Chronic Achilles Peritendinitis: Etiology, Pathophysiology, and Treatment

Transcription

1 Chronic Achilles Peritendinitis: Etiology, Pathophysiology, and Treatment NANCY L. REYNOLDS, MEd, PT, ATC,' TEDDY W. WORRELL, EdD, PT, ATC2 Journal of Orthopaedic & Sports Physical Therapy Overuse injuries represent a significant percentage of injuries seen in a sports medicine setting. Sports medicine health professionals evaluate and treat patients with the overuse injury of chronic Achilles peritendinitis. This paper reviews the anatomy of the Achilles tendon and presents recent literature concerning the etiology, pathophysiology, and rehabilitation of chronic Achilles peritendinitis. A rehabilitation program is outlined addressing the specific demands of the chronically injured Achilles tendon. Athletes participating in running and jumping sports are at risk for developing Achilles tendon disorders (2, 5, 7, 10, 12-14). Since the onset of the fitness explosion, the frequency of occurrence of this injury has increased (1 0, 12). Furthermore, these injuries often recur and have a propensity for becoming chronic problems (1, 5, 7, 12, 13). Physicians, physical therapists, athletic trainers, and athletes are well aware of the prolonged nature of disability that can occur with Achilles peritendinitis and often become frustrated with the protracted rehabilitation process. The purpose of this paper is to discuss etiological factors related to the development of Achilles peritendinitis, including anatomical and biomechanical factors, faulty footwear, lack of flexibility, and training errors. Also, the pathology of Achilles peritendinitis is examined. Finally, a rehabilitation program that emphasizes the role of eccentric muscle contraction is presented. ANATOMY Gross Structure The gastrocnemius and soleus muscles form the superficial muscle group of the posterior leg. The ' Ms. Reynolds is an independent contracting physical Merapist in Indianapolis. Indiana. She was a graduate student at the University of Virginia's Graduate Program in Athletic Training at the time this paper was completed. Correspondence may be addressed to her at Progresswe Physical Therapy Hadley Road. Mooresville. IN Assistant professor of physical therapy. Krannert School of Physical Therapy. Un~vers~ty of Ind~anapolis. Ind~anapol~s. IN /1991/ $03.00/0 THE JOURNAL OF ORTHOPAED~C AND SPORTS PHYSICAL THERAPY Copyright by The Orthopaedic and Sports Physical Therapy Sections of the American Physical Therapy Association gastrocnemius acts as a knee flexor and foot plantarflexor. The soleus acts only on the foot as a plantarflexor. The two muscles join to form a common tendon, the tendo calcaneus, or Achilles tendon (1 5). The tendo calcaneus is broad and flat near its proximal insertion to the gastrocnemius and becomes more narrow and round distally. On the anterior surface, the gastrocnemius receives muscle fibers from the soleus that continue almost to the gastrocnemius' distal end. The gastrocnemius portion of the tendon ranges from 11 to 26 cm long, with its most rounded portion approximately four cm above the calcaneus. The soleus tendon length can vary from three to 11 cm (2). The distal portion of the tendon expands from approximately four cm distally and attaches to the midposterior calcaneus via a stiff fibrocartilaginous expansion. As the tendon descends, it may spiral up to 90 degrees laterally, so that the medial aspect becomes posterior at the distal end. The rotation is variable and depends on the amount of fusion between the soleus and gastrocnemius. The more proximal the fusion, the less the degree of rotation (2). The significance of the rotation is that a region of concentrated stress may be produced where the two tendons meet. This is most prominent at two to five cm proximal to the calcaneal insertion and corresponds to the region of the tendon with the poorest vascular supply (2). Tendon Structure The Achilles tendon is composed primarily of collagen fibers arranged in increasing order of size: JOSPT 13:4 April 1991 CHRONIC ACHILLES PERITENDINITIS 171

