Tendon Problems in Athletic Individuals

Tendon Problems in Athletic Individuals*†BY CAROL C. TEITZ, M.D.‡, SEATTLE, WASHINGTON, WILLIAM E. GARRETT, JR., M.D., PH.D.§, DURHAM, NORTH CAROLINA, ANTHONY MINIACI, M.D.¶, M. H. LEE, M.D.¶, TORONTO, ONTARIO, CANADA, AND ROGER A. MANN, M.D.#, OAKLAND, CALIFORNIA An Instructional Course Lecture, The American Academy of Orthopaedic Surgeons Tendons attach muscle to bone and transmit the forces generated by muscles across joints to bone in order to achieve movement or stability of the body in space. Even when the muscle-tendon unit is not shortening, it can be performing a useful function when activated under conditions of constant length (isometric) or lengthening (eccentric) contractions. The compliance of tendons varies. Tendons of the digital flexors and extensors are very stiff, and their length changes very little when muscle forces are applied through them. In contrast, the tendons of some muscles, particularly those involved in locomotion and ballistic performance, are more elastic. The Achilles tendon, for example, is stretched in late stance phase as the triceps surae contracts and the ankle dorsiflexes. Near the beginning of plantar flexion, the muscle activation ceases and energy stored in the stretched tendon helps to initiate plantar flexion. Tendons that transmit large loads under eccentric and elastic conditions are more subject to injury73. A muscle has a much larger cross-sectional area than does its tendon near its attachment to bone. The tendon fans out into a much broader and thinner structure as it joins the muscle. This junctional area is the location of most injuries caused by tensile forces in a normal muscle-tendon unit, and it is the site of most common muscle strains in the active population21. Histologically, the tendon is seen to be a densely packed connective-tissue structure, consisting of a matrix of many type-I collagen-fiber bundles that are oriented along the axis of the tendon7. The tightly packed *Printed with permission of The American Academy of Orthopaedic Surgeons. This article will appear in Instructional Course Lectures, Volume 46, The American Academy of Orthopaedic Surgeons, Rosemont, Illinois, March 1997. †No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study. ‡University of Washington, 300 HEC Edmundson Pavilion, Box 354060, Seattle, Washington 98195-4060. §Duke University Medical Center, Box 3435, Durham, North Carolina 27710. ¶Toronto Western Hospital, 399 Bathurst Street, Suite ECW 1-038, Toronto, Ontario M5T 258, Canada. #3300 Webster Street, Suite 1200, Oakland, California 94609. and highly oriented collagen-fiber matrix makes the tendon ideal for sustaining tensile load73. Between the bundles are spindle-shaped fibroblasts that are responsible for creating and maintaining the matrix. A loose connective-tissue matrix surrounds the bundles of collagen fibrils and is organized within the primary collagen bundles as well as between the bundles and surrounding them. A peritendinous connectivetissue sheath (paratenon) surrounds the entire tendon. This sheath consists of two layers: an inner (visceral) layer and an outer (parietal) layer with occasional connecting bridges (mesotenon). If there is synovial fluid between these two layers, the paratenon is called tenosynovium; if not, it is termed tenovagium. Pathophysiology Histological Findings Painful areas of tendon are traditionally diagnosed by clinicians as tendinitis. This term implies an inflammatory nature of the lesion. However, histological studies of operative specimens do not show the characteristic signs of an inflammatory response as there are few inflammatory cells such as macrophages or polymorphonuclear leukocytes. There is little formation of granulation tissue. Rather, the histological pattern is more characteristic of a degenerative condition. The matrix is very disorganized without the usual axial, tightly woven collagen bundles. Fibroblasts are more numerous, and vascularity is generally increased. The degenerative pattern can assume fatty, mucoid, or hyaline features histologically. The better and more commonly used term for this degenerative condition is tendinosis7,59. Necropsy studies have shown that these degenerative changes may also be present in asymptomatic tendons35. The degree of degeneration increases with age and may represent part of the normal aging process. The degeneration appears to be activity-related as well. Operative specimens obtained from younger or middleaged patients who put high demands on the involved muscle-tendon units through recreational or occupational activities, such as using a strong grip to hold a THE JOURNAL OF BONE AND JOINT SURGERY 138 TENDON PROBLEMS IN ATHLETIC INDIVIDUALS 139 tennis racquet or a hammer, often show degenerative changes in the affected tendon34. Tendon Failure High forces created by eccentric muscle activation usually are responsible for tendon failure34,41,59. Biomechanical studies of the effect of loading on normal bone-tendon-muscle-tendon-bone preparations have shown that failure rarely occurs in the tendon22. Biopsy specimens obtained soon after the spontaneous failure of tendons showed degenerative changes in the ruptured tendon ends35. Specimens of Achilles tendon obtained on exploration for operative repair almost always demonstrate that degenerative changes were present within the tendon before it failed. These changes presumably weakened the tendon to such a degree that it became the weakest link in the chain. Research aimed at understanding the pathophysiology and treatment of tendinosis has been limited by the lack of a good and affordable animal model57. Injection of collagenase into the center of an equine tendon produces a histological picture similar to that seen in biopsy specimens of human tendinosis71. However, this lesion tends to heal and, therefore, may be more of a model for tendon sprain than for chronic tendinosis. Perhaps the model most closely resembling tendinosis occurs in the superficial digital flexor tendon of the horse. Lesions in this tendon are responsible for poor performance or lameness, especially in racehorses. The condition is characterized by fusiform swelling of the tendon with a degenerative core lesion and more normal tissue in the tendon peripherally. The tendon undergoes rapid loading and high strains in the galloping horse. Tendons store energy on stretching and return most of it when released. However, the energy that is not returned is dissipated as heat within the tendon, and the temperature in the central area of the tendon can reach nearly 45 degrees Celsius. Fibroblast viability is at risk at this temperature, and death of the central fibroblasts may create the central core degeneration that is seen histologically. In summary, the pathophysiology of tendinosis has not been well studied and is not well understood. Susceptible tendons are those that undergo large loads in an eccentric or stretching mode in which the tendons are storing and releasing energy. Susceptibility appears to be related both to activity and to age. The basic lesion can be identified within the tendon core and is characterized as degenerative rather than inflammatory. The term tendinitis is, therefore, less applicable than tendinosis. Possible factors in the etiology include agerelated changes in tendon structure and exercise-related hyperthermia within the tendon. Tendinosis of the Rotator Cuff Disorders of the