Surgical Treatment for Chronic Disease and Disorders of ...

Surgical Treatment forChronic Disease andDisorders of the AchillesTendon

AbstractChronic Achilles tendon disorders range from overuse syndromesto frank ruptures. Numerous forms of treatment have been used,depending on the nature of the disorder or injury. Ultrasonographyand magnetic resonance imaging are commonly used forevaluation. The spectrum of disease comprises paratenonitis,tendinosis, paratenonitis with tendinosis, retrocalcaneal bursitis,insertional tendinosis, and chronic rupture. However, there is noclear consensus on what defines a chronic Achilles disorder.Nonsurgical therapy is the mainstay of treatment for most patientswith overuse syndromes. Surgical techniques for overusesyndromes or chronic rupture include débridement, local tissuetransfer, augmentation, and synthetic grafts. Local tissue transfermost commonly employs either the flexor hallucis longus or flexordigitorum longus tendon to treat a chronic rupture. Reports onlong-term outcomes are needed before useful generalizations can bemade regarding treatment.

Chronic Achilles tendon dys-function and disease are chal-

lenging to manage. Numerous treat-ment options are available, withselection based on the nature of thedisorder. At one end of the spec-trum is a variety of overuse syn-dromes that continue to be furtherdefined; at the other end is frankrupture of the tendon in the settingof chronic tendon pathology andchronic rupture. The confusing lit-any of terms used to describechronic Achilles tendon disordershighlights the lack of consensus re-garding which classification systembest illustrates what is seen clini-cally and microscopically. For in-stance, what was once termed ten-

dinitis is now known to be acondition in which inflammatorycells are not involved.1 The term“chronic” has been used differentlyin various settings, leading to diffi-culty in interpreting results.2 Fur-ther complicating any proposedtreatment algorithm is that the as-sorted Achilles tendon pathologycan and often does present in twodistinct patient populations: theyounger athlete and the older com-munity ambulator, neither of whommay be an optimal candidate for anyof the available treatment modali-ties. Surgical treatments are myriadand can involve local tissue transfer,augmentation procedures, and syn-thetic graft.

Sudheer S. Reddy, MD

David I. Pedowitz, MD, MS

Selene G. Parekh, MD, MBA

Imran M. Omar, MD

Keith L. Wapner, MD

Dr. Reddy is Sports Medicine Fellow,Department of Orthopaedic Surgery,University of California–San Francisco,San Francisco, CA. Dr. Pedowitz isAttending Physician, Department ofOrthopaedic Surgery, Crystal RunHealthcare, Middletown, NY. Dr. Parekhis Assistant Professor, Foot and AnkleSurgery, Department of OrthopaedicSurgery, University of North CarolinaSchool of Medicine, Chapel Hill, NC.Dr. Omar is Fellow, Department ofRadiology, Thomas Jefferson UniversityHospital, Philadelphia, PA. Dr. Wapneris Clinical Professor, Department ofOrthopaedic Surgery, University ofPennsylvania School of Medicine,Philadelphia.

Reprint requests: Dr. Parekh,Department of Orthopaedic Surgery,University of North Carolina School ofMedicine, 3135 Bioinformatics Bldg,CB#7055, Chapel Hill, NC 27599.

J Am Acad Orthop Surg 2009;17:3-14

Copyright 2009 by the AmericanAcademy of Orthopaedic Surgeons.

Volume 17, Number 1, January 2009 3

Imaging

Imaging of the Achilles tendon is pri-marily limited to ultrasonographyand magnetic resonance imaging(MRI). Standard radiographic imagingis useful for diagnosis of some con-ditions. Ultrasonography providesmany advantages, including speed,safety, and low cost. It can verify theexistence and location of intraten-dinous lesions. The results of ultra-sonography have been found to be re-

liable, particularly in chronic casesinvolving adhesions around the ten-don. In the acute phase of Achillestendinopathy, ultrasonography candemonstrate fluid surrounding thetendon.3,4 In the chronic form, peri-tendinous adhesions can be seen asa thickening of the hypoechoicparatenon with poorly defined bor-ders.4,5 Localized tendon swelling andthickening, discontinuity of tendonfibers, and focal hypoechoic intraten-dinous areas are the most character-

istic ultrasonographic findings in thepatient with a surgically verifiedAchilles intratendinous lesion.4

Ultrasonography has drawbacks,however. It is operator-dependentand is not as readily accessible asMRI.4,6 Neither is it as accurate asMRI in delineating isolated paraten-onitis unassociated with focal intra-tendinous disease. With ultrasound,it is difficult to differentiate a partialrupture from a discrete area of tendi-nosis. In evaluating Achilles tendon

Figure 1

Algorithm for the treatment of Achilles tendinopathy. FHL = flexor hallucis longus tendon, MAFO = molded ankle-foot orthosis,MRI = magnetic resonance imaging, PT = physical therapy

Dr. Wapner or a member of his immediate family has received research or institutional support from EBI and serves as a consultant to or is anemployee of Wright Medical Technology and MemoMetal. None of the following authors or a member of their immediate families has receivedanything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Reddy,Dr. Pedowitz, Dr. Parekh, and Dr. Omar.

Surgical Treatment for Chronic Disease and Disorders of the Achilles Tendon

4 Journal of the American Academy of Orthopaedic Surgeons

disorders, ultrasound has a sensitiv-ity of 0.80 and specificity of 0.49.7

MRI has been used extensively tovisualize tendons. It provides exten-sive information on the internalmorphology of the tendon and thesurrounding structures. It is usefulfor evaluation of acute ruptures aswell as various stages of chronic de-generation. It can aid in differentiat-ing paratenonitis from tendinosis.As with ultrasound, excellent corre-lation has been reported betweenMRI results and intraoperativepathologic findings.8 MRI has a sen-sitivity of 0.95 and a specificity of0.50 in evaluating Achilles tendonpathology.7,9 Unlike ultrasonogra-phy, it is not operator-dependent,and it allows multiplanar imaging.

Standard radiography has also beenused in the evaluation of retrocalca-neal bursitis and Haglund deformity(ie, prominence of the posterosuperiorangle of the os calcis). The promi-nence can cause a mechanical irrita-tion of the retrocalcaneal bursa. Ona lateral radiograph, the prominenceof the posterosuperior calcaneal tu-berosity can be measured using par-allel pitch lines. This line can be mea-sured by placing a line from thecalcaneal tuberosity to the anteriorcalcaneal tubercle. A second line isdrawn parallel to this at the level ofthe posterior lip of the posterior facet.Bony prominences extending abovethis line are abnormal.10 Although apatient with a Haglund deformity hasan element of retrocalcaneal bursitis,multiple studies have attempted todelineate Haglund deformity radio-graphically as related to calcanealanatomy. However, no particular ra-diographic view has been consistentlyhelpful in making a diagnosis or inplanning treatment.11

After an exhaustive search of theliterature, we have realized that thereis no uniform classification or treat-ment scheme for Achilles tendonpathology. In regard to surgical plan-ning, MRI is the most useful imagingtool as it allows for evaluation of theAchilles tendon in the sagittal plane

to determine the length of the injuredor diseased tendon and subsequentsurgical planning. We present twotreatment algorithms based on imag-ing findings, albeit not on any directevidence, to guide the surgeon in thetreatment of chronic Achilles tendondisorders and disease (Figures 1 and 2).

Classification ofChronic AchillesTendon Disorders

Clancy et al12 proposed a schemethat classified Achilles tendinitis asbeing acute (symptom duration ≤2weeks), subacute (symptom durationbetween 3 and 6 weeks), and chron-ic (symptom duration ≥6 weeks). Amore descriptive and frequentlyused classification scheme based onclinical and anatomic-pathologicfindings was created by Puddu etal.13 Disorders are classified as pureperitendinitis (stage 1), peritendini-tis with tendinosis (stage 2), and ten-dinosis (stage 3).

In this scheme, the peritendi-nous structures, which include theparatenon and the septum, are sup-ported by loose connective tissuewith abundant cellularity that canpredispose them to an inflammatoryprocess.13 With regard to tendinosis,because of diminished vascularityand hypocellularity, the tendon isunlikely to undergo an inflammato-ry process and has been found histo-logically to undergo degeneration.13

Because the tendon itself does notundergo true inflammation, theterm tendinitis as it refers to theAchilles tendon is a misnomer.Paratenonitis would be a more de-scriptive term as it specifically refersto the tissue surrounding the tendonproper. Although Achilles parateno-nitis and tendinosis are independententities, they can coexist. Further-more, disease in the retrocalcanealbursa and the Achilles tendon inser-tion can result in retrocalcaneal bur-sitis and insertional tendinosis. Ex-cluding rupture, the spectrum of

Figure 2

Algorithm for treatment of chronic Achilles tendon rupture. FDL = flexor digitorumlongus tendon, FHL = flexor hallucis longus tendon

Sudheer S. Reddy, MD, et al


chronic Achilles tendon disease canbe subdivided into five disorders:paratenonitis, tendinosis, parateno-nitis with tendinosis, retrocalcanealbursitis, and insertional tendino-sis11 (Table 1).

Achilles ParatenonitisFamiliarity with the anatomy of

the Achilles tendon sheath is neces-sary to fully understand Achilles

paratenonitis (Figure 3). The Achil-les tendon is not encased in a truesynovial sheath but rather in a singlelayer of paratenon made up of a sin-gle layer of cells. The paratenon iscomposed of fatty, mesentery-likeareolar tissue that is highly vascular-ized and is responsible for a signifi-cant portion of the blood supply tothe tendon. Perfusion of the tendonoccurs through a series of vincula

that serve as thoroughfares for bloodvessels to reach the tendon. Most ofthe blood supply to the tendon is an-terior. Angiographic studies have re-vealed that there is an area of tenu-ous blood supply approximately 2 to6 cm proximal to the insertion to thecalcaneus.11

Although uncommon in theolder, more sedentary population,paratenonitis is commonly seen inathletes, especially long- and middle-distance runners.14 Because of itsvascularity, the paratenon is suscep-tible to inflammation, and the pa-tient with paratenonitis commonlypresents with diffuse discomfort andswelling of the tendon. Acutely, theAchilles tendon may appear sausage-like, with fusiform swelling (Fig-ure 4). Tender nodules can often oc-cur within the paratenon, reflectinglocalized hypertrophy of connectivetissue.11

External pressure from poor-fitting shoes is thought to cause fric-tion between the Achilles tendonand the overlying paratenon.11 Addi-

Figure 3

Magnetic resonance imaging (MRI) scans of a normal Achilles tendon in a 12-year-old girl with right ankle inversion. SagittalT1-weighted non–fat-suppressed (A) and T2-weighted fat-suppressed (B) scans indicating the tendon is uniform in caliber andof homogeneously low signal, with no paratendinosis or edema in Kager fat. C, Axial proton density non–fat-suppressed MRIscan of the mid tendon (arrowhead) demonstrating a homogeneously low tendon signal with a flat or slightly concave anteriortendon margin.

Table 1

Classification of Chronic Achilles Tendon Dysfunction3

Disorder Pathology

Paratenonitis Inflammation of the peritendinous structures,including the paratenon and septum

Tendinosis Asymptomatic degeneration of tendon withoutinflammation, with regional focal loss of tendonstructure

Paratenonitis withtendinosis

Inflammation of the peritendinous structures alongwith intratendinous degeneration

Retrocalcanealbursitis

Mechanical irritation of the retrocalcaneal bursa

Insertionaltendinosis

Inflammatory process within the tendinous insertion ofthe Achilles tendon



tionally, fluid may accumulate adja-cent to the tendon, and adhesionsmay develop. Macroscopically, thetendon is thickened and adherent tothe normal surrounding tissue. In apatient with isolated paratenonitis, ahistologic study will show capillaryproliferation and inflammatory infil-trate confined to the paratendinoustissue.15 Kvist et al14 found that theblood vessels within the paratenonwere often obliterated and degener-ated, with fibronectin and fibrinogencommonly found in the proliferatingconnective tissue areas and in thevascular walls. It is thought thatmyofibroblasts in the peritendinoustissue synthesize abundant amountsof collagen in response to mechani-cal stress, resulting in scarring andshrinkage of the peritendinous tis-sue. This contracted state can alsolead to vascular constriction, furtherimpeding the circulation to theAchilles tendon.3

Given that Achilles paratenonitisoften has a mechanical origin andfrequently affects distance runners, adetailed history tailored to the activ-ity of the runner should be sought.Pain is the cardinal symptom ofAchilles tendinopathy.3 In the earlyphase of paratenonitis, the patientmay complain primarily of pain fol-lowing strenuous exercise; if thecondition is progressive, pain mayaccompany routine activities. Forathletes, the pain may be disablingenough to curtail training regi-mens.16

Physical examination findingsvary, depending on the degree ofinflammation present within theparatenon. Decreased ankle dorsi-flexion, often due to tightness of thegastrocnemius-soleus-Achilles ten-don complex, and hamstring tight-ness are commonly found in patientswith Achilles tendon pathology.16,17

The Silfverskiold test can be used tomeasure tightness of the gastroc-nemius-soleus complex by alter-nately relaxing and incorporatingthe muscle by flexing and extendingthe knee, respectively, while dorsi-flexing the ankle.10 A patient withparatenonitis will exhibit tendernessand thickness that remain fixed withactive range of motion of the ankle.

There is often palpable tendernesson both sides of the tendon, with themedial side being more tender thanthe lateral.11 Imaging of paratenoni-tis primarily involves two modali-ties: ultrasonography and MRI.15

Ultrasound frequently reveals fluidsurrounding the tendon acutely andchronically and can reveal adhesionsthat can be visualized as thickeningof the hypoechoic paratenon (Fig-ure 5). T1-weighted MRI scans willshow a thickened paratenon, with ahigh signal seen within the paraten-on on T2-weighted imaging (halosign)18 (Figure 6).

Nonsurgical treatment is initiallyindicated for Achilles paratenoni-tis. For the less active, older patient,treatment generally focuses onimmobilization with a nonarticu-lated solid molded ankle/foot ortho-sis, nonsteroidal anti-inflammatorydrugs (NSAIDs), and possibly a shortcourse of physical therapy. For themore active patient, conservativemodalities typically consist of mod-ification of training regimens (eg,

Figure 5

Sagittal grayscale ultrasound image ofa 61-year-old man with left posteriorankle pain demonstrating a tendon withfusiform enlargement (arrow) andsurrounding hypoechoic fluid(arrowheads), indicating Achillesparatendinitis.

Figure 6

Axial T2-weighted fat-suppressed MRIscan of a 47-year-old man with rightposterior ankle pain. The imagedemonstrates a convex anterior marginof the Achilles tendon, seen in criticalzone tendinosis, with a circumferentialrim of hyperintense signal (arrowhead)depicting paratendinitis.

Figure 4

Sagittal T2-weighted fat-suppressedMRI scan demonstrating critical zoneAchilles hypoxic tendinosis andfusiform enlargement of the tendoncritical zone with uniform low signal(arrowhead) in a 40-year-old womanwho presented with right posteriorankle pain.



staged cross-training regimen), rest,ice, massage, and NSAIDs. A smallheel lift or a shock-absorbing orthot-ic device may also help reduce acutesymptoms but may allow the in-jured tendon to contract. Nightsplints may be added as needed toprevent this.

In a series of 41 patients, Johnstonet al19 found that 51% improved withan average of 18 weeks of nonsurgi-cal therapy alone. Brisement can alsobe performed to break up adhesionsin paratenonitis, particularly in pa-tients with audible crepitus with am-bulation. This procedure involves in-jecting slowly into the paratenonsheath approximately 5 to 10 mL ofa dilute local anesthetic, such aslidocaine, or saline solution underpressure. Ultrasound guidance can beused, if available, to guide proper nee-dle placement. Two or three injec-tions can reduce symptoms approx-imately half of the time.10,11,15

Rarely, surgical treatment is con-sidered for chronic paratenonitisthat is resistant to nonsurgical mea-sures. A medial longitudinal inci-sion can be used, with developmentof full-thickness flaps of skin, subcu-taneous tissue, and crural fascia. Theanterior aspect of the paratenon isavoided to protect the blood supplyto the Achilles tendon. Thickenedparatenon can be excised posteriorly,medially, and laterally around thetendon.15 For cases of paratenonitisonly, postoperative therapy shouldfocus on immediate range-of-motionexercises to prevent scarring and re-currence of adhesions. For the first 3weeks, weight bearing is restrictedin a removable boot to limit swellingand aid wound healing. Schepsis andcolleagues8,11 reported a satisfactionrate of 87% for surgical treatment ofrecalcitrant paratenonitis. Endoscop-ic methods, consisting of a proximalportal for visualization and a distalportal for instrumentation, have alsobeen used to release, in a retrogradelongitudinal fashion, and débride theconstricting paratenon, by means ofa shaver. Patients were allowed to

begin range-of-motion exercises andwere progressed to full weight bear-ing by 3 to 6 days. Satisfactory sub-jective results were reported byMaquirriain et al20 in using thistechnique for paratenonitis.

Achilles TendinosisGiven that tendinosis is a degen-

erative process, the Achilles tendonwith tendinosis on gross examina-tion may appear thick, soft, and yel-lowish, owing to an accumulation ofmucinoid material within the ten-don.13 The condition is often definedas an asymptomatic degeneration ofthe tendon without inflammation,caused by accumulated microtrau-ma, aging, or both. Because of itsasymptomatic nature, tendinosis isoften detected after frank rupture ofthe tendon.1 Such frank ruptures areoften preceded by partial ruptures,typically in middle-aged men whohave suddenly increased their levelof physical activity. The paratenon israrely involved. Central to thispathologic process is the poor heal-ing response following repetitivemicrotrauma.3

Although the pathogenesis of ten-dinosis is unknown, several theorieshave been proposed, including hy-poxic degeneration, the effect of freeradicals, and exercise-induced hyper-thermia; however, all of these theo-ries lack direct scientific evidence.Pathologic changes within the ten-don matrix also occur, including cal-cification and accumulation of adi-pose tissue (ie, tendolipomatosis).3

Systemic factors such as hyperten-sion and hormone replacement ther-apy have been linked to tendinopa-thy in women, while obesity is anetiologic factor in both men andwomen because of diminution in lo-cal microvascularity.21 Perhaps mostimportant in determining the causeof this condition is defining the rolethat biomechanics plays in the disor-der. Specifically, increased foot pro-nation has been proposed to be asso-ciated with Achilles tendinopathyand to result in tendinosis.3 Prona-

tion of the foot generates a resultantinternal rotation of the tibia thattends to draw the Achilles tendonmedially. When the foot remains ex-cessively pronated as the knee ex-tends during the stance phase of gait,there will be a resultant “whipping”action of the Achilles tendon withrepetitive walking or running thatcan lead to microtears in the medialaspect of the tendon, which can pre-cipitate tendinosis.9

In their series of 109 runnerstreated conservatively for Achillestendon overuse injuries, Clement etal9 reported that most affected run-ners presented with a gradual evolu-tion of symptoms, including painand swelling approximately 2 to 3cm proximal to the calcaneal inser-tion. A feature distinguishing tendi-nosis from paratenonitis is the mo-bility of the intratendinous noduleor thickening with the point of max-imal tenderness during active rangeof motion (ie, painful arc sign). Onultrasonography, tendinosis can ap-pear as a hypoechoic lesion with orwithout intratendinous calcification(Figure 7). MRI would also revealtendon abnormalities, such as ten-don thickening on sagittal imagingand altered signal appearance withinthe tendon tissue3 (Figure 8).

As with paratenonitis, and foroveruse injuries of the Achilles ten-don in general, initial nonsurgicaltreatment should be directed towardrelieving symptoms, correcting train-ing errors in athletes, modifying limbmalalignment with orthoses, and im-proving flexibility.3 Physical therapy,concentrating on enhancing dorsi-flexion (ie, eccentric training), is ben-eficial, given that most patients withchronic tendinopathy possess limitedpassive dorsiflexion. To treat the ex-cess pronation often found in pa-tients with Achilles tendinosis, afull-length, flexible or semirigidorthotic device has been found towork well; a shock-absorbing insolemay also be helpful.11 Althoughbrisement can be used in the patientwith chronic paratenonitis, it is not



used for tendinosis. It is also criticalto note that the use of corticosteroidsfor chronic tendinopathy is contrain-dicated because of the risk of causinga frank rupture. When a patient failsto respond adequately to traditionalnonsurgical treatment with NSAIDs,rest, bracing, and physical therapywithin a 3- to 6-month period, atten-tion should be directed toward man-aging the pathology surgically.16

In approximately 25% of cases,nonsurgical therapy is ineffective,and the ineffectiveness has beenfound to be correlated with patientage, duration of symptoms, and se-verity of tendinopathic change.22

Surgical treatment of tendinosisconsists of removing the areas of de-generated tendon. The extent of de-generation and the age of the indi-vidual can have a profound effect onpostoperative outcomes. It has beenrecommended that if more than50% to 75% of the tendon is in-volved, autogenous tendon transfer,such as with the flexor hallucis lon-gus (FHL) or the flexor digitorumlongus (FDL), or even allograft recon-struction should be done.11 Patientsolder than age 50 years with a great-er degree of tendon involvement alsohad less satisfying results with dé-bridement alone. Den Hartog23 re-

ported 88% good to excellent resultswith regard to improved functionand pain in a series of 26 patients(mean age, 51.3 years) when using anFHL transfer for chronic Achillestendinosis.

Achilles Paratenonitis WithTendinosis

Paratenonitis can coexist withtendinosis and is manifested as mac-roscopic tendon thickening, nodu-larity, softening, and yellowing ofthe tendon with fibrillation.4 Prag-matically, Achilles tendinopathy re-garding paratenonitis and tendinosiscan be viewed as a spectrum, as orig-inally classified by Puddu et al:13

stage 1, pure paratenonitis; stage 2,paratenonitis with tendinosis; andstage 3, tendinosis.

Stages 2 and 3 are less likely to re-spond to nonsurgical treatment.10

One of the earliest changes that canbe seen histologically in tendinosiscoexistent with paratenonitis is frag-mentation of collagen fibers withinthe substance of the tendon.3 Typi-cally, it is the chronic form of para-tenonitis that is associated with ten-dinosis.

With the onset of tendinosis, thephysician should have a high indexof suspicion for a partial rupture

within the tendon. A cardinal sign ofthis would be a history of transientsharp pain or repeated episodes ofsharp pain within the tendon whilerunning.8 Similar to the presentationof paratenonitis, in the acute phaseof coexistent tendinitis, swelling andtenderness are usually found in themiddle third of the tendon. As theinjury becomes chronic, exercise-induced pain is the cardinal symp-tom, while crepitus and swelling arediminished. The development of fo-cal, tender nodules heralds the onsetof tendinosis in the setting ofparatenonitis.3

Imaging and treatment must betailored based on the existence ofboth tendinosis and paratenonitis.Imaging, in particular, can help iden-tify those patients who are unlikelyto respond to nonsurgical treatment.The patient with clinical signs oftendinosis with confluent areas of

Figure 8

Sagittal T2-weighted fat-suppressedMRI scan of a 60-year-old man with leftposterior ankle pain demonstratingmucoid degeneration in Achillestendinosis. The image shows markedfusiform enlargement of the Achillestendon critical zone with abnormal, highintrasubstance signal, which is lowerthan the signal intensity of fluid(arrowhead).

Figure 7

Ultrasonographic image of a 52-year-old woman with right posterior heel pain nearthe Achilles tendon insertion, demonstrating intratendinous calcifications. The long-axis grayscale image demonstrates abnormal thickening, hypoechoic appearance,and disruption of the normal fibrillar arrangement of the tendon fibers (arrowhead).There are also at least two echogenic foci with posterior shadowing in the distaltendon from calcification (arrows), a pattern that is commonly seen in tendinosis.



intrasubstance signal changes onMRI is unlikely to respond to non-surgical treatment. Earlier surgicalintervention in these patients maylead to earlier return of function.24

Surgical treatment involves excisionof the diseased paratenon along withdegenerated tendon. Schepsis andcolleagues8,11 reported a 70% satis-faction rate with débridement pro-vided that <50% of the tendon wasinvolved. When 50% of the tendonis involved, then augmentation con-sisting of a turndown flap or tendontransfer should be performed. Simi-lar to Den Hartog,23 Wilcox et al25 re-ported 90% good to excellent resultswhen using an FHL transfer forchronic Achilles tendinopathy.

Retrocalcaneal BursitisUnlike paratenonitis or tendino-

sis, retrocalcaneal bursitis is a dis-tinct entity that is characterized bypain anterior to the Achilles tendonand that involves inflammation ofthe retrocalcaneal bursa. The bursais roughly horseshoe-shaped and is 4mm in width from anterior to poste-rior and 8 mm from medial to later-al. Its anterior surface is composed offibrocartilage; the posterior aspect ofthe bursa merges with the paratenonof the anterior Achilles tendon. Thebursa can become inflamed, hyper-trophied, and adherent to the under-lying Achilles tendon; this can leadto degenerative changes within thetendon. This condition is often asso-ciated with Haglund’s deformity,which causes mechanical irritationof the bursa. Compression of thebursa between the calcaneus and theanterior aspect of the Achilles ten-don occurs when the ankle is dorsi-flexed. Commonly, the athlete whotrains uphill is subject to this condi-tion because of the extreme dorsi-flexion of the ankles.11

Given the location of the bursa,perhaps the best method for detect-ing retrocalcaneal bursitis is thetwo-finger squeeze test, in which thepain response is observed on applica-tion of pressure medially and lateral-

ly anterior to the Achilles tendoninsertion.8 It is important to distin-guish this entity from the conditionknown as “pump bump.” Pumpbump is a generic term that refers toany prominence in the subcutaneousAchilles tendon area. It can be attrib-uted to an inflammation of the sub-cutaneous Achilles tendon bursacaused by an abrasive heel counteror from a bony protrusion.11

Routine radiographs can be help-ful with the use of parallel pitchlines to measure the posterosuperiorcalcaneal tuberosity on a lateral ra-diograph. If changes within theAchilles tendon are present, ultra-sound or MRI may demonstrate apartial Achilles tendon tear, periten-dinous thickening, tendinosis, or os-sification.

NSAIDs and modification oftraining regimens can also be helpfulin the early phase of nonsurgicalcare. Additionally, abnormal exter-nal pressure, such as from a hard ath-letic shoe heel counter, should beavoided. When these measures fail,then a short period of immobiliza-tion in a short leg walking cast mayreduce the acute symptoms. Corti-costeroid injection is contraindicat-ed because it may lead to tendonrupture. Occasionally a patient mayfail to respond to these measures andrequire surgical treatment. Partialcalcaneal ostectomy is a generallysuccessful procedure in this popula-tion and can often restore patients totheir original level of activity with-in 6 months.11 An endoscopic ap-proach has also been used. In a seriesof 28 patients (30 heels), there were29 good or excellent results based onthe American Orthopaedic Foot andAnkle-Hindfoot Scale, with oneAchilles tendon rupture 3 weeks fol-lowing surgery.26

Insertional TendinosisInsertional tendinosis is a true in-

flammatory process within the ten-dinous insertion of the Achilles. It isoften associated with Haglund defor-mity and, in athletes, is commonly

seen in those doing aggressive hillrunning and interval programs.11

Like retrocalcaneal bursitis, inser-tional tendinosis causes posteriorheel pain, thought to be due to bonyimpingement from the calcaneus, lo-cal bursitis, or both. Differentiatingbetween the conditions that causeposterior heel pain can be difficult,and these conditions can be viewedas a spectrum of a single disease pro-cess. However, a diagnosis of inser-tional tendinosis requires that thepatient have tenderness at the bone-tendon interface. There is also limit-ed dorsiflexion. If the tendinosis be-comes chronic, the tendon may alsobecome palpably thickened.27

Radiographs can reveal a promi-nence of the posterior calcaneal tu-berosity, possible calcification, or anintratendinous spur. MRI can beused to rule out abnormalities with-in the tendon and can demonstratehigh signal intensity within the ret-rocalcaneal bursa, which is oftenbest seen on T2-weighted imaging. Itcan also reveal degenerative or in-flammatory changes within the ten-don insertion11 (Figure 9).

Most cases of insertional tendino-sis improve with nonsurgical inter-vention aimed at relieving stress onthe tendon insertion (85% to90%).27 Initial treatment should beguided toward Achilles tendonstretching, with use of a nonarticu-lated solid molded ankle-foot ortho-sis, heel-lift orthoses, and physicaltherapy. Should nonsurgical mea-sures fail, surgical therapy may benecessary. McGarvey et al27 reportedon the use of a central-splitting ap-proach, beginning with a skin inci-sion 2 cm proximal to the Achillesinsertion and extending 6 cm distal-ly. The tendon insertion was thenincised in its midline, and any calcif-ic or degenerate regions were dis-sected free and removed. When ex-cess débridement was required(>50% of the tendon insertion), thenthe plantaris tendon was used toaugment the insertion; only one pa-tient required this in a series of 22



Achilles tendons. Excision of thebursa was also done, followed by aposterosuperior calcaneal ostecto-my. These authors reported an 82%satisfaction rate with this surgery.

Wagner et al28 also evaluatedcomplete detachment and recon-struction of the Achilles tendon at-tachment for insertional bursitis. Ina series of 75 patients treated over 5years for insertional tendinopathy,49 patients underwent débridementand complete detachment, followedby reattachment with suture an-chors and, for severe involvement,proximal V-Y lengthening. The au-thors reported satisfactory results in92% of patients at a mean follow-upof 33 months, with no reruptures.Good to excellent results have alsobeen reported with the use of an FHLtransfer for insertional tendinosis.23

Chronic Rupture

Although chronic rupture is a dis-tinct entity among the variouschronic Achilles disorders discussedhere, the methods of treatment, suchas augmentation and tendon transfer,are pertinent to the treatment of de-generated, nonfunctional tendons.Gross observation of neglected hu-man Achilles tendon ruptures hasnot demonstrated great healing po-tential, a finding similar to that withtendinosis and rupture in the settingof a chronic Achilles tendon disorder.

There is no single rationale for de-termining what is to be considered alate, chronic, or neglected rupture asauthors have modified these termsand used them differently acrossstudy groups. Excluding acute rup-ture, a perusal of the English-languageliterature on the subject reveals min-imum time points used, varying from4 weeks to 2.5 months.29 Chronic rup-tures typically occur 2 to 6 cm abovethe calcaneal insertion in the vascu-lar watershed area, with extensivescar tissue deposition between the re-tracted tendon stumps.30 Porter et al29

documented the presence of a highlyvascularized collagen scar interposed

between the retracted tendon seg-ments at 4 weeks. To the best of ourknowledge, this is the earliest timepoint used that has demonstrated his-tologic evidence of a chronic healingprocess. For that reason, we use 4weeks as the minimum period to con-sider a rupture neglected.

Surgical Techniques

In the neglected rupture, restorationof function is dependent on reestab-lishing appropriate resting length inthe gastrocnemius-soleus complex.A variety of techniques has been de-veloped for use, depending on thesize of the tendon gap following dé-bridement.31 If the defect is smallerthan 3 cm following débridementand is less than 12 weeks old, thenoften direct repair can be per-formed.29 However, if the tendon gapis larger than 3 cm (more common-ly observed), then additional tech-niques must be used; these tech-niques include local tissue transfer,tissue augmentation, synthetic bio-materials, and allograft.30

Local Tissue TransferTo reestablish the functional in-

tegrity of the Achilles tendon, sur-geons have developed a myriad ofoptions for local enhancement ofchronic tendon repair. These tech-niques can provide long, durable ten-don grafts, which may augment thestrength of the gastrocnemius-soleuscontractile unit and supply vascular-ity to the relatively hypoxic frayedtendon ends. Local tissue transfer isparticularly useful to span defectslarger than 3 cm when the remain-ing Achilles tendon tissue is nothealthy.30

Use of the FHL tendon was re-ported on by Wapner et al32 and wasdescribed as having multiple advan-tages over previously recognized ten-don transfers. In reporting on sevenpatients, the authors postulated thatuse of the FHL provided a long andreliable tendon source that wasstronger than the FDL and peroneal

tendons, contracted along an axisvery similar to that of the nativeAchilles, and fired in phase with thegastrocnemius-soleus complex. TheFHL also was closer than the FDL tothe Achilles tendon, and it preservedthe normal muscle balance of thefoot. Wapner’s technique involvedharvesting the FHL through a medi-al arch incision (Figure 10). The ten-don was then introduced into theposteromedial exposure (Figure 11,A) and passed superior to medialthrough a drill hole in the calcaneus(Figure 11, B) before being weavedproximally through the Achilles ten-don (Figure 11, C and D). Using nu-merous outcomes measures, Wapneret al32 reported good or excellent re-sults with this technique in six of

Figure 9

Sagittal T2-weighted MRI scan of a61-year-old woman with rheumatoidarthritis as well as posterior right anklepain and swelling, demonstratingretrocalcaneal bursitis. The imagereveals fluid distention of theretrocalcaneal bursa resulting frombursitis (thin arrow) and reactive edemain the posterior calcaneus with erosionat the Achilles insertion (thick arrow).There is abnormally high signal in thetendon, likely related to mucoiddegeneration (arrowhead).



seven cases. Den Hartog23 used atechnique similar to that describedby Hansen,33 in which the FHL isharvested from the posterior inci-sion, and reported no functional def-icit from loss of strength at the firstinterphalangeal joint.

Mann et al34 used an FDL graftand central slip turndown to recon-struct and span large gaps in theAchilles tendon in seven patients.The FDL was harvested through amedial arch incision, after which thestump was sutured to the FHL ten-don. The FDL was then passed medi-al to lateral through the calcaneusand sewn back on itself under appro-priate tension. The authors postulat-ed that this tendon transfer wouldhelp reestablish the more medialpull of the normal Achilles andwould not create the imbalancethought to exist when a peronealtransfer is used. Although no stan-dardized outcome survey or ques-tionnaire was used, six of seven pa-tients had excellent or good resultsat an average of 39 months. Two pa-tients required additional soft-tissueprocedures for wound complica-tions. All patients retained activeflexion of the lesser toes and had nohammer toe deformities. There wereno reported reruptures in this se-ries.

The peroneus brevis tendon maybe routed lateral to medial through a

drill hole in the calcaneus to bridgethe gap between the ends of a ne-glected rupture. Once rerouted, theproximal part of the peroneus brevisis sutured to the proximal stump ofthe Achilles. The Turco modifica-tion involved routing the tendonthrough the distal stump as opposedto the calcaneus.35 Excellent resultswere reported in four reruptures andfour neglected ruptures.

AugmentationThe concept of Achilles tendon

repair augmentation has expandedover time to include a variety oftechniques and donor tissues. Arner

and Lindholm36 developed a tech-nique of medial and lateral apo-neurotic fascial turndown flaps. Theindications for this method werelater expanded by Inglis and Sculco37

to include chronic ruptures withgaps. These authors used a doubleweave, creating four strands of aug-mentation across the gap. Additionalaugmentation sources include theplantaris, sliding V-Y advancementof the gastrocnemius-soleus complexaponeurosis, and fascia lata.38,39 V-Yadvancement and fascial turndownflaps are particularly useful for gapsof 3 to 5 cm when the remainingAchilles tendon tissue is healthy.10,30

Figure 10

Intraoperative photograph demonstrat-ing the medial arch incision used torelease the flexor hallucis longus ten-don of the patient in Figure 9.

Figure 11

Intraoperative photographs demonstrating the introduction of the flexor hallucislongus (FHL) tendon into the posteromedial exposure (A), preparation of thecalcaneal drill hole for the FHL transfer (B), and weaving of the FHL tendonproximally through the Achilles tendon (C). D, Completion of the FHL weavethrough the Achilles tendon.



Synthetics and AllograftsVarious synthetic materials have

been employed to address chronicruptures, including carbon fiber,composite carbon fiber/absorbablepolymer, polyester tape, and Marlexmesh (Phillips Sumika, The Wood-lands, TX).2,5 Recently, an acellularhuman dermal tissue matrix (Graft-jacket; Wright Medical Technolo-gies, Arlington, TN) was used as anaugmentation material for chronicAchilles ruptures. Lee40 reported ona series of nine patients with chron-ic Achilles ruptures treated with pri-mary repair in conjunction with adermal tissue matrix sewn aroundthe repair. At a mean follow-up of 20months, there was no rerupture, re-current pain, or adverse reaction tothe graft. However, none of the re-pair techniques using synthetic orbiologic materials have found wide-spread use, primarily because of con-cerns regarding the introduction of aforeign body into an area with rela-tively poor healing capacity. Asfunctional tissue engineering tech-niques become more refined andproduce more reliable outcomes,new interest in the use of these ma-terials is anticipated.

Achilles allografts have also beenused to reconstruct large defects (ap-proximately 10 cm) that are not suit-able for a tendon transfer. Results arelimited to case reports, and long-term clinical follow-up is lacking,but successful use of an allograft toreconstruct the Achilles tendon hasbeen demonstrated in these situa-tions.41

Summary

Surgically managing chronic Achil-les tendon pathology, which rangesfrom paratenonitis to the neglectedrupture, is neither simple norstraightforward. Whether a combina-tion of turndown fascial flaps, ten-don transfers, or the use of synthetic/biomaterials in the construction of aneotendon will yield superior long-term results is unknown. The prefer-

ence for any one technique should bebased on evidence-based medicine,review of current techniques, sur-geon comfort, and the likelihood ofa favorable outcome. The long-termfollow up for many of these proce-dures must be studied and reportedby comparative randomized studies.Additionally, a randomized prospec-tive study design to compare the useof two or more techniques for repairof chronic Achilles disorders is re-quired before generalizations con-cerning the efficacy of any specificsurgical treatment can be made.

References

Evidence-based Medicine: Referenc-es 7 and 14 are level II prospectiverandomized studies. References 1, 4,8, 18, 19, 21, and 28 are level III casecontrol studies. The remaining refer-ences include level IV case series (2,5, 6, 12, 20, 23-27, 29, 31-36, and 38-41) and level V expert opinion (3, 9,11, 13, 15-17, 22, and 30).

Citation numbers printed in boldtype indicate references publishedwithin the past 5 years.

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