2 collagen fibers grouped together form primary fiber bundles, and groups of primary fiber bundles form fascicles (secondary bundles). A group of fascicles forms a tertiary bundle, and the tertiary bundles make up the tendon (12). A fine sheath, the epitenon, surrounds the tertiary bundles. Deeper, the sheath surrounds the fascicles as the endotenon. The paratenon covers the epitenon and allows the tendon to move freely against the surrounding tissues. Where the paratenon serves to prevent friction, it is replaced by a synovial sheath. The epitenon and paratenon together make up the peritendon (2, 12). Vascular Supply Small branches from the posterior tibial and peroneal arteries supply the Achilles tendon. The major areas of vascularity are: the musculotendinous junction, along the length of the tendon, and at the tendon-bone junction. The majority of the blood supplied to the Achilles tendon comes through the paratenon (12). Small branches from the posterior tibial and peroneal arteries run transversely through the paratenon. These then branch repeatedly, becoming longitudinally and transversely oriented along the fascicles to form a uniform, mesh-like vascular system along the length of the tendon (1 2). The significance of the blood supply is that an area of decreased vascularity exists between two and six cm above the tendon insertion (4, 9). Several authors speculate that this reduced vascularity may be an important etiological factor in the development of Achilles tendinitis (1, 2, 12). BIOMECHANICS Prolonged Pronation As the foot moves from heel strike to foofflat, a certain amount of pronation is necessary to allow the foot to adapt to the surface contour (1 1). However, during excessive pronation, the Achilles tendon is at risk for injury (1,12,13). Factors that may cause excessive pronation are forefoot and rearfoot varus, forefoot valgus, and a plantarflexed fifth ray (1 1). Also, internal torsional deformities of the hip, femur, or tibia, leg length inequalities, and muscular shortness of the iliopsoas, hamstrings, or gastrocnemius/soleus complex preventing full dorsiflexion of the ankle require abnormal, excessive, subtalar joint pronation (1, 11,12). Clement et a1 (1) and Smart et al (12) have reported through observations of slow-motion cinematography that prolonged pronation causes tibial internal rotation, pulling the Achilles tendon medially. As push-off occurs, there is a resultant bowstring or "whipping" effect, pulling the tendon laterally. The authors postulate that this whipping effect may contribute to microtears in the tendon, especially on the medial side. Clement et al (1) and Smart et al (12) also describe the role of internal tibial rotation and knee extension occurring simultaneously during prolonged pronation. As the foot moves from midstance to push-off, the tibia is being externally rotated by knee extension and foot supination. Ideally, this should occur simultaneously. However, if the foot is excessively pronated and the knee begins to extend, the forces of external tibia rotation at the knee and internal tibia rotation at the ankle occur simultaneously. These authors propose that the resultant torsional force on the Achilles tendon may cause an ischemic "wringing out" at or near the avascular zone, predisposing the tendon to degenerative changes. Tendon Mechanics Long tendons are most suited for absorbing large forces placed on them during athletic activity. Since tendon is stronger than muscle per unit area (2), it would appear that the Achilles tendon is ideally designed to withstand the high forces of running and jumping. However, the tendon is derived from two muscles and has interdigitating fibers that twist as they descend. This may produce areas of high stress concentration (2). Also, the Achilles tendon absorbs forces in two planes: the sagittal plane (dorsiflexion and plantarflexion), and the frontal plane (eversion and inversion). These combined stresses can create unequal tensile forces on different parts of the tendon. This relates to the torsional ischemic "wringing out" effect described by Clement et a1 (1) and Smart et al (1 2). Maximal stress values to failure for mammalian tendon have been estimated at 49 to 98 MPa (3). Estimated stress on the Achilles tendon during slow and fast running is 52.3 to 78.5 MPa and MPa, respectively (2). Curwin and Stanish (2) note that these values have been obtained from animal studies, and data for humans has been limited to estimations from force plates or in vitro studies. However, it appears that stress values produced during athletic activity greatly exceed the maximum values for tendon load, making the tendon at risk for injury (2, 13). Forces that tend to place highest stress on the Achilles tendon occur during eccentric contraction of the gastrocnemius/soleus muscle complex (2, 13). Examples of these include: pushing off the weightbearing foot while simultaneously extending the knee, as in uphill running; sudden ankle dorsiflexion that occurs unexpectedly, such as when stepping up a step and then slipping off with the heel dropping; and rapid, involuntary dorsiflexion of a plantarflexed foot (2). 172 REYNOLDS AND WORRELL JOSPT 13:4 April 199 1