rotator cuff occur commonly. Overuse or repetitive stress of the upper extremity in the VOL. 79-A, NO. 1, JANUARY 1997 overhead position may be an important cause of rotator cuff tendinosis11,37,46,48. Poor vascularity and primary degenerative changes also may contribute to the development of the lesion. Codman11 described a so-called critical zone, located approximately one centimeter medial to the supraspinatus tendon insertion, where tears usually occur. Rathbun and Macnab60 showed that there was relative avascularity in this critical zone, and they hypothesized that this was the reason for the degenerative changes. Lohr and Uhthoff42 also found this to be an area of hypovascularity, but they noted that the articular side of the tendon was poorly vascularized whereas the bursal side was well vascularized. Ogata and Uhthoff56 suggested that primary tendinosis was also an important etiological factor, especially for the deep-surface or intratendinous tears that are seen more often than tears on the bursal side. Shoulder pain and rotator cuff tendinosis are frequently seen in athletes who are involved in sports, such as baseball, tennis, and swimming, that require overhead actions. Jobe et al.33 suggested that subtle glenohumeral instability was one of the causes of rotator cuff tendinosis in this group. The overhead throwing motion of baseball pitchers and the service motion of tennis players require eccentric muscle contractions as the rotator cuff and shoulder-girdle muscles attempt to maintain stability of the glenohumeral joint23,33,65. These eccentric contractions can injure structures such as the bicepslabrum complex2. Because the static stabilizers in patients who have shoulder laxity or multidirectional instability are relatively incompetent, the rotator cuff and other shouldergirdle muscles must work harder to limit glenohumeral translation. This may lead to overuse tendinosis. Fowler and Webster19 as well as Richardson et al.61 observed a close relationship between rotator cuff tendinosis and shoulder laxity in competitive swimmers. Neuromuscular imbalance, especially between the internal and external rotators, also may result in rotator cuff tendinosis23. For athletes who use the arms overhead, an imbalance between the internal and external rotators may compromise the stabilizing function of the rotator cuff, causing secondary impingement as the humeral head migrates superiorly. The internal rotators usually are stronger than the external rotators, causing further migration of the humeral head anteriorly and superiorly. Shoulder pain is a common presenting symptom for many conditions about the shoulder. Although most patients who have rotator cuff tendinosis report pain, others may describe clicking, catching, weakness, stiffness, crepitation, or symptoms of instability. In addition, problems of the neck and the shoulder often have overlapping symptoms, and they may exist concomitantly, complicating diagnosis and management. The age and occupation of the patient; the duration and location of the symptoms; and the radiation, timing, quality, and severity of the pain can be important differentiating 140 C. C. TEITZ ET AL. factors. The patient should be asked about any alleviating or aggravating factors as well as about any specific traumatic event that precipitated the problem. Athletes should be questioned about the level and intensity of their participation in sports activities, particularly those that require overhead use of the upper extremity, such as baseball, tennis, volleyball, and swimming. They should be questioned about the time that the pain occurs during each activity and asked to note specific movements or other factors, such as the position of the upper limb, that induce the symptoms. The shoulder examination should be approached systematically for every patient by following the consecutive steps of inspection, palpation, assessment of the range of motion, strength-testing, neurological assessment, and the performance of special tests. In addition, the physical examination should include a thorough assessment of the cervical spine and the rest of the upper extremity. During inspection, scapular winging may be noted, which suggests an underlying scapulothoracic dysfunction that may be associated with shoulder instability, muscle imbalance, or muscle fatigue. Scapular winging may become more evident with range-of-motion and strength-testing. Osseous and soft-tissue structures are palpated in order to identify specifically any areas of tenderness. The range of motion, both active and passive, should then be assessed and documented in all planes. When there is pain, its severity and the arc of motion at which it occurs should be noted. An attempt should be made to determine if any loss of motion is secondary to pain or to capsular contracture. Loss of internal rotation may be due to posterior capsular contracture, a condition that is often associated with glenohumeral instability43. Muscles should be isolated and tested specifically for strength. Special tests may be helpful for differentiating the etiology of the shoulder pain. Impingement tests such as the Neer49 test and the test of Hawkins and Kennedy25 may be positive regardless of the cause of the rotator cuff tendinosis. Pain during crossed-arm adduction at 90 degrees suggests a lesion in the acromioclavicular joint. The tests of Yergason75 and of Speed13 are used to check for a lesion in the biceps. Tests for instability include the apprehension sign and the relocation test27. The load and shift test, as described by Hawkins et al.26, assesses the degree of translation in all planes. A sulcus sign may indicate multidirectional instability26. Field and Savoie17 described a test to check for labral tears involving the anchoring point of the long head of the biceps. Radiographic evaluation should consist of an anteroposterior, a transscapular lateral, and an axillary radiograph. The supraspinatus outlet radiograph, a lateral radiograph of the erect scapula with a downward tilt of 10 degrees, can help in the assessment of acromial morphology50. The examiner should note any osseous abnor- malities, such as a variation in the shape and slope of the acromion, osteoarthrosis of the acromioclavicular joint, spurring of the distal aspect of the clavicle, and calcification of the rotator cuff tendons. The examiner should also look for evidence of an osseous Bankart lesion or a Hill-Sachs lesion. Cystic changes or sclerosis in the region of the greater tuberosity, proximal migration of the humeral head, decreased acromiohumeral distance, or glenohumeral osteoarthrosis may be indicative of a rotator cuff tear. Arthrography, ultrasonography, and magnetic resonance imaging can be helpful in the diagnosis of full-thickness tears of the rotator cuff, but their clinical value in the assessment of rotator cuff tendinosis remains questionable16,28,47,51. In our experience, shoulder arthroscopy has been extremely useful in demonstrating the exact location and extent of partialthickness tears of the rotator cuff and in identifying other pathological conditions in the shoulder, such as labral tears or ligamentous laxity. Regardless of the etiology of the condition, patients who have rotator cuff tendinosis have similar symptoms and most can be managed conservatively with an appropriate rehabilitation program. Physiotherapists often play an important role in this program, using a variety of modalities such as heat, cold, ultrasound, laser, friction, and transcutaneous electrical nerve stimulation. Good communication between the physician, the patient, and the physiotherapist is essential for a successful outcome. The role of the patient in the treatment program should be clearly defined at the onset, and realistic goals and expectations of therapy also should be established at the start. The first phase of the rehabilitation process is pain control, which is achieved by having the patient rest the shoulder and modify or avoid activities that aggravate the pain. Anti-inflammatory medications may be helpful. Subacromial injections of corticosteroids may be considered, but they usually are used only in the later stages of the conservative treatment protocol. We limit treatment to a maximum of three injections. The second phase of the rehabilitation protocol is restoration of the range of motion. Patients are instructed in circumduction exercises and in the use of pulleys to improve motion. Specific stretching exercises also are taught as a standard part of this program. The third phase is muscle-strengthening. Emphasis is placed on the strength of the rotator cuff, the deltoid, and the scapular stabilizing muscles. Overhead activities should be avoided, especially during the early phases of treatment. A progressive resistive program is initiated with use of Therabands (DePuy, Warsaw, Indiana), elastic tubing, free weights, or a combination of these. Therabands and elastic tubing are easily adapted for use at home. They create a closed kinetic system, which may be preferable to the high torque stresses generated at the shoulder by free weights. Restoration of the power, endurance, and smooth coordination of the shoulder THE JOURNAL OF BONE AND JOINT SURGERY TENDON PROBLEMS IN ATHLETIC INDIVIDUALS 141 muscles is emphasized and should be sport-specific. Any muscle imbalance, especially one between the internal and external rotators, must be identified and addressed. Glenohumeral instability should be identified early, and a proper strengthening program should be directed at improving the dynamic stabilizers of the shoulder. If symptomatic glenohumeral instability continues despite a comprehensive rehabilitation program, operative intervention should be considered to restore stability. Operative intervention for rotator cuff tendinosis should be considered only after all attempts at conservative treatment have failed. For patients who demonstrate primary mechanical impingement, the operative procedures available are resection of the coracoacromial ligament25,31,36,58, anterior acromioplasty, resection of the distal part of the clavicle, and resection of inferior osteophytes from the acromioclavicular joint, depending on the specific underlying disorder. Glenohumeral instability that is unresponsive to a program of musclestrengthening and balancing should be treated with operative stabilization. The use of shoulder arthroscopy has enhanced the ability to diagnose and evaluate various pathological conditions in the shoulder, including rotator cuff tendinosis and, in particular, partial-thickness tears. Although we agree with those investigators15,68 who have advocated repair of sizable or delaminated partialthickness tears of the rotator cuff, there is little in the literature describing the treatment of partial-thickness tears of the rotator cuff and controversy still exists regarding the effectiveness of treatment. Snyder68 described an arthroscopic suture-repair technique for partial-thickness tears as well as for small full-thickness tears of the rotator cuff. Tendinosis of the Elbow The term tennis elbow is widely used to describe a series of overuse injuries that are characterized by pain and tenderness in the region of the humeral epicondyles and that involve the extensors or flexors of the wrist. The peak prevalence of tennis elbow is in the fourth decade of life, when it is four times higher than the prevalence in any other decade12. The lateral epicondyle is involved seven times more often than is the medial epicondyle. Although it is termed tennis elbow, the condition occurs very commonly in non-athletes. Lateral Tendinosis of the Elbow Although lateral epicondylitis was first described64 in 1873, some controversy still exists regarding the etiology and the pathogenesis of this condition. The basic underlying lesion seems to be a macroscopic or microscopic tear in the origin of the extensor carpi radialis brevis tendon that heals with immature reparative tissue52. Gross examination of this region characteristically shows grayish, gelatinous, friable immature scar tissue that appears shiny and edematous. Light microscopy VOL. 79-A, NO. 1, JANUARY 1997 reveals a characteristic invasion of fibroblasts and vascular granulation, which has been described as so-called angiofibroblastic hyperplasia55. Although lateral tendinosis of the elbow most commonly involves the origin of the extensor carpi radialis brevis, the origins of the extensor digitorum communis, the extensor carpi radialis longus, and the supinator can also be involved in the process. Inflammation of the lateral collateral and orbicular ligaments also can be observed. The patient usually is first seen because of the gradual onset of aching pain in the region of the lateral epicondyle and in the proximal muscles of the forearm. The pain often is related to flexion and extension of the wrist and to pronation and supination activities. Other conditions that should be considered in the differential diagnosis include nerve entrapment (radial tunnel syndrome) and intra-articular disorders such as radiocapitellar osteoarthrosis, osteochondritis dissecans, and an osseous tumor. Physical examination usually reveals localized tenderness directly over the lateral epicondyle in the region of the origin of the extensor carpi radialis brevis; however, the area of tenderness often can be quite diffuse. Pain may be increased with resisted wrist or finger extension, particularly with the forearm in pronation. Patients may have a positive coffee-cup test, as described by Coonrad12, in which grasping or pinching with the wrist in extension reproduces the pain at the point of maximum tenderness. They also may have a positive chair test, as described by Gardner20, in which the patient has pain in the region of the lateral epicondyle while lifting a chair with one hand with the forearm pronated. Isokinetic strength deficits also may be observed. Anteroposterior and lateral radiographs of the elbow should be made routinely, as they are helpful for ruling out other conditions such as radiocapitellar osteoarthrosis or the presence of a loose body or an osseous tumor. Oblique radiographs occasionally demonstrate calcifications in the region of the lateral epicondyle. The findings of electromyography studies are usually normal, even for patients who have radial tunnel syndrome. Magnetic resonance imaging may demonstrate abnormal changes in signal intensity at the extensor origin on the lateral aspect of the elbow, but a change in signal intensity does not necessarily correlate with the histological findings or with the symptoms53. The pain needs to be brought under control before the patient can start any extensive rehabilitation. Pain control can be achieved with the use of non-steroidal anti-inflammatory medications, rest, and modification of activity. Physical modalities such as ice or heat, ultrasound, and electrical stimulation may help to control the pain; phonophoresis with 10 per cent hydrocortisone cream has been found to be useful38. Injections of corticosteroids can be tried in resistant cases, with a maximum of three injections during a period of one year. Care should be taken to inject the medications directly 142 C. C. TEITZ ET AL. into the area of maximum tenderness. Counterforce braces have been shown to be effective in the treatment of elbow tendinosis as well24. These braces are straps, approximately five to six centimeters wide, that are applied just distal to the elbow over the origin of the common extensor tendon. Biomechanical and electromyographic analysis has shown inhibition of maximum contraction of the wrist and finger extensors by use of a counterforce brace24. For the tennis player, stroke mechanics should be evaluated and modified as necessary to help control symptoms. When the pain has been controlled, an exercise program that focuses on eccentric strengthening (as described by Stanish et al.69) and the restoration of flexibility and endurance can be initiated. Seven per cent (eighty-eight) of 1213 elbows in one series55 had resistant lateral tendinosis that needed operative intervention. Operative treatment should be considered only after non-operative treatment has failed for at least one year. The principles of operative treatment were previously described by Nirschl and Pettrone55. The origin of the extensor carpi radialis brevis is exposed, and tears as well as any granulation tissue that is seen on the underside of the extensor carpi radialis brevis tendon are excised. A small area of the lateral condyle can be decorticated or drilled to improve the blood supply for healing of the detached tendon. Intra-articular examination usually is not necessary unless an associated abnormality was anticipated preoperatively. Usually, the elbow is splinted in 90 degrees of flexion for three weeks postoperatively. Then, range-of-motion and gradual strengthening exercises of the hand and wrist are performed daily for three additional weeks. From six to twelve weeks postoperatively, resisted and eccentric exercises of the wrist are performed. Weights are gradually increased to a maximum of five pounds (2.3 kilograms). After twelve weeks, patients should return gradually to full activities. They may return to sports activities at four to six months after the operation or when strength and endurance are approximately 80 per cent of normal. Medial Tendinosis of the Elbow Medial tendinosis of the elbow occurs much less commonly than lateral tendinosis of the elbow and results from overuse of the forearm flexor muscles or from repetitive valgus stress in throwing athletes. The condition is seen also in patients who play racquet sports, such as tennis, squash, and racquetball, in which the forehand stroke creates excessive stress on the medial elbow structures. In medial tendinosis of the elbow, the tendons of the pronator teres, the flexor carpi radialis, and occasionally the flexor carpi ulnaris are principally affected. Patients who have medial tendinosis of the elbow usually report aching pain that originates from the region of the medial epicondyle and radiates into the muscles of the forearm. They may also report decreased grip strength, but this problem is usually related to pain rather than to an injury of nerve or muscle. Some of these patients are seen with an acute disruption of the common flexor origin or the ulnar collateral ligament, or both. These conditions, chronic tendinosis and acute disruption, must be differentiated clinically because acute rupture of the ulnar collateral ligament is best treated operatively, especially in an athlete who uses overhead motion. In medial tendinosis of the elbow, the pain increases with resisted wrist flexion when the forearm is held in pronation. With a disruption of the ulnar collateral ligament, a valgus stress test of the elbow produces pain. Ulnar-nerve entrapment can also cause medial pain in the elbow, and it should be included in the differential diagnosis. Nirschl54 reported ulnar-nerve dysfunction in 60 per cent of patients who had operative treatment for medial epicondylitis. Entrapment of the ulnar nerve usually is found in zone 3, distal to the medial epicondyle. Non-operative treatment of medial tendinosis of the elbow should follow the same steps as those described for lateral tendinosis of the elbow. Operative treatment involves a medial longitudinal incision with the surgeon carefully avoiding the medial antebrachial cutaneous nerve. The tendons of the pronator teres and flexor carpi radialis are split longitudinally, distal from their origin on the medial epicondyle. Care should be taken not to detach the common flexor origin, as this can lead to posteromedial instability of the elbow. All abnormal, torn, or degenerative tissue should be sharply excised. If there is evidence of ulnar neuropathy preoperatively, a formal ulnar-nerve transposition should be performed because the results of cubital tunnel decompression alone have not been satisfactory39. Tendinosis about the Hip (Snapping Hip) Two distinct conditions, which have been characterized as internal and external, can cause symptomatic snapping with motion of the hip. The internal type is due to the iliopsoas tendon snapping over the femoral head, over the iliopectineal eminence, or, less commonly, over a ridge on the lesser trochanter. Internal snapping hip often is found in athletes who frequently flex and extend this joint, especially in association with abduction and external rotation, as occurs commonly in dance and in the martial arts. The patient is first seen because of the gradual onset of a reproducible, audible, and palpable low-pitched clunk in the groin. Typically, the problem is unilateral. On physical examination, there is no tenderness and no pain when the rectus femoris works against resistance. Occasionally, the examiner can elicit pain with resisted use of the iliopsoas muscle. Although arthrography or magnetic resonance imaging can be considered in order to rule out a loose body or a labral tear within the hip joint, no workup is necessary when the clinical findings are typical. The diagnosis can be made definitively by iliopsoas bursography, THE JOURNAL OF BONE AND JOINT SURGERY TENDON PROBLEMS IN ATHLETIC INDIVIDUALS 143 dition is most common in cyclists and runners, particularly those who run up and down hills. Anatomical factors that maintain the iliotibial band in a stretched position and make it more likely to rub as it passes over the greater trochanter include genu varum, a true limblength discrepancy or a functional short limb (the downhill limb while an individual is running on a canted surface), and a crossover running style. Occasionally, a causative factor for external snapping hip in cyclists is the position of the cleat or other shoe-fixation device on the bicycle. When these patients are first seen, they report the gradual onset of pain and a high-pitched snapping over the greater trochanter. Typically, the problem is unilateral and is sometimes difficult to distinguish from greater trochanteric bursitis. The patient has tenderness FIG. 1-A Figs. 1-A through 1-D: Drawings showing the Ober test for assessing contracture of the iliotibial band. The patient lies on the unaffected side with the unaffected hip and knee flexed enough to eliminate lumbar lordosis. The examiner holds the extremity to be tested with the knee flexed. The examiner’s other hand stabilizes the pelvis. The hip is then flexed, abducted, and hyperextended to catch the iliotibial band on the greater trochanter. The limb is then adducted. If the iliotibial band is tight, the limb cannot be adducted back down to the examining table or to the contralateral limb but remains passively abducted. Fig. 1-A: Flexion. FIG. 1-C Hyperextension. FIG. 1-B Abduction. which will demonstrate the snapping tendon66. The internal snapping hip is treated first by encouraging the patient to stop intentional snapping. Nonsteroidal anti-inflammatory medications may be helpful in relieving any inflammation that may have resulted from repeated snapping. Stretching and strengthening exercises of the iliopsoas are helpful as is repatterning muscle use during the affected motions. Operative lengthening of the iliopsoas tendon is rarely necessary1. The external snapping hip is caused by the iliotibial band snapping over the greater trochanter. This conVOL. 79-A, NO. 1, JANUARY 1997 FIG. 1-D Adduction. 144 C. C. TEITZ ET AL. to palpation over the greater trochanter when tendinosis is present and behind it when bursitis is present. In either case, the patient has pain when the lower extremity is adducted across the midline. The hip usually is painful to lie on when the patient has bursitis, but not when the patient has iliotibial tendinosis. Resisted abduction is painful when tendinosis is present, but not when the patient has bursitis alone. An Ober test reveals tightness of the iliotibial band (Figs. 1-A through 1-D). The initial treatment of both bursitis and tendinosis includes the use of non-steroidal anti-inflammatory drugs and ice-friction massage. Stretching the iliotibial band is helpful, but it may aggravate bursitis initially. The physician should look for and correct any training, biomechanical, or anatomical factors that may have contributed to the problem. Differentiation of bursitis from tendinosis is more important when initial treatment is unsuccessful. When a patient has chronic bursitis of the greater trochanter, an injection of steroids into the bursa often relieves symptoms. When the problem is chronic iliotibial tendinosis, however, injections of steroids are less likely to provide relief, and lengthening of the iliotibial band should be considered in order to achieve long-lasting relief4. Lateral Runner’s Knee (Iliotibial Band Tendinosis) The condition that is termed lateral runner’s knee is caused by the iliotibial band rubbing over the lateral femoral epicondyle. This is most commonly an overuse condition with the same predisposing biomechanical and anatomical factors as those noted previously for the iliotibial band snapping over the greater trochanter. In addition, a mild varus position of the heel can predispose a runner to iliotibial band tendinosis at the knee because of the varus moment imposed by this deformity on the knee during heel-strike and mid-stance10. The patient is first seen with unilateral pain in the lateral aspect of the knee, proximal to the joint line, at the level of the lateral femoral epicondyle. Occasionally, a patient reports snapping as well. The pain is insidious in onset, but it is made worse by going up or down stairs, riding a bicycle, or running. Tenderness to palpation at the epicondyle and, sometimes, crepitation are noted. The Ober test is positive for tightness of the iliotibial band (Figs. 1-A through 1-D). The examiner should also check the shoes of the runner for abnormal wear along the lateral part of the midsole and forefoot. The treatment for this condition is identical to that for external snapping hip, as described previously. One way to correct the common biomechanical problems is to encourage the patient to run in alternate directions on the track or on alternate sides of the road to avoid always having the same lower extremity in the downhill position. In addition, a lateral wedge in the shoe of a patient who has varus heels or knees can help to decrease the varus moment during running. If all else fails, an injection of steroids into the area of maximum tenderness may produce relief, as an inflamed bursa may have developed deep to the tendon. Lengthening of the iliotibial band may be performed, but it is rarely necessary18. Jumper’s Knee Jumper’s knee, or so-called patellar tendinosis, results from microtears of the patellar ligament followed by a chronic inflammatory response. It is an overuse injury that is most commonly seen in athletes who participate in sports that require a great deal of jumping or kicking, such as basketball, volleyball, and soccer. Symptoms may occur during an adolescent growth spurt, perhaps because the ligament does not lengthen as fast or as much as the adjacent bones are growing. FIG. 2 Photograph showing a brace for jumper’s knee. The pad must be positioned directly over the patellar ligament. THE JOURNAL OF BONE AND JOINT SURGERY TENDON PROBLEMS IN ATHLETIC INDIVIDUALS 145 The patient is first seen with tenderness over the patellar ligament. The area may be red, swollen, or crepitant. Resisted use of the quadriceps and full passive flexion of the knee produce pain. Quadriceps tightness is frequently present. Treatment includes decreasing or stopping the inciting activity, use of non-steroidal anti-inflammatory drugs, and ice-friction massage. A program of quadriceps stretching is critical, particularly for the adolescent. Isometric exercises to strengthen the quadriceps can be started immediately, but isotonic or isokinetic exercises for strengthening the quadriceps should begin only when the tenderness has subsided. It is very important that the athlete eventually advance to eccentric quadriceps strengthening in order to train for his or her sport. Although the precise reason for its clinical effectiveness is not known, application of a brace that contains a pad over the patellar ligament is useful when the pain has resolved and the athlete wishes to return to participation in sports (Fig. 2). When patellar tendinosis does not respond to nonoperative intervention, diagnostic ultrasonography may reveal an area of angiofibroblastic hyperplasia and fibrinoid necrosis deep within the ligament (Fig. 3-A). With use of a local anesthetic, excision of this area can be carried out by splitting the ligament longitudinally (Fig. 3-B), and the surgeon should look for gelatinous material between normal fibers. This material should be excised, and the remainder of the ligament should be closed with absorbable sutures. Roels et al. reported that operative treatment allowed all ten patients in their series to return to participation in sports62. Dysfunction of the Posterior Tibial Tendon The posterior tibial muscle is the main invertor of the subtalar joint. The short fiber length of this muscle produces a great deal of force on its five insertions into the plantar aspect of the foot. The posterior tibial tendon has an excursion of two centimeters 14. If the hindfoot is in an abnormal amount of valgus or the forefoot is in too much varus, excessive tension is placed on the posterior tibial tendon, a situation that may lead to tenosynovitis. Dysfunction of the posterior tibial tendon can be acute or chronic. Most commonly, the condition consists of an acute tenosynovitis secondary to overuse, without any structural change in the hindfoot. In one series, this condition was reported in fifty-eight (6 per cent) of 974 runners6. Chronic tenosynovitis, which usually is found in the non-athletic population, is associated with tendinosis and structural changes in the hindfoot. An acute rupture of the posterior tibial tendon before the age of thirty years has been reported in only four patients9. Woods and Leach reported one other series of six patients who had had an acute rupture (complete or partial) of the posterior tibial tendon and emphasized the necessity for early recognition and treatment 74. VOL. 79-A, NO. 1, JANUARY 1997 Patients who have tenosynovitis of the posterior tibial tendon report pain along the posteromedial aspect of the foot and ankle. The pain is minor at first, but swelling and progressive disability develop as the condition progresses. The evaluation should begin with careful questioning regarding history, with particular attention paid to the onset of the condition, changes in training habits, the nature and frequency of training, the type of footwear, and the use of orthotic devices. The single most important aspect in the assessment of a patient who has suspected dysfunction of the posterior FIG. 3-A Figs. 3-A and 3-B: A patient who had jumper’s knee. Fig. 3-A: Ultrasonogram showing the hypoechoic area (arrow) within the fibers of the patellar ligament. This area corresponds to the area of angiofibroblastic hyperplasia and fibrinoid necrosis in the ligament. FIG. 3-B Photograph showing the gross appearance of the patellar ligament. Note the discoloration and the loss of fibrous integrity in the damaged area deep in the ligament (arrow). 146 C. C. TEITZ ET AL. tibial tendon is the physical examination. The hindfoot should be observed with the patient standing. A patient who has posterior tibial tendon dysfunction may have an increased valgus posture of the calcaneus and a fullness that is seen just distal to the medial malleolus. The patient should be asked to stand on tiptoe so that the examiner can assess the degree of active inversion of the calcaneus that occurs at the subtalar joint. Lack of heel inversion usually indicates dysfunction or weakness of the posterior tibial tendon. Next, the patient should be asked to repeat a toe-rise on one foot approximately eight to ten times. The examiner should carefully observe how high the patient is able to rise on the toes as well as the degree of heel inversion that occurs. Frequently, during an acute episode of tenosynovitis, the patient is unable to stand on tiptoe at all because of pain. The examiner should carefully note the degree of dorsiflexion and plantar flexion of the ankle (specifically looking for any lack of dorsiflexion), the range of subtalar joint motion (looking particularly for diminished inversion), and the motion of the transverse tarsal joint. The tendon sheath should be palpated carefully, with the examiner looking for thickening, increased warmth, and crepitation. The strength of the tendon should be evaluated by having the patient both bring the foot actively from a fully everted position into inversion and attempt to hold the foot in an inverted position against resistance. Weight-bearing anteroposterior, lateral, and oblique radiographs of the foot should be made. The anteroposterior radiograph can demonstrate subluxation of the talonavicular joint and the relationship of the talus to the calcaneus. The lateral radiograph should be studied for any sagging of the talonavicular, naviculocuneiform, or first metatarsal-cuneiform joint. No single specific pattern of radiographic changes is observed in these patients. Treatment Acute tenosynovitis: When acute tenosynovitis is mild, it can be treated with a decrease in the level of activities. However, when the symptoms are moderate, the extremity should be rested and stressful activities should be stopped. An anti-inflammatory medication or ice, or both, should be utilized at this stage. If the symptoms do not respond within four to six weeks, immobilization in a weight-bearing below-the-knee cast for four to six weeks is recommended. If the symptoms still fail to respond, operative treatment should be recommended. The operative procedure consists of exploration of the tendon between the medial malleolus and the tendon insertion. Most frequently, varying degrees of synovial proliferation are found. The tendon and sheath should be carefully debrided of the exuberant synovial tissue. If necessary, the débridement may be continued proximal to the medial malleolus, but a one-centimeter section of sheath should be left in place to act as a pulley behind the medial malleolus. Occasionally, when the posterior tibial tendon is explored, the tendon itself appears to be intact, but the abnormality lies at the insertion of the tendon into the navicular. Although excision of the affected portion and advancement of the posterior tibial tendon into the navicular is preferable in this situation, often there is not enough excursion of the musculotendinous unit to allow advancement of the tendon into the navicular. Therefore, we have found that it is better to carry out a reconstruction with use of the flexor digitorum longus tendon as a transfer into the navicular and then to suture the end of the posterior tibial tendon into the flexor digitorum longus. Acute rupture: A patient who sustains an acute rupture of the posterior tibial tendon, a rare injury, demonstrates no active inversion of the subtalar joint. A defect in the tendon may be palpable because the rupture usually occurs between the medial malleolus and the navicular. However, blood in the tendon sheath may mask this finding. When an acute rupture is present, a reconstruction with use of the flexor digitorum longus should be performed as soon as possible in order to avoid the development of a flatfoot deformity44. Chronic tenosynovitis: A patient who has had tenosynovitis of the posterior tibial tendon for more than a year probably has a mild-to-moderate degree of tendinosis. The foot probably has structural changes (such as mild flattening of the longitudinal arch secondary to sagging of the talonavicular joint), although the deformities may be mild and usually are not fixed. These patients retain fair-to-good strength of the posterior tibial muscle and can be managed with an orthosis. The orthosis should include a varus heel-wedge and a medial forefoot post. When the symptoms persist and interfere with activities of daily living or athletic activities, exploration, decompression, and reconstruction of the tendon with use of the flexor digitorum longus is indicated. Chronic rupture: Patients who have chronic rupture of the posterior tibial tendon note a flatfoot deformity that has progressed over a period of several years. The physical examination often demonstrates loss of subtalar joint motion, especially inversion, and a fixed varus deformity of the forefoot that usually exceeds 15 degrees. When this is the case, tendon decompression and transfer is not effective and a double or triple arthrodesis is indicated. It should be realized that fusion of this type can be a substantial impediment to running activities; however, walking, golf, and doubles tennis are still feasible. Dysfunction of the Achilles Tendon The gastrocnemius-soleus complex spans two joints and is the largest and strongest muscle in the calf. It is a stance-phase muscle that undergoes both eccentric (lengthening) and concentric (shortening) contractions THE JOURNAL OF BONE AND JOINT SURGERY TENDON PROBLEMS IN ATHLETIC INDIVIDUALS 147 during walking and running. Normally, the Achilles tendon twists as it passes to its insertion, particularly in the area approximately two to six centimeters proximal to the insertion. This anatomical configuration results in increased internal stress on the tendon30. In addition, the blood supply to this area has been demonstrated to be tenuous29,40. Problems that commonly occur in the area that is proximal to the insertion of the tendon and to the level of the retrocalcaneal bursa are termed non-insertional problems. These include Achilles tendinitis, which is an inflammation of the tendon sheath without intrinsic tendinous changes; Achilles tendinosis, which is the occurrence of intrinsic tendinous changes with or without associated tendinitis; and Achilles tendon rupture. Another set of problems occurs in the area posterior to the retrocalcaneal bursa and at the insertion of the tendon. These are termed insertional problems and include calcification within the Achilles tendon at its insertion into the calcaneus without tendinosis; Achilles tendinosis at its insertion with or without associated calcification; and Achilles dysfunction associated with a Haglund deformity, which is a prominence of the posterosuperior aspect of the calcaneus. Such categorization of the various pathological entities that occur about the Achilles tendon is important for accurate diagnosis, prognosis, and treatment. The prevalence of Achilles tendinitis has been estimated to be 11 per cent (twenty-five of 232) in runners32, 9 per cent (thirty-three of 352) in dancers63, 5 per cent (eight of 147) in gymnasts5, 2 per cent (two of eighty-nine) in tennis players72, and less than 1 per cent (twenty-three of 2820) in football players76. Tendinitis is brought about most frequently by training-related errors, although mechanical factors, such as hyperpronation of the foot, contracture of the gastrocnemiussoleus complex, or faulty footwear, may be involved as well. Conversely, Achilles tendinosis represents a degenerative process of the tendon and probably has nothing to do with training errors or other mechanical problems. Achilles tendon ruptures, which are not described in the present report, are thought to be due to underlying tendinosis3,8, although usually the tendinosis is subclinical. Evaluation of a patient who has a painful Achilles tendon begins with careful questioning regarding the history, including the onset of the condition, the level of activities, the training techniques, the type of footwear, and the previous treatment. The patient is asked to place a finger on the area of maximum pain. The patient should then stand while the examiner notes the posture of the foot. Next, a toe-rise should be done three, four, or five times on each foot individually. A patient who has tendinosis often is unable to do a single toe-rise, whereas a patient who has tendinitis can perform a toe-rise without as much difficulty. The tendon should be palpated for thickening, increased warmth along the tendon sheath, and crepitation. The range of VOL. 79-A, NO. 1, JANUARY 1997 motion of the ankle and the subtalar joint should be determined carefully. The physical findings in tendinitis consist of inflammation that is limited to the peritenon, as demonstrated by increased warmth and tenderness and, possibly, by crepitation. Nodularity is not present with acute Achilles tendinitis. During dorsiflexion and plantar flexion, the fingertips of the examiner feel no nodules in the Achilles tendon. When tendinosis is present, the tendon is thickened FIG. 4-A Figs. 4-A and 4-B: A patient who had insertional tendinosis. Fig. 4-A: Radiograph demonstrating calcification at the insertion of the Achilles tendon (arrow). FIG. 4-B Computerized tomography scan localizing the area of calcification (arrow). 148 C. C. TEITZ ET AL. over a length of two to five centimeters. This area may or may not demonstrate increased warmth, depending on the extent and duration of the tendinosis. Squeezing the area of tendinosis often causes substantial pain. Tendinosis may limit the ability of a patient to stand on tiptoe. On occasion, an inflamed retrocalcaneal bursa may be the cause of pain. In this case, most of the pain is located between the calcaneus and the Achilles tendon but proximal to the insertion of the tendon. There may be focal tenderness over the bursal area anterior to the Achilles tendon, but usually there is no substantial thickening of the tendon per se. Palpation of the tendon does not cause pain. Sometimes, the swollen bursa can be palpated. Insertional tendinosis includes two basic types. The first type is characterized by generalized thickening of the tendon at its insertion, where there is an area of increased warmth, frequently an osseous prominence, and marked tenderness to palpation. Performing a single toe-rise is often difficult for patients who have this type of tendinosis, and only rarely can these patients repeat a toe-rise more than two or three times. The second type of insertional tendinosis involves a well localized area that a patient can pinpoint at the insertion of the Achilles tendon. Frequently, the tendon itself is not particularly thickened except in the localized area where the pain is located. Patients who have this type of tendinosis usually can perform a single toe-rise without difficulty. Radiographs often demonstrate calcifica- tion about the insertion of the tendon (Fig. 4-A). The radiographs of a patient who has a focal area of pain usually show a localized area of calcification, as opposed to a large area, which is frequently seen in a patient who has generalized tendinosis. Computerized tomography scans of a patient who has localized calcification frequently demonstrate an area of calcification that corresponds to the area of the pain (Fig. 4-B). For patients who have generalized tendinosis, a magnetic resonance image may demonstrate cystic areas within the substance of the tendon, either proximal to or at the level of the insertion (Figs. 5-A and 5-B). The extent of the involvement varies greatly among patients. Treatment of all of these conditions depends on the severity of the problem. The initial treatment consists of rest, ice massages, non-steroidal anti-inflammatory medication, and stretching of the Achilles tendon. Athletes may need to change their training program or footwear. Effective modifications of footwear may include a softer heel-counter, an orthotic device to correct severe pronation if it is present, or a softer heel-cushion. If the symptoms fail to respond to these measures, we have found that immobilization in a weight-bearing cast, particularly for a patient who has insertional tendinosis, is extremely useful. If the symptoms respond to the use of a below-the-knee cast and subsequently recur but the patient is not a good candidate for an operation, a polypropylene ankle-foot orthosis with no motion of the ankle joint often provides effective longterm relief. FIG. 5-A FIG. 5-B Figs. 5-A and 5-B: Magnetic resonance images showing abnormalities within the Achilles tendon. Fig. 5-A: A defect in the mid-substance of the Achilles tendon, representing the area of tendinosis (arrow). Fig. 5-B: Insertional tendinosis with probable obliteration of the retrocalcaneal bursa because of adhesion of the tendon to the calcaneus. THE JOURNAL OF BONE AND JOINT SURGERY TENDON PROBLEMS IN ATHLETIC INDIVIDUALS 149 FIG. 6-A FIG. 6-B Figs. 6-A and 6-B: Drawings showing the reconstruction of the Achilles tendon with use of a flexor digitorum transfer. Fig. 6-A: The flexor digitorum longus or the flexor hallucis longus is freed from the plantar aspect of the foot and brought posteriorly through a drill-hole in the calcaneus, after which it is sutured back onto itself. It is important to tension the transplant to approximate the tension felt with manual dorsiflexion of the contralateral extremity. Usually, this procedure will hold the foot in approximately 10 degrees of plantar flexion. Fig. 6-B: A flap of the Achilles tendon is developed either by the turndown method, as demonstrated, or by some type of advancement somewhat more proximally, depending on the nature of the abnormality. The flap is brought down under tension in order to reconstruct the Achilles tendon. Sutures are then placed between the transferred tendon and the Achilles tendon. Operative management should be undertaken only after conservative treatment has been exhausted. In a patient who has Achilles tendinitis, chronic inflammation may create a thickening of the tendon sheath. Release of the tendon sheath has been reported to be successful67, but we have not found the procedure to be necessary for these patients because tendinitis virtually always responds to non-operative treatment. In patients who have recalcitrant Achilles tendinosis, we explore the area of tendinosis but rarely find any substantial lesion or cyst formation other than an occasional area of cholesterol deposition. We do not attempt to excise small lesions of two centimeters or less but rather we weave the plantaris tendon back and forth through the area to stimulate an inflammatory healing response. Postoperatively, the leg is kept in a non-weight-bearing below-the-knee cast for one month and in a weightbearing below-the-knee cast for another month. During the second month, a removable cast is utilized to allow the patient to work on range-of-motion exercises and to use an elastic band to keep some tone in the muscles during the later healing phase. The enlarged area of tendinosis usually does not disappear, but it often becomes much less painful. We do not permit a patient to resume unrestricted activities until the enlarged area is no longer warm or tender to palpation. For some patients, this may take three to six months. Eight of our ten patients who were managed with this technique had a successful result. VOL. 79-A, NO. 1, JANUARY 1997 When the tendinosis involves the entire segment of tendon and has failed to respond to conservative treatment, a procedure is used to bypass the involved area, whether it is in the mid-substance or at the level of the insertion of the tendon into the calcaneus44. In this procedure, either the flexor hallucis longus or the flexor digitorum longus is transplanted from the plantar aspect of the foot and is used to bypass the segment of tendinosis (Fig. 6-A). Depending on the severity and the length of the segment involved, a portion of the Achilles tendon may need to be excised. The tendon of the flexor hallucis longus or flexor digitorum longus is freed from the midfoot and tunneled through the calcaneus to reinforce the reconstructed tendon and to create one stable musculotendinous unit. The transferred tendon acts as a splint for the area of the Achilles tendon where the segment has been advanced and, in this way, a sort of scaffolding is created to support the Achilles tendon until it heals. Next, the central portion of the Achilles tendon is advanced across the excised area, either into the calcaneus if the distal portion of the Achilles tendon was resected or into the substance of the tendon if a more proximal area was excised (Fig. 6-B). This procedure is technically demanding. Caution must be used in handling the skin, as it has a marginal blood supply and a skin slough may occur. Postoperatively, the patient is not allowed to bear weight on the limb for three months. Afterward, progressive weightbearing is begun, but full mobilization without a cast is 150 C. C. TEITZ ET AL. not permitted until the involved area is no longer warm or painful to palpation. When there is a well localized area of calcification within the tendon, a transverse incision is made in the skin. Then, a longitudinal incision is made over the area of calcification, and the calcified area is shelled out. Postoperatively, a below-the-knee non-weight-bearing cast is worn for three weeks and then a weight-bearing cast is worn for an additional three weeks. The result is usually successful for these patients as the problem is well localized and extensive tendinosis usually is not present. This operative approach cannot be used for a large area of calcification within the substance of the tendon, as that type of lesion usually is located in the anterior aspect of the tendon and cannot be reached from a posterior approach. A patient who has chronic retrocalcaneal bursitis, with or without an associated Haglund deformity but with no tendinosis, often is managed successfully with simple excision of the posterosuperior aspect of the calcaneus in order to decompress the bursa67. Not infrequently, it has been observed that the Achilles tendon actually has become adherent to the posterior aspect of the calcaneus. Relieving this irritation of the Achilles tendon usually benefits the patient. Overview Tendinitis, although not life-threatening, is an extremely common problem that interferes with an active lifestyle. Although it is used often, the term tendinitis is probably a misnomer. Tendinosis should be used to describe problems that are predominantly degenerative, such as those that occur in the rotator cuff and in the extensor tendons of the wrist. In tendons with a tenosynovial layer, such as the posterior tibial tendon, the visceral layer of paratenon can become inflamed in response to microtrauma or to degenerative changes in the tendon proper. The semantic difficulties arise from a paradox between the histological and the clinical find- ings. The results of histological examination of chronically painful tendons are more consistent with tendinosis, revealing angiofibroblastic hyperplasia and fibrinoid necrosis with few or no inflammatory cells. These findings are seen, perhaps, because operative treatment is rarely undertaken early in the process. Yet, early in the clinical setting, the symptoms in many patients respond favorably to anti-inflammatory drugs and modalities. One can speculate that the anti-inflammatory drugs are acting solely as pain relievers, much as they do in osteoarthrosis. Alternatively, perhaps in some patients, a microscopic tear in the tendon initiates an inflammatory response that, if not treated, is replaced by tissue that resembles a failed repair or degenerative process: it is poorly organized, has numerous blood vessels, and contains fibroblasts and areas of hyaline or mucoid degeneration. Questions remain about the exact pathophysiology and appropriate terminology for what are predominantly overuse problems in the tendon. In the evaluation of a patient who has a tendon problem, it is important to obtain a detailed history of the onset of pain and the examiner must look carefully for contributing anatomical or biomechanical factors. As we have pointed out, most of these tendon problems are due to overuse caused by errors in training by either a younger enthusiastic athlete or an older, unconditioned recreational athlete. 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