is usually seen in older athletes and is considered secondary to degenerative changes within the joint itself. Impingement may also be associated with instability caused by repetitive microtrauma on the labrum (the ring of fibrocar-
Subscapularis
Figure 1. Superior view of the rotator cuff muscles. (From Hartley A: Practical joint assessment. In Weimer R (ed):A Sports Medicine Manual. St. Louis, Mosby-Year Book, 1991, p 92; with permission.)
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tilage that forms the glenoid cavity of the scapula) and the capsular ligaments. Inherent hyperelasticity can lead to instability and impingement as well. Ultimately, all impingements can progress to rotator cuff tears.Is The glenohumeral joint is considered to be ”inherently unstable.” The stability is provided by the static glenohumeral ligaments and dynamic musculotendinous units of the rotator cuff, which together restrain the limits of motion of the humeral head; however, the position of abduction, coupled with external rotation, applies significant stress to the anterior shoulder. Repetitive motion from this position initially leads to damage of the glenohumeral ligaments, and even vascular compromise due to pressure from the acromion, eventually stretching the joint capsule. Any abnormal capsuloligamentous laxity or muscle weakness then allows greater humeral head motion.’ With injury to the static stabilizers of the joint, the musculotendinous units (the rotator cuff) must act to maintain stability. The eccentric overload (which refers to contraction of muscle fibers as they lengthen) of the rotator cuff will eventually result in fatigue and inflammation of the tendons as well as asymmetric weakness of the muscles. This further compromises stability and allows translation of the head of the humerus. As the humeral head moves further anteriorly and superiorly, with abrasion of the labrum, impingement of the rotator cuff tendons occurs as they approximate against the coracoacromial arch.’, 25 The unusual location of the rotator cuff tendons, confined between the humeral head on one side and the acromion on the other, also contributes to the confinement of the swelling and the chronicity of tendinitis. Ultimately, this degeneration results in attrition of the tendons.’ The muscle-tendon complex of the biceps brachii assists in the maintenance of the anterior stability of the glenohumeral joint. Together with the rotator cuff it controls the deceleration of the arm after striking or throwing the ball and minimizes the stress placed on the inferior glenohumeral ligaments. Irritation and inflammation of the biceps tendon may also occur with impingement. Although biceps tendonitis may be the initial presentation of overuse, the possibility of humeral instability should be considered because a more extensive treatment and rehabilitation would be necessary.’” 25 In the early 1970s, Neer23stated that 95% of rotator cuff tears are associated with impingement (not including those secondary to one-time traumatic events). He described three stages in the development of rotator cuff tears from overuse, which still remains clinically useful. Stage One-Edema and hemorrhage within and around the tendons are the pathologic manifestation of this stage. Clinically, the patients describe a ”toothache-like” pain extending from the shoulder to the mid-upper arm, usually occurring after activities involving flexion and abduction of the arm. On physical examination, point tenderness is present over the greater tuberosity of the humerus.’ A positive impingement sign is demonstrated by pain with forward flexion and internal rotation of the arm, which compresses the supraspinatus tendon of the rotator cuff between the greater tuberosity of the humerus and the anterior-inferior acromial s ~ r f a c e . At ’ ~ this point, no weakness or loss of motion is present. Stage Two-The shoulder pain becomes constant but often worsens at night. Any activity involving overhead movement of the arm will exacerbate the pain. On physical examination, tenderness is more diffuse than in stage one and more intense. The range of motion may be limited by pain, but passive range is usually normal. Involvement of the acromioclavicular joint may also be present.’