3 POOR FLEXIBILITY Lack of flexibility in the calf musculature predisposes an individual to Achilles tendon injury (1, 2, 12, 13). The relationship of length to injury can be described in terms of the muscle-tendon unit's resting length. When the resting length is increased, decreased strain (deformation) takes place during a particular range of movement (2). A shortened Achilles tendon is placed under greater strain than a longer tendon. Also, lack of adequate dorsiflexion may cause unwanted compensation by excessive pronation (1, 1 1, 12). FAULTY FOOTWEAR Curwin and Stanish (2). Smart et al (12), and Clement et al (1) agree that faulty footwear can be a major contributing factor toward develop ment of Achilles tendon disorders. Control of the rearfoot is essential. Shoes should have firm, close-fitting heel counters of proper depth (distal to the lateral and medial malleolus, but not in contact with them) and wide heel bases in order to provide adequate rearfoot stability. There should also be adequate heel wedging of 12 to 15 mm vertical height. Lastly, shoe sole flexibility must allow extension of the metatarsophalangeal joints during running. If the toes cannot bend, the lever arm from the ankle to the forefoot is lengthened, thus increasing strain on the Achilles tendon. TRAINING ERRORS Training errors include changes in frequency, duration, intensity, terrain (hills), and change of sport (1, 2, 10, 12). Increasing frequency, duration, and intensity of training too rapidly is related to an increased incidence of Achilles tendon problems (1, 10, 12). Also, changing from soft to hard running surfaces or instituting an increase in hill running are factors that predispose athletes to Achilles tendon injury (1, 12). Classification of Achilles Peritendinitis Since the Achilles tendon does not have a true synovial sheath, classification of acute and chronic conditions of the Achilles tendon can sometimes become confusing. Although, in the case of acute injury, crepitus is present with movement of the tendon, it cannot be named a tenosynovitis since there is only a paratenon (1, 2, 13, 14) and no true synovial sheath. Several authors (1,2, 10, 13) recommend use of the term peritendinitis or paratenonitis to refer to inflammation of the tendon sheaths and the term ten- dinitis to refer to the inflammation and degeneration of the tendon itself. For purposes of clarification, the remainder of this paper will use the term peritendinitis to refer to any acute or chronic inflammation of the tendon sheaths. Development of Chronic Achilles Peritendinitis Acute peritendinitis is usually the result of blunt trauma or acute muscle fatigue (10). There is subsequent circulatory impairment and edema formation. Crepitus, a major diagnostic sign of acute injury, is due to movement of the tendon within the peritendon, which now contains a fibrinrich exudate. If treatment of the acute condition fails, or goes untreated, the fibrin within the sheath organizes and begins to form adhesions to the tendon and surrounding tissues (5,7). The tendon is then predisposed toward development of chronic Achilles peritendinitis (CAP). More commonly, CAP occurs as a result of overuse in combination with one or more of the etiological factors mentioned previously. Symp toms have a gradual onset, and if not treated immediately, become rapidly resistant to conservative treatment (1,2,10, 1 1,13, 14). In CAP there is usually no crepitus or effusion. Frequently there are tender nodules around the tendon (most frequently on the medial border) and diffuse thickening of the soft tissues surrounding the tendon (1 0). Common symptoms of individuals in the process of developing CAP include pain and stiffness with the first steps taken in the morning and pain at the onset and shortly after an exercise bout. Left untreated, these symptoms progress until the athlete is functionally disabled for his or her sport. Even walking becomes painful (1, 10, 13). Cellular Changes As the condition progresses, several pathological, structural, metabolic, and vascular changes occur in the peritendon. Kvist et al (6) examined tissue samples from 16 athletes having CAP an average of six months who were undergoing surgery for removal of tendinous adhesions and compared them with three normal controls. Biopsies were obtained from five sites: next to the crural fascia, the paratendineal tissue, the epitenon, adhesions in Kager's triangle (anterolateral to the Achilles tendon), and the gliding membranes of the paratenon. Macroscopically, they found all peritendineal tissue to be thickened and edematous. This hypertrophy serves to increase friction between the peritendon and tendon that interferes with the gliding function of the paratenon membranes. Also present was widespread fat necrosis with connective tissue proliferation and adhesion forrna- JOSPT 13:4 April CHRONIC ACHILLES PERITENDINITIS 173

4 tion. These further interfered with the gliding function of the paratenon membranes. Enzyme studies demonstrated marked changes of increased catabolism and decreased oxygenation of the affected tissue. Vascular changes included proliferation of small vessels, with thickening of the intima that caused narrowing and even obliteration of capillaries, small arteries, and veins. Also, stasis and hemorrhage of small vessels, along with atherosclerotic and thrombotic alterations, were found. Kvist et al (7) also found increased secretion of ground substance, type I and type Ill collagen fibrils, and proliferation of myofibroblasts in a study of 14 athletes with CAP. The increase in ground substance and collagen fibrils indicates an attempt at tissue repair. Myofibroblasts occur only in wounds requiring contraction. Therefore, the authors believe that the myofibroblasts cause contraction of the chronically inflamed peritendon which, in turn, decreases blood flow via constriction of the vascular lumen, thus perpetuating the chronic nature of the inflammation. The authors speculated that the marked vascular changes may cause ischemic pain felt during exercise. In addition, morning stiffness and pain may be due in part to the disturbance in blood supply caused by the previous proliferation of ground substance, collagen, and myofibroblasts. Kvist et a1 (5) reported the role of fibronectin and fibrinogen in perpetuating CAP. Fibronectin is a glycoprotein, which together with fibrin, promotes the organization of collagen. During normal healing, fibronectin soon disappears from the affected site. However, in this study of 11 athletes having CAP an average of 20 months, the tissue biopsies obtained at surgery contained high amounts of fibronectin and fibrinogen. The presence of these substances indicates the immature nature of scar tissue in chronically inflamed peritendineal tissue. In addition, these substances may play an important role in the development of the vascular lesions seen in CAP. Because they increase vascular permeability, the cycle of vessel leakage, edema, pressure, and tissue necrosis is continued. TREATMENT AND REHABILITATION Conservative Measures Common conservative treatment for CAP includes stretching of both the soleus and gastrocnemius, use of quarter-inch heel pad inserts to decrease strain on the tendon, biomechanical assessment and appropriate orthotic prescription, modified rest, oral anti-inflammatories, ice, ultrasound, and strengthening exercises (1, 2, 10, 1 1, 13, 14). Steroid injections and prolonged cast immobilization are now being recognized for their potential deleterious effects on tendon degeneration, muscle atrophy, and joint degeneration, respectively (2,11, 13). Several authors agree that more often than not, these measures fail, and surgery then becomes the treatment of choice (1, 8, 10, 1 1, 13, 14). One recent study describes a treatment that may help prevent surgery. Sundqvist et al (14) performed a double-blind study on 60 recreational athletes with CAP. The subjects received either local injections around the Achilles tendon of glycosaminoglycan polysulfate (GAGPS), an anticoagulant, in 50 mg/ml doses three times a week for two weeks and placebo tablets, or oral indomethacin in doses of 50 mg a day for two weeks and placebo injections. One year follow-up results showed that 66 percent of those treated with GAGPS and only 33 percent of the indomethacin treated group had a good therapeutic result (described as symptom-free or minor symptoms). Sundqvist et al(14) theorized that the therapeutic benefit achieved with the GAGPS injections may be due to its inhibition of the formation of thrombin and fibrin. This supports the work of Kvist et al(5), who found increased fibrinogen and fibrin in the peritendineal tissues of CAP patients. The presence of these substances delays collagen formation, leading to the eventual hypertrophic scarring often seen in CAP (6-8, 14). Finally, Sundqvist et al(14) point out that while GAGPS may be a new and successful alternative to surgery, it should be augmented with a rehabilitation program and biomechanical correction as indicated. Role of Eccentrics Curwin and Stanish (2) and Stanish et al (13) theorize that trauma to the Achilles tendon occurs specifically under eccentric loading and that eccentric exercises must be included in the rehabilitation process. Their theory is based on the fact that an eccentric contraction places greater load on the tendon than concentric or isometric contractions. Therefore, if the injured tendon is strengthened via the eccentric mode, the tendon will develop sufficient strength to withstand the applied eccentric forces of activity. There are three factors upon which Curwin and Stanish base their eccentric exercise program: length, load, and speed of contraction. The longer the resting length of the muscle-tendon unit, the less strain placed upon it for a given force applied. As load and speed of contraction increase, an increase in force development also occurs. Exercises are performed in a pain-free progression, although early-on, delayed muscle soreness may be experienced. Patients should be made aware of the expected response to eccentric exercise. The use of warm-up and flexibility REYNOLDS AND WORRELL JOSPT 13:4 April 1991

5 exercises prior to the exercise program and ice following the exercise program are essential to its success. To the knowledge of this study's authors, no controlled clinical studies other than that of Curwin and Stanish have been reported in the literature. It should be noted that the success of this study's reported program is based solely on clinical observation. The Exercise Program The eccentric exercise is performed on a fourinch box or step. Both legs perform a concentric toe raise. Once maximum plantarflexion range of motion is reached, the uninvolved leg is picked up and the involved leg lowers into dorsiflexion. Speed, sets, and weight are increased to tolerance. Table 1 presents an example of a typical exercise progression. This progression is modeled after the work of Curwin and Stanish (2), but has been modified based on the authors' experience. Pain is the rate-limiting factor during exercise. Each level of progression must be performed symptom-free before moving up to the next level. It is better to keep the progression slow, allowing healing to occur, than to force a more rapid recovery, thereby prolonging the rehabilitation process. Ideally, the exercises should be preceded by a five to 10 minute warm-up. Stretching consists of three, 30-second stretches of the gastrocnemius and soleus. The exercises are then performed, followed again by stretching, and then ice TABLE 1 Example of eccentric exercise program is applied in a slightly dorsiflexed position for 15 minutes. Alternative forms of exercise to maintain some level of cardiovascular conditioning should be included in the rehabilitation program. However, if the peritendinitis is severe, even swimming or stationary biking may exacerbate symptoms. If so, upper extremity exercise or one-legged stationary cycling should be utilized. A cycle ergometer with moving upper extremity handles is ideal for this purpose as it allows both upper and lower extremity exercise while the involved extremity is rested. Also the eccentric exercise protocol can be performed in a swimming pool if the athlete is unable to bear full weight during the eccentric loading phase. A brick can be used to provide elevation. Submersion can begin at shoulder height and progress to waist height. At this point, the exercise can probably be performed out of water without pain. When the patient has progressed through the strengthening progression to phase six, emphasis is placed on the walkljog program. Total walkljog time should increase up to one hour. At this point, jog duration should be decreased and intensity gradually increased. Gradual return to sport also begins during this period. During the walkljog phase of rehabilitation, frequent stops for stretching will extend the duration of the pain-free activity. If patients feel onset of symptoms during any running activity, they should be instructed to stop and stretch. If the stretching alleviates symptoms, they may continue activity. Phase SetsPeps Speed WMM Frequenc~ Function' Slow Body 2xlday ADLs sx-free Mod Body Fast Body 2x/day 2xlday Mod walk up to 15 min sxfree Fast walk up to 20 min sxfree Slow Body+lOIbs 2xlday Walkljog 5 min/l min sx-free up to 20 min Mod Body+lOIbs 2x/day Walkljog 5 min/3 min sx-free up to 20 min Fast Body+lOIbs 2xlday Walkljog 5 min/5 min sx-free up to 25 rnin 'sx, symptom; min, minutes; mod, moderate. JOSPT 13:4 April CHRONIC ACHILLES PERITENDINITIS 175

