Diagnosis and Treatment of Chronic Ankle Pain€¦ · The PDF of the article you requested follows this cover page. € This is an enhanced PDF from The Journal of Bone and Joint

The PDF of the article you requested follows this cover page.

This is an enhanced PDF from The Journal of Bone and Joint Surgery

2010;92:2002-2016. J Bone Joint Surg Am.Dane K. Wukich and Dominic A. Tuason

Diagnosis and Treatment of Chronic Ankle Pain

This information is current as of August 20, 2010

Reprints and Permissions

Permissions] link. and click on the [Reprints andjbjs.orgarticle, or locate the article citation on

to use material from thisorder reprints or request permissionClick here to

Publisher Information

www.jbjs.org20 Pickering Street, Needham, MA 02492-3157The Journal of Bone and Joint Surgery

http://www2.ejbjs.org/misc/reprints_perms.dtl

http://www.jbjs.org

http://www.jbjs.org

Selected

Instructional

Course Lectures

The American Academy of Orthopaedic Surgeons

KENNETH A. EGOL

EDITOR, VOL. 60

COMMITTEEKENNETH A. EGOLCHAIR

FREDERICK M. AZARMARY I. O’CONNORMARK PAGNANOPAUL TORNETTA III

EX-OFFICIO

DEMPSEY S. SPRINGFIELDDEPUTY EDITOR OF THE JOURNAL OF BONE AND JOINT SURGERY

FOR INSTRUCTIONAL COURSE LECTURES

Printed with permission of the American Academy ofOrthopaedic Surgeons. This article, as well as other lecturespresented at the Academy’s Annual Meeting, will be availablein February 2011 in Instructional Course Lectures, Volume 60.The complete volume can be ordered online at www.aaos.org,or by calling 800-626-6726 (8 A.M.-5 P.M., Central time).

2001

Diagnosis and Treatment ofChronic Ankle PainBy Dane K. Wukich, MD, and Dominic A. Tuason, MD

An Instructional Course Lecture, American Academy of Orthopaedic Surgeons

Chronic ankle pain is common. Thecauses are numerous, and all ages areaffected. Trauma is not necessary but isoften the initiating event, so an efficientmethod for evaluation is beneficial. Adetailed history, careful physical exam-ination, and judicious selection of theappropriate imaging modalities are allvital to making an accurate diagnosisand providing effective treatment.

Tarsal Tunnel SyndromeThe tarsal tunnel is bordered by thedistal part of the tibia anteriorly and theposterior border of the talus and calca-neus posteriorly. The roof of the tunnelis formed by the flexor retinaculum,which begins 10 cm proximal to themedial malleolus. The contents of thetarsal tunnel include the posterior tibial

artery and vein, the posterior tibialtendon, the flexor hallucis and flexordigitorum longus tendons, and theposterior tibial nerve. The posteriortibial nerve has three terminal branches:the medial plantar, lateral plantar, andmedial calcaneal nerves. The threeterminal nerve branches typically arisein the tarsal tunnel, although variationsmay occur. Recent evidence has identi-fied separate fascial tunnels distal to theflexor retinaculum for the medial plan-tar nerve, the lateral plantar nerve, andthe medial calcaneal nerve1. Tarsaltunnel syndrome is defined as thesymptomatic entrapment of the tibialnerve and/or its branches within theconfines of the tarsal tunnel or distally.Space-occupying lesions such as gan-glion cysts, lipomas, varicose veins,

nerve-sheath tumors, and synovitis canresult in nerve compression. Similarly,a hypertrophic tarsal coalition or a non-union of a sustentaculum tali fracturecan cause compression of the neuralstructures within the tunnel. Pathologichindfoot valgus can produce tension onthe posterior tibial nerve and can causesymptoms of nerve irritation. Intra-operative pressure measurements havedemonstrated that pronation and plan-tar flexion increase the pressures in themedial and lateral plantar tunnels2.Patients usually complain of a burningor tingling sensation along the plantaraspect of the foot or pain radiatingproximally into the distal part of themedial aspect of the leg. Symptoms areusually exacerbated by activity such aswalking or prolonged standing.

The hallmark of the physicalexamination is the reproduction ofparesthesias with percussion over theposterior tibial nerve (i.e., Tinel sign).On physical examination, it is importantto inspect for soft-tissue masses on themedial aspect of the ankle and to makenote of any varicosities as well as thepresence of any hindfoot malalignment.Positioning the ankle and foot in dorsi-

Look for this and other related articles in Instructional Course Lectures,Volume 60, which will be published by the American Academy of Orthopaedic

Surgeons in February 2011:

� ‘‘The ‘Not So Simple’ Ankle Fracture: Avoiding Problems and Pitfalls to

Improve Patient Outcome,’’ by David J. Hak, MD, Kenneth Egol, MD,

Michael Gardner, MD, and Andrew Haskell, MD

Disclosure: The authors did not receive any outside funding or grants in support of their research for or preparation of this work. Neither they nora member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercialentity.

J Bone Joint Surg Am. 2010;92:2002-16

2002

TH E J O U R N A L O F B O N E & JO I N T SU R G E RY d J B J S . O R G

VO LU M E 92-A d NU M B E R 10 d AU G U S T 18, 2010DI AG N O S I S A N D TR E AT M E N T O F CH R O N I C A N K L E PA I N

flexion and eversion may reproducethe symptoms, analogous to the Phalensign in the hands3. Evaluation of thelumbosacral spine is important becauseradiculopathy can present in a similarfashion. The patient should also bequestioned about other causes of neu-ropathy such as diabetes and alcoholism.Electrodiagnostic studies are useful forconfirming the site of nerve compres-sion and can eliminate more proximalnerve compression as a source ofsymptoms. Electrodiagnostic studies areaccurate approximately 80% to 90% ofthe time, and sensory nerve conductionvelocity studies are more likely to beabnormal than motor nerve conductionvelocity studies. The utility of needleelectromyography is uncertain in thediagnosis of tarsal tunnel syndrome4.Magnetic resonance imaging is used toexclude a mass within the tunnel.

If there is a mass within the tarsaltunnel, removal is usually recom-mended, but otherwise the initial treat-ment is rest of the foot and ankle ