Everything Achilles: Knowledge Update and Current Concepts in Management AAOS Exhibit Selection

1187 COPYRIGHT Ó 2015 BY THE JOURNAL OF BONE AND JOINT SURGERY,INCORPORATED Exhibit Selection Everything Achilles: Knowledge Update and Current Concepts in Management AAOS Exhibit Selection Carlos A. Uquillas, MD, Michael S. Guss, MD, Devon J. Ryan, BA, Laith M. Jazrawi, MD, and Eric J. Strauss, MD Investigation performed at the Department of Orthopaedic Surgery, NYU Hospital for Joint Diseases, New York, NY Abstract: Achilles tendon pathology is common and affects athletes and nonathletes alike. The cause is multifactorial and controversial, involving biological, anatomical, and mechanical factors. A variety of conditions characterized by Achilles tendon inflammation and/or degeneration can be clinically and histologically differentiated. These include insertional Achilles tendinopathy, retrocalcaneal bursitis, Achilles paratenonitis, Achilles tendinosis, and Achilles paratenonitis with tendinosis. The mainstay of treatment for all of these diagnoses is nonoperative. There is a large body of evidence addressing treatment of acute and chronic Achilles tendon ruptures; however, controversy remains. Peer Review: This article was reviewed by the Editor-in-Chief and one Deputy Editor, and it underwent blinded review by two or more outside experts. The Deputy Editor reviewed each revision of the article, and it underwent a final review by the Editor-in-Chief prior to publication. Final corrections and clarifications occurred during one or more exchanges between the author(s) and copyeditors. Anatomy and Function 3.5 cm distal to the musculotendinous junction5, making it he Achilles tendon, composed of fibers from the gastrocne- vulnerable to iatrogenic injury6, particularly with minimally Tmius and soleus muscles, is the body’sstrongestandthickest invasive repair techniques5. The Achilles tendon is relatively tendon. Beginning at the midportion of the calf, the Achilles ten- hypovascular, especially at its midportion7,8; in contrast, the don internally rotates 90° as it courses distally in the posterior as- paratenon is a highly vascular structure9 (Figs. 1 and 2). pect of the leg, with the soleus contribution medial to that of The Achilles tendon is part of a musculotendinous unit the gastrocnemius1,2. It then inserts into the middle third of the that spans three joints, producing knee flexion, tibiotalar flat surface on the posterior aspect of the calcaneal tuberosity. flexion, and subtalar inversion (exerting a medial pull on the The Achilles tendon does not have a true synovial sheath; calcaneus). Loads as great as 12.5 times body weight are placed instead, it has a paratenon composed of flexible connective on the tendon during running, contributing to its high rate of tissue that allows for 1.5 cm of tendon gliding with activity 3,4. injury4,10. Male individuals have a higher maximum tendon The paratenon and tendon are innervated by nerves from attached rupture force and stiffness, in part due to a larger cross-sectional muscles and small fascicles from local cutaneous nerves—in area, than female individuals. Younger individuals have a higher particular, the sural nerve3. The sural nerve crosses the tendon maximum tendon rupture force and lower stiffness than their approximately 11 cm proximal to the calcaneal tuberosity and older counterparts11,12. Disclosure: None of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in support of any aspect of this work. None of the authors, or their institution(s), have had any financial relationship, in the thirty-six months prior to submission of this work, with any entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written in this work. Also, no author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to influence what is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the online version of the article. J Bone Joint Surg Am. 2015;97:1187-95 d http://dx.doi.org/10.2106/JBJS.O.00002 1188 T HE J OURNAL OF B ONE &JOINT SURGERY d JBJS. ORG EVERYTHING ACHILLES:KNOWLEDGE UPDATE AND CURRENT VOLUME 97-A d NUMBER 14 d J ULY 15, 2015 CONCEPTS IN MANAGEMENT gout, and use of fluoroquinolone antibiotics21.Reportedprevalence rates range from 6.5% to 18% in runners and 9% in dancers21. Insertional Achilles tendinopathy is thought to be an inflammatory process, at least in its initial phase. It may be associated with a Haglund deformity, which is a prominent posterosuperior aspect of the calcaneal tuberosity that causes an overlying bursitis and tendinopathy 20,21. In its chronic form, insertional tendinopathy may no longer be an inflammatory process. Insertional Achilles tendinopathy is primarily a clinical diagnosis, and patients will often report a history of pain and stiffness at the back of the calcaneus in the morning that worsens with activity and severe pain the day after exercising. Commonly, the Achilles tendon insertion will be painful at the midportion of the posterior aspect of the calcaneus21. In addition, an enlarged posterior border of the calcaneus may be palpable20.MRI(mag- netic resonance imaging) will reveal focal microtears and can be useful in confirming the diagnosis (Fig. 3)22. For most cases of insertional Achilles tendinopathy (85% to 90%), nonoperative treatment consisting of a short period of immobilization followed by gradual integration of reduced load-bearing activities and physical therapy provides pain re- lief 23. Prolonged periods of immobilization should be avoided. Platelet-rich plasma (PRP) therapy can be considered for re- fractory cases, although evidence supporting its use is scant 24,25. Surgical treatment to remove the diseased portions of the tendon, an osseous prominence irritating the tendon, and the inflamed bursa is rarely indicated, unless the condition becomes chronic Fig. 1 Gross anatomy of the Achilles tendon, showing innervation from the sural nerve and insertion on the posterior aspect of the calcaneus. Etiology and Risk Factors for Injury he Achilles tendon is the most commonly ruptured ten- Tdon2, and the incidence of injuries is increasing13. Injury causes are often multifactorial, related to overuse combined with mechanical overload and host susceptibility14. Both internal (anatomical conditions or systemic diseases) and external (training conditions and equipment) influencing factors have been de- scribed. Internal risk factors include decreased blood supply with advancing age15,16, corticosteroid or fluoroquinolone use, and male sex17. External risk factors may include high-intensity plyometric exercises, training on unfamiliar surfaces, and the use of improper footwear18,19. Achilles Tendon Pathology (Table I) nsertional Achilles tendinopathy, as its name suggests, occurs fi I secondary to degeneration of tendinous bers at their insertion Fig. 2 on the calcaneus20. The condition is associated with inflammatory Microscopic anatomy of the Achilles tendon. The paratenon is a flexible arthropathies, corticosteroid use, diabetes, hypertension, obesity, connective tissue structure that surrounds the tendon itself. 1189 T HE J OURNAL OF B ONE &JOINT SURGERY d JBJS. ORG EVERYTHING ACHILLES:KNOWLEDGE UPDATE AND CURRENT VOLUME 97-A d NUMBER 14 d J ULY 15, 2015 CONCEPTS IN MANAGEMENT Noninsertional tendinopathy can be divided into three his- topathologic entities: paratenonitis, paratenonitis with tendinosis, and tendinosis alone20. The term tendinopathy encompasses the broad spectrum of inflammation levels that may be present histologically in a given injury. The terminology for these disor- ders can be confusing, and different descriptive paradigms have been advocated to provide clarification28. Paratenonitis involves inflammation of only the paratenon; grossly, the paratenon appears thickened and adherent to normal tendon. Histologic evaluation classically shows inflammatory cell infiltration and capillary proliferation in the paratenon or peritendinous tissue20. Clinical signs include swelling, pain, crep- itus, local tenderness, and warmth. Paratenonitis with tendinosis is defined as paratenon inflammation present in the setting of intratendinous degeneration, thought to be secondary to a failed healing response29. Histology shows the same findings as paratenonitis with additional loss of tendon collagen, fiber disori- entation, and scattered vascular ingrowth. However, there is typically no intratendinous inflammation at this juncture20. The clinical signs and symptoms are similar to paratenonitis, often with the additional finding of a palpable asymptomatic tendon nodule20. Finally, isolated tendinosis can occur without Fig. 3 paratenonitis. It is thought that this condition results from an Sagittal T2-weighted MRI cut demonstrating insertional Achilles tendin- early inflammatory infiltrate followed by a failed healing re- opathy with surrounding paratenonitis. There is no evidence of a tendon sponse and ultimately tendon degeneration29. Histologically, tear. There is a trace amount of fluid within the retrocalcaneal bursa and the tendon has a noninflamed appearance with collagen de- a small dorsal calcaneal enthesophyte is visible. generation, hypocellularity, local necrosis, areas of calcification, and minimal vascular ingrowth20. Clinically, tendinosis is often and debilitating. In these cases, lengthening of the Achilles tendon painless and without swelling. may be necessary,

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