6 Other Rehabilitation Considerations A critical factor that is not addressed in the reviewed literature is the importance of prevention. The role of the clinician is to recognize the signs and symptoms of a specific musculoskeletal problem and initiate treatment before that problem becomes chronic. Obviously, many individuals do not come for help until the problem is already chronic. However, in the athletic training room setting, where contact with athletes is daily, close monitoring is feasible and necessary to prevent injuries. Any athlete-recreational, collegiate, or professional-should be made aware of the signs and symptoms of Achilles peritendinitis, the need for immediate therapeutic intervention, and the severe and prolonged debilitation that can occur if treatment is delayed. Even the best attempts at prevention some times fail; once a case of CAP is identified, the difficulty of rehabilitation and the need for 100 percent compliance from the patient should be discussed. Even then, success is not guaranteed. Stanish et al (13) reported on 200 patients having CAP for an average duration of 18 months. They performed an eccentric exercise protocol once a day for six weeks. Eighty-seven percent had either complete or marked decrease in pain and functional impairment at 16 months followup. Two percent were worse, and nine percent were unchanged. Curwin (2) feels that the presence of severe scarring (i.e., the longer the CAP is present) reduces the chance of successful conservative treatment. Again, the importance of prevention and early recognition and treatment is demonstrated. SUMMARY There are several factors that may explain the etiology of the development of chronic Achilles peritendinitis. The clinician must be aware of all of them when assessing a particular patient. Not only the symptoms, but the causative factors must be corrected. The pathophysiology of CAP is complex and not yet well understood. The use of GAGPS may be a successful alternative to surgery for severe cases recalcitrant to conservative treatment. The role of eccentrics should be understood and utilized by the clinician in the rehabilitation of CAP. Further study is necessary to clarify the role of eccentrics in rehabilitation of Achilles tendinitis-specifically, prospective studies comparing eccentric versus concentric exercise protocols. Finally, the role of prevention cannot be overemphasized. 0 The author wishes to acknowledge Joe G i for his valuable input concerning exercise progression. REFERENCES 1. Clement D. Taunton J, Smart G: Achilles tendinitis and peritendi nitis: e t i and treatment. Am J Sports Med Curwin S. Stanlsh WD: Tendinitis: Its Etiology and Treatment, pp Lexington. MA: Collarnore Press. D. C. Health and Co Elliot DH: Structure and function of mammalian tendon. Bii Rev 40: , Hastad K. Larsson LG. Lindholm A: Clearance of radiiium after local deposit in the Achilles tendon. Acta Chir Scand 116: /59 5. Kvlst M. Lehto M, Jozsa L. Jarvinen M. Kvist H: Chronic Achilles paratenonitis: an immunohistological study of fibronectin and fibrinogen. Am J Sports Med 16: Kvlst M. Josza L. Jarvinen M. Kvlst H: Chronic Achilles paratenmtls in athletes: a histological and histochemical study. Pathology 19:l Kvist M. Josza L. Jarvinen M. Kvist H: Fine structural alterations in chronic Achilles paratenonitis in athletes. Pathd Res Pract 180: Kvist H. Kvist M: The operative treatment of chronic calcaneal paratenonits. J Bone Joint Surg (Br) Lagergren C. Lindholm A. Vascular distribution in the Achilles tendon-an angiographii and m~croangiographic study. Acta Chir Scand 116: / Leach R. James S. Wasilewski S: Achilles tendinitis. Am J Sports Med 9: Root M. Onen W. Weed J: Normal and Abnonnal Function of the Foot. Clinical B~ornechanics. 11. pp Los Angeles. CA: Cllnlcal Biomechanics Cop Smart G. Taunton J. Clement D: Achilles disorders in runners-a revlew. Med Sci Sports Exerc 12: Stanlsh W. Rubinovich R. Curwin S: Eccentric exercise in chronic tendmitis. Clin Orthop 208: Sundqvist H. Forsskahl B. Kvist M: A promising nod therapy for Achllles peritend~nltls: double-blind comparison of glycosaminoglycan polysulfate and highdose indomethacin. Int J Sports Med 8: , Wtlhams P. Warwick R: Gray's Anatomy. 36th Ed. pp Philadelphia: WB Saunders REYNOLDS AND WORRELL JOSPT 13:4 April 1991