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Stage Three-Although the symptoms of this stage are similar to stage two, athletes usually have had a long history of shoulder problems. Athletes may feel weak secondary to pain or prolonged disuse. The range of motion is decreased, either secondary to disuse or a partial rotator cuff tear. Pathologically, tendon degeneration and attrition are present. Partial thickness tears, the next stage in the continuum of rotator cuff disease, may then easily occur or extend with minor trauma or stress. Rotator cuff tears usually involve the supraspinatus muscle; therefore, subtle changes in strength may reflect partial tears or extensions of tears. Isolation of the supraspinatus muscle can be accomplished by abducting the athlete's outstretched arm to 90 degrees, forward flexing to 30 degrees, and maximally internally rotating it (thumbs down). Strength can then be tested by forced resistance and compared for ~ymmetry.'~ Several signs on physical examination suggest complete tears of the rotator cuff. These include supraspinatus wasting, with or without infraspinatus wasting; a painful arc of motion at 90 degrees of abduction or forward flexion; and greater passive than active range of motion, especially in abduction and external rotation. The inability to slowly lower the arm from 90 degrees of abduction, the "drop arm test," may also be elicited. In addition, weakness in abduction and external rotation may be present.' Radiographs, especially the anterior-posterior view, allow for the visualization of the undersurface of the acromion, the acromioclavicular joint, and the glenohumeral joint. If the distance between the undersurface of the acromion and the superior surface of the humeral head is less than 6 mm, then the possibility of a rotator cuff tear should be considered. In addition, a complete tear is often associated with sclerosis and osteophyte formation along the anterior-inferior acromion and over the greater tuberosity of the humerus.2 Calcification of the tendons composing the rotator cuff may also occur with prolonged inflammation. The differential diagnosis should include subacromial bursitis and acromioclavicular osteoarthritis, both of which can be aggravated by overuse, especially in older adults. Both are usually associated with pain on palpation of the involved structure. Local injection of lidocaine may be used to differentiate the cause of the shoulder pain if necessary. Treatment of stage one overuse involves avoidance of the inciting activity (overhead sports), NSAIDs, and intensive physical therapy to strengthen the muscles involved in internal and external rotation. The strengthening program should use isometric (contraction with both ends of the muscle held fixed), isokinetic (contraction with constant motion), and isotonic (contraction leading to shortening with a constant load) exercises.15Local steroid injections with a low dose of a short-acting glucocorticoid may also be used, but no more than twice and with at least 3 months between injections. Some orthopedic surgeons believe that athletes who require a steroid injection for pain relief should have more aggressive evaluation involving an MRI or arthroscopy. The vast majority of cases of stage one tendinitis is reversible with conservative treatment.' Athletes with stage two impingement have a fibrotic supraspinatus tendon and persistent pain. They should initially receive conservative treatment with intensive physical therapy and NSAIDs. If athletes do not respond within 3 to 6 months, then more aggressive diagnostic and even surgical management should be considered.' Many orthopedic surgeons initially obtain an MR image to evaluate the diagnosis of a cuff tear. Arthroscopy is also a diagnostic alternative because it allows direct inspection of the glenohumeral joint and subacromial
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area as well as the rotator cuff. At the same time, repair of small tears with dbbridement to initiate healing can be carried out. Removal of acromial spurs and subacromial decompression can also be performed, in which the anterior acromion is exposed and shaved at the lateral tip of the acromioclavicular joint. These manipulations are designed to diminish any pathology from the acromion that may be contributing to impingement of the rotator cuff tendons. This allows increased free movement between the humeral head and the undersurface of the acromion. Up to 90% of patients describe dramatic pain relief, and hopefully the future inflammatory response will be minimized.2 Early surgical intervention in the shoulder of patients with impingement unresponsive to conservative treatment or patients with a partial rotator cuff tear results in improved function, pain relief, and most importantly, the prevention of progression to complete tears. In addition, small tears are more easily repaired and have better outcomes.2 Prevention of complete rotator cuff tears also decreases the incidence and severity of secondary arthropathy. By stage three, the rotator cuff deficiency will usually have resulted in some degree of glenohumeral arthritis. Of note, two factors that contribute to a poor prognosis of surgical repair of a rotator cuff tear are the size of the tear and the duration of the restricted motion preoperatively, further supporting the argument for early, aggressive surgical intervention.2 PATELLO-FEMORAL DYSFUNCTION
Anterior knee pain is the most common complaint presenting to sports medicine physicians, and overuse is a major contributing factor, especially in sports involving running, jumping, quick stops, and turns. The most common cause of anterior knee pain is abnormal patellar tracking produced by mechanical overload and excessive lateral vector forces on the joint (patello-femoral dysfunction).z' In fact, patello-femoral dysfunction is often seen in the general population, occurring in up to one in four patients, and is considered to have a higher incidence in athletes.13 The primary function of the patella, a special sesamoid bone, is to increase the "lever arm" of the quadriceps muscle during extension. Throughout the entire range of motion of the knee, the patella has been demonstrated to increase the force of extension by as much as 50Y0.~~ The patella also transmits load from the quadriceps to the trochlear surface of the femur. Biomechanical studies have demonstrated forces on the patello-femoral joint as among the highest per unit area of any joint in the body.I4 The patella also has the thickest cartilage in the body, which enables it to withstand forces that may exceed seven times the body weight during squatting.14 Disturbances of patellar mechanics are due to abnormalities in the position of the patella as it moves through the trochlear groove of the femur. The patella does not articulate with the trochlea until 20 degrees of flexion (full extension is 0 degrees). Disturbances range from an abnormal tilt of the patella to abnormal tracking in the trochlear groove to frank dislocation. Athletes who have shallow trochlear grooves or low lateral walls of the trochlea have an increased risk for patellar malalignment or subluxation. Other risk factors for patellar dysfunction include general ligamentous laxity and abnormal limb alignment (e.g., knee valgus or foot ~ r o n a t i o n ) .Because ~~ the vastus medialis muscle functions throughout the range of motion of the knee to align the patella, this muscle is a factor in patello-femoral malalignment. Focal strengthening of the vastus medialis muscle is a major factor in rehabilitation. Straight-leg raising exercises are
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considered the most effective means of focal strengthening, although they are not uniformly used (Fig. 2).13 One type of malalignment is characterized by a lateral tilt of the patella within the trochlear groove, which leads to an adaptive shortening of the lateral retinaculum, and as a result, the medial retinaculum may stretch or tear? With flexion of the knee, the patella is forcefully drawn into the lateral trochlear groove. Eventually, the cartilage of the undersurface of the patella can be di~rupted.'~ The relationship between abnormal patellar tracking and changes in articular cartilage are often causally liked." An association between changes in articular cartilage and tilt-subluxation patterns of malalignment has been similarly suggested. The incidence of chondromalacia is higher in patients with subluxation (93%)than in those with frank dislocation (62%)of the patella. Any increase in compressive forces that exceed physiologic range, which are normally quite high, may lead to damage of the cartilage or ch~ndromalacia.'~ The historical causal relationship between chondromalacia and patello-femoral pain due to malalignment has recently been reexamined, in part because of the lack of correlation of arthroscopic findings of fibrillation, cartilage softening, or disruption in many patients with the clinical syndrome of patello-femoral
Vastus Lateralis
Rectus Femoris
Vastus Medialis
Patella Lateral Retinacul urn
Medial Retinaculum
Patellar Ligament
Figure 2. The knee, illustrating the medial and lateral retinaculum. ( f r o m Wertheimer C: Patellofemoral mechanics as a cause of anterior knee pain. Your Patient and Fitness 9:21, 1995; with permission.)
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pain. This does not mean that cartilage degeneration will not cause pain when bone is exposed, but rather that other factors related to patellar malalignment, such as chronic strain on the retinaculum (which is richly innervated), may also result in similar pain. It is now generally agreed that chondromalacia is most likely caused by chronic patello-femoral dysf~nction.~, ’. l7 Chondromalacia is considered a gross pathologic diagnosis and is reserved for findings from arthroscopy or s ~ r g e r yThe . ~ relationship to osteoarthritis is still debated. The diagnosis of patello-femoral dysfunction may be somewhat difficult. Athletes complain of gradual onset of a dull ache in the peri- or retro-patellar region. In milder cases, symptoms are initiated by activities involving running (especially long distance) as well as jumping and quick stops and starts. Pain initially resolves if the inciting activity is discontinued; however, as the condition worsens, pain may become constant. Classic activities that exacerbate pain include squatting, walking up or down stairs, and prolonged sitting. Some athletes will describe a popping, grinding, or a catching sensation under the patella. Continued aggravation of the patello-femoral joint dysfunction will lead to constant pain and the sensation of weakness in the quadriceps.’? On physical examination, atrophy of the vastus medialis may be present. Tight hamstring muscles (the muscles of the posterior thigh, which include the semimembranosus, semitendinosus, gracilis, sartorius, and biceps femoris) may be noted. Tight hamstrings are thought to lead to increased knee flexion during running, which in turn increases the patello-femoral joint forces.I3Patellar stability should be evaluated by having the athlete flex the knee to 20 degrees over a pillow, which engages the patella into the trochlear groove. The patella should then be manually pushed medially and laterally to determine the percentage of its total width that can be forced out of the trochlear groove. Displacement to the side by more than 75% of its total width suggests an increased risk for subluxation. If the patella can barely be pushed out of the groove medially, a tight lateral retinaculum is present and suggests the possibility of patellar tilt. Both are indicative of patello-femoral malalignment /dysfunction.?? The amount of patellar tilt can also be evaluated by having the athlete relax the knee in extension (the patella will not be in the trochlear groove). The patella is then grasped between the examiner’s thumb and index finger and the lateral edge is pulled straight upward and tilted. A normal patella will only tilt approximately 20 degrees above horizontal. Any tilt greater than 20 degrees is abnormal. Again, inability to pull the patella to or above the horizontal plane is strongly suggestive of a tight lateral r e t i n a c ~ l u m . ~ ~ A positive apprehension sign, occurring when the knee is flexed to 30 degrees and lateral pressure is placed against the medial aspect of the patella, is suspicious for recurrent subluxation. Patellas at higher risk for subluxation are those which are ”high-riding” or have a lateral rotation over the trochleas on inspection. Lastly, patellar cartilage or bone may be assessed by compressing the patella against the trochlea while the knee is passively moved from full extension to partial flexion. Pain and crepitus elicited with compression suggests cartilage degeneration or exposure of bone, which may accompany long-term patellar rnalaligr~ment.~~ Differentiation between a plica and patello-femoral malalignment in the affected knee is important because some symptoms are similar. A synovial plica is a redundant fold in the synovial lining of the knee, which is present in 60% of the population. It is usually crescent shaped, extending from the infrapatellar fat pad medially, looping around the femoral condyle, crossing under the suprapatellar tendon, and then passing laterally over the lateral femoral condyle to
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the lateral retinaculum. When chronically inflamed and fibrotic from overuse and stress, anterior knee pain results (Fig. ,).I4 Common complaints of an inflamed plica include gradual onset of pain over the anterior knee, which increases when sitting with the knee in flexion for a prolonged period of time. More severe pain then occurs upon rising, but diminishes after 8 to 10 steps. This occurs because the plica is trapped over the femoral condyles in flexion. With extension of the knee, the articularis genus muscle acts to extract it to prevent impingement in the patello-femoral joint; however, sufficient elevation of the plica may require 8 to 10 steps. If the plica does become entrapped as the quadriceps contract, the athlete will feel pain and the sensation that the knee may give out or b~ck1e.I~ On physical examination, palpation of the fibrotic and inflamed plica along the anterior femoral condyle may elicit pain. Otherwise, examination of the knee and patella will be normal and no effusion is noted. Treatment includes rest, ice, stretching of hamstrings, and strengthening of the quadriceps. If symptoms become chronic, surgical intervention may be necessary and is usually curative.13 In regard to patello-femoral malalignment and dysfunction, radiographs may be helpful. Lateral views provide information as to patellar thickness and height. The presence of a patella alta (a high-riding patella) can be determined by comparing the length of the patella to the length of the inferior patellar tendon (distance from the inferior pole to the tibia1 tubercle). If the tendon length is greater than 1.2 times the length of the patella, then patella alta is present and the risk for subluxation is higher.33An infrapatellar, or sunrise view, allows for evaluation of patello-femoral articulation. A lateral tilt of the patella may be appreciated on this view as well. Low femoral condyles or a shallow groove provide less of a sulcus for tracking and suggest poor patellar stability and malalignment.14 Treatment of patello-femoral dysfunction should initially include an aggres-
Figure 3. The knee, demonstrating the anatomy and location of the suprapatellar plica. Note also the articularis genu muscle, which inserts on the superior portion of the plica. (Adapted from Jacobson K, Flandry F: Diagnosis of anterior knee pain. Clin Sports Med
8:88,1989.)
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sive physical therapy program that involves stretching of the iliotibial band and the hamstring muscles as well as the lateral retinaculum if it is tight. Strengthening of the vastus medialis muscle should also be included to help provide dynamic medial stabilization of the ~atel1a.I~ Taping of the patella (McConnell method), which supposedly facilitates proper tracking, may decrease or eliminate pain and allow muscle strengthening.l3Patellar stabilization braces (usually neoprene with a hole for the patella), which can be obtained off the shelf in many sports stores, may also be of use. The best approach is to diminish symptoms as much as possible during the athletic activity. To allow continued participation in the activity while undergoing physical therapy,I3 it is important to remind the athlete that it may take several months of continuous exercise to achieve the increased strength and flexibility necessary to resolve the pain. At least 8 to 9 months of conservative management should be attempted before considering surgery. Realignment of the patello-femoral joint is generally considered a major surgical procedure. Clear-cut evidence of poor tracking of the patella, with or without subluxation, should be present either radiographically or arthroscopically before considering corrective surgery, which is usually done by arthroscope as well.R The lateral release of the patella is an appropriate procedure for correction of mild malalignment, without history of subluxation, as well as denervation of the painful, tight lateral retinaculum, which also serves to reduce the pathologically tilted r at el la.^ This procedure limits articular cartilage contact under stress with the associated decrease in soft-tissue strain. Athletes with more advanced malalignment do not do as well with a lateral release procedure alone.KAdditional surgical techniques that serve to change the position and dynamics of the patella, such as patellar realignment and tibia1 tubercle anteromedialization, may be required if the athlete has recurrent patellar subluxation or considerable patellar tilting and degenerati~n.~
ACHILLES TENDINITIS
Achilles tendinitis i s another common overuse injury seen among recreational athletes. It most typically affects adult male athletes involved in sports requiring constant running and repetitive jumping3' Epidemiologic studies have shown that Achilles tendinitis accounts for 15%of all running injuries.?' The Achilles tendon is the strongest and largest tendon in the body. It arises from both the medial and lateral heads of the gastrocnemius muscle as well as the deeper layers of the soleus. These layers join together to form the oblongshaped Achilles tendon, which inserts on the proximal aspect of the calcaneal t~berosity.~ The Achilles tendon is subjected to the highest forces in the body, able to withstand tensile loads of up to eight times the body's weight during running. Blood supply may also have a role in the development of tendinitis. A watershed area exists 2 to 6 cm above the calcaneal insertion, which coincides with the location of most noninsertional Achilles tendon overuse injuries.3" Overuse injuries have been described in the Achilles tendon as a progression through stages defined by the site of involvement.2hInitially, the sheath surrounding the tendon (paratendon) becomes inflamed and then thickened and edematous. If the inciting activity is continued, the paratendinitis spreads to the tendon itself. Tendinosis occurs when the inflammation leads to focal, poorly organized scar tissue and degeneration, all of which tend to weaken the tensile strength of the tendon. Tendon rupture is considered the most serious Achilles
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tendon overuse injury and usually occurs as a result of eccentric contraction leading to tensile overload at the site of tendinosis. The rupture can be partial or complete. All of these stages can be differentiated histologically, but this differentiation can be clinically difficult despite its vital importance in defining therapeutic option^.^, l9 The cause of Achilles tendinitis is usually multifactorial. It is considered a combination of poor body mechanics, training errors, and environmental factors that can relate to malalignment of the hip, knee, ankle, or foot. Extrinsic factors, such as athletic shoes that do not stabilize the hindfoot sufficiently to prevent excessive varus/valgus rotation or do not contain maximal shock absorbing material, can also contribute to increased stress on the Achilles tendon. Even the type of exercise surface, especially firm or banked, can also be associated with tendinitis in recreational runners or aerobic exercisers.'" As with all overuse injuries, poor warm-up or abrupt increases in intensity, duration, or frequency of training can be seen as contributing factors to this tendiniti~.~' Clinically, in the early phase, athletes complain of pain primarily after strenuous activity. If the athlete continues to exercise, pain occurs with activity, usually running or repetitive jumping.'" The pain is localized to the inferior aspect of the posterior calf. The athlete may also note weakness during activity.31 Morning stiffness may be present in more chronic cases.'" Physical examination varies depending on the degree of tendon involvement. Decreased ankle dorsiflexion and tight hamstring muscles are common. Tenderness to palpation is usually present 2 to 6 cm above the insertion of the tendon on the calcaneus. Paratendinitis usually has a fixed point of tenderness and swelling near the malleolus as the ankle moves from dorsiflexion to plantar flexion. A thickened, possibly nodular area of tenderness on the Achilles tendon that moves as the ankle flexes is characteristic of involvement of the tendon itself? Paratendinitis and tendinosis may occur together. A retrocalcaneal bursitis can result from impingement between the inflamed Achilles tendon and the prominent superior angle of the calcaneus.'" Both ultrasound and MR imaging are useful in the evaluation of the extent of Achilles tendon injuries. Ultrasound can fairly reliably help to determine the extent of paratendon thickening and degeneration. MR imaging more effectively illustrates the degree of tendon injury, including partial or complete rupture, and also provides detailed information regarding the surrounding tissue.'" Although response to conservative management seems to be controversial and most likely related to part of tendon involvement as well as the chronicity of symptoms, noninvasive treatment is always advocated initially. The mainstay of conservative treatment is abstinence from the inciting activity together with physical therapy that emphasizes stretching and progressive resistance strengthening of the calf muscles.'o Correction of limb malalignment and the use of orthotics may be helpful. Heel wedges of 3/8 inches can help to diminish symptoms during daily activities; however, close monitoring to avoid further tendon contracture must be employed. Heel pads have not been demonstrated to be of help in the treatment of Achilles tendinitis.'" Because it is difficult to confine steroid injections to the paratendon (because a true sheath is not present), their use is not advocated because of their potential risk of causing intratendinous injury and subsequent rupture. Athletes are then usually instructed to gradually return to their previous activities once pain and tenderness have resolved and flexibility and strength are restored. For athletes who remain unresponsive to conservative management, surgery is an option, although the period of time to allow for noninvasive treatment is also controversial, ranging between 2 to 6 months.'", 31 Chronic fibrotic paraten-
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dinitis is considered a definite indication for surgery because the symptoms always recur with activity because of tightness of the paratendon.” For chronic tendinosis, surgery involves release of the posterior fascia and debridement of the focal areas of degenerated tendon.’(’Many athletes who have been diagnosed with chronic tendinosis are found to have partial tears upon exploration that were not detected by MR image. In these cases, the necrotic areas are then excised and the tendon is reinforced and r e ~ a i r e d Surgery .~ has actually been shown to allow 75% of athletes to return to high performance sport activity and 90% of recreational athletes to return to full previous a ~ t i v i t y . ~ Achilles tendon ruptures, partial and complete, may occur as the result of overuse and chronic tendinosis. Complete ruptures are most common in middleaged men involved in recreational athletics. Partial ruptures tend to occur in athletes between 20 and 40 years of age who perform at a more elite athletic level.”, 31 Ruptures usually result from rapid, eccentric loading of the Achilles tendon with the knee extended and the ankle flexed. The athlete often experiences a sensation of a ”pop” in the calf, and although the pain may not be disabling, the athlete will be unable to continue the activity because of weakness and acute swelling from edema and hem~rrhage.~’ Initially, a palpable gap in the tendon at the rupture site may be present acutely; however, over the ensuing hours a hematoma may fill the defect.‘ Athletes are unable to perform a single toe raise, indicating significant strength loss. It is important to be aware that active plantar flexion is possible in some cases of complete rupture of the Achilles tendon because of intact tibialis posterior, peroneals, and long-toe flexor muscles. Complete rupture of the tendon is most reliably indicated on physical examination by squeezing the posterior calf while the athlete is in the prone position with the feet off the edge of the table. An absence of plantar flexion represents discontinuity between the calf muscles and the foot, known as a positive Thompson‘s test.31 MR imaging and ultrasound are both useful adjuncts to confirm the diagnosis, especially in cases of partial ruptures. Many recent reports indicate that early surgery is the treatment of choice for ruptures.” Nonoperative management has been shown to carry a higher rate of re-rupture and a lower level of subsequent performance.” Although a fibrous scar band forms without surgery, only 10% to 30% of athletes return to preinjury activity level whereas approximately 75% of elite athletes and 90% of recreational athletes are able to return to pre-injury level with surgery.lY STRESSFRACTURES
A stress fracture is considered the ultimate overuse injury. It is defined as a partial or complete fracture of bone that occurs when the rate of microfractures in trabecular bone (the result of nonviolent, repetitive stress) surpasses the rate of repair.zyStress fractures can occur in any bone, but usually are seen in the lower extremities and are associated with running. It should be considered as a diagnosis in any athlete with continuous and unrelenting pain.21 Two theories exist to explain the occurrence of stress fractures in athletes; both involve muscle function in a key role. The most widely accepted theory is that muscles normally act to absorb energy when loaded and then gradually transmit this energy into the bone, functioning like a shock absorber. During prolonged exercise, muscle fatigues, and its capacity to absorb energy decreases, resulting in the transmission of undampened forces directly to bone. This redistribution of force to the bone increases stress at focal points causing microfrac-
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tures, which, if not allowed to repair, may lead to a stress fracture.22According to the second theory, which is less accepted, muscles act to dynamically cause stress fractures. It is proposed that the pull of the contracting muscle on bone produces sufficient repetitive force to create microfractures. The occurrence of stress fractures in non-weight-bearing bones supports this concept.20, 22 Several extrinsic factors are believed to be associated with the occurrence of stress fractures as well; the most important is the training regimen. A rapid increase in the running mileage or the intensity of workouts per unit of time have been found to be directly related to the incidence of stress f r a c t u r e ~ . ~ ~ Malalignment of lower extremities and alterations in the type of running surface and shoe type are also risk factors.29Stress fractures have an incidence up to 12 times higher in female athletes than in males under similar training conditions. Possible explanations include gait, diminished cortical bone thickness, and altered biomechanics secondary to a wider pelvis.29The high incidence of amenorrhea (especially in distance runners), which leads to some level of osteoporosis, most likely plays a contributing role as well. Therefore, the diagnosis of a stress fracture should also signal the need for an evaluation of training habits, athletic technique, and, if female, menstrual function.2 The diagnosis of a stress fracture may be difficult, which is why the clinician’s index of suspicion must always be high. Athletes characteristically describe localized pain with an insidious onset. Initially, the pain occurs after the activity (often running), but with continued training the pain will occur during exercise and soon limit activity.12Physical examination may reveal localized tenderness and swelling.12 Imaging of the involved bone is often not particularly helpful. Approximately two thirds of radiographs are normal early in the course of the condition, and only one half of these ever develop any radiographic evidence of a stress fracture. The characteristic radiographic findings include periosteal new bone formation, endosteal thickening, and a radiolucent line.2 Radionucleotide imaging is considered more sensitive than x-rays, especially early in the condition. Bone scans are able to detect small areas of new bone formation and therefore reflect the early accelerated remodeling that occurs in response to the microfractures. The bone scan also helps to determine the age of the stress fracture. Diffuse uptake in the early stages of the stress reaction is demonstrated, then a sharply marginated, fusiform uptake is present in the more advanced stages of the fracture.I2 Differentiation from other common soft-tissue abnormalities is another important use of the bone scan. The triple-phase bone scan has become particularly useful. It has three phases, including an angiogram, blood pool, and delayed image phase. In shin splints, which are a common cause of anterior shin pain, the angiogram and blood pool phases are negative, but are positive in the delayed image phase. Other soft-tissue disorders, such as plantar fasciitis and retrocalcaneal bursitis, also have characteristic patterns on bone scan, allowing differentiation from stress fractures.12 The incidence and location of the stress fracture vary depending on the sport. One study of 320 athletes with stress fractures confirmed by bone scan found the distribution to be 69% runners, 8% aerobic dancers, 5% racquet sport players, and 4% basketball players.1zThe majority of stress fractures involve the lower extremities. The head of the femur is one of the most serious locations for a stress fracture. Clinically, the athlete complains of groin pain and demonstrates a painful range of motion. The fracture occurs perpendicular to the lines of stress, and due to tension forces, displacement is a common complication. Ultimately, avascular necrosis, nonunion, or malunion can occur if the diagnosis
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is not made. Often, internal fixation with multiple threaded pins is the preferred treatment whether or not displacement has occurred.lz Runners tend to have stress fractures involving the tibia, fibula, and metatarsals. The shaft of the tibia is the most common site, accounting for approximately half of all stress fractures.1ZMost tibial stress fractures involve the proximal one third of the shaft and heal well with treatment. Stress fractures of the anterior midshaft of the tibia are not as common and are associated with jumping sports, such as basketball and ballet. They also have the potential to develop into a serious problem. These fractures often continue to delayed union and may fracture completely. The pathogenesis is not clear, but may involve the poor vascularity of the tibial cortex; they may eventually require bone grafting to heal completely.12 Another uncommon site for stress fractures is the tarsal navicular bone, occurring most often in basketball players. Clinicians must be aware of it as a diagnosis because early recognition is crucial for appropriate treatment to avoid chronic complications. The tarsal navicular bone is at high risk for this complication because of the relative avascularity of the central core of the bone. The discomfort may be mild but is usually located over the tarsal navicular bone or along the medial longitudinal arch. Limited dorsiflexion or subtalar motion is sometimes present. Immediate cast immobilization with non-weight-bearing for 6 to 8 weeks is recommended.z2A Jones’ fracture, which occurs at the metaphyseal-diaphyseal junction of the fifth metatarsal, typically occurs in basketball and football players. Poor local blood supply may contribute to its pathogenesis. Early bone scanning of any athlete with pain and tenderness in this area is advocated. Prolonged immobilization to try to avoid nonunion is recommended, but is not always successful. A high incidence of refracture after nonoperative treatment has been shown as well.zz The location, duration of symptoms, and the associated activities are all crucial factors in the management of stress fractures. In the majority of patients who receive prompt diagnosis, conservative management is most effective. A two-stage treatment program is often employed.’ Stage one involves use of NSAIDs and local physical therapy that emphasizes stretching and flexibility. The athlete is also restricted to a modified rest program, including normal weight bearing as tolerated during daily activities, but no sport activity. Once the athlete is free of pain at rest, which usually occurs in 2 to 3 weeks, the second stage is instituted. The inciting activity is gradually re-introduced, initially every other day with rest periods between as needed. Pain is used as the guideline for assessment of progress and when to advance or rest during rehabilitati~n.’~ If compliance is a problem, immobilization in a cast may be necessary. In general, exercise to maintain cardiac conditioning should be encouraged, such as bicycling and swimming. References 1. Beach W, Caspari R Arthroscopic management of rotator cuff disease. Orthopedics 16:1007, 1993 2. Bonutti P, Hawkins R Rotator cuff disorders. Baillieres Clin Rheumatol 3:535, 1989 3. Clement DB: Tibia1 stress syndrome in athletes. J Sports Med 2:81, 1974 4. DeMaio M, Paine R, Drez D Achilles tendonitis. Orthopedics 18:195, 1995 5. Ficat P, Hungerford D Disorders of the Patello-Femoral Joint. Baltimore, Williams and Wilkins, 1977 6. Field L, Altcheck D: Elbow injuries. Clin Sports Med 14:59, 1995
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7. Fulkerson J: Evaluation of peripatellar soft tissue and retinaculum in patients with patello-femoral pain. Clin Sports Med 8:197, 1989 8. Fulkerson J, Schutzer S After failure of conservative treatment for painful patellofemoral malalignment: Lateral release or realignment? Orthop Clin North Am 17283, 1986 9. Galea A, Albers J: Patello-femoral pain. Physician and Sports Medicine 22:48, 1994 10. Galloway M, Jokl P, Dayton 0 Achilles tendon overuse injuries. Clin Sports Med 11:771, 1992 11. Hart L: Exercise and soft tissue injury. Baillieres Clin Rheumatol 8:137, 1994 12. Hershman EB, Mailly T Stress fractures. Clin Sports Med 9:183, 1990 13. Host J, Craig R, Lehman R Patello-femoral dysfunction in tennis players. Clin Sports Med 14177, 1995 14. Jacobson K, Flandry F: Diagnosis of anterior knee pain. Clin Sports Med 8:179, 1989 15. Jobe F, Bradley J: The diagnosis of non-operative treatment of shoulder injuries in the athlete. Clin Sports Med 8:419, 1989 16. Keifhaber T, Stem P: Upper extremity tendonitis and overuse syndromes in the athlete. Clin Sports Med 11:39, 1992 17. Kelly M, Insall J: Historical perspectives of chondromalacia patellae. Orthop Clin North Am 23:517, 1992 18. Kibler W: Pathophysiology of overload injury around the elbow. Sports Med 14:447, 1995 19. Kvist M: Achilles tendon injuries in athletes. Sports Med 18:173, 1994 20. Matheson GO, et al: Stress fractures in athletes. Am J Sports Med 15:46, 1987 21. Mattalino A, Deese J, Campbell E: Office evaluation and treatment of lower extremities in the runner. Clin Sports Med 8:461, 1989 22. Meyer SA, et al: Stress fractures of the foot and leg. Clin Sports Med 12:395, 1993 23. Neer C: Anterior acromioplasty for chronic impingement syndrome in the shoulder. J Bone Joint Surg 54A:4, 1972 24. Paty J: Diagnosis and treatment of musculoskeletal running injuries. Semin Arthritis Rheum 18:48, 1988 25. Plancher K, Litchfield R, Hawkins R Rehabilitation of the shoulder in tennis players. Clin Sports Med 14:111, 1995 26. Puddu G, Ippolito E, Postacchini F: A classification of Achilles tendon disease. Am J Sports Med 4:145, 1976 27. Renstrom P, Johnson R Overuse injuries in sports. Sports Med 2:316, 1985 28. Roetert E, Brody H, Dillman C: The biomechanics of tennis elbow: An integrated approach. Clin Sports Med 1447, 1995 29. Sallis RE, Jones K: Stress fractures in athletes. Postgrad Med 89:185, 1991 30. Scioli M: Achilles tendonitis. Orthop Clin North Am 25:177, 1994 31. Soma C, Mandelbaum 8: Achilles tendon disorders. Clin Sports Med 13:811,1994 32. Steindler A: Kinesiology of the Human Body. Springfield, Illinois, Charles C Thomas, 1955 33. Wertheimer C: Patello-femoral mechanics as a cause of anterior knee pain. Your Patient and Fitness 9:19, 1995 34. Williams J: Achilles tendon lesions in sport. Sports Med 3:114, 1986
Address reprint requests to N. Nichole Barry, MD 760 Elizabeth Street San Francisco, CA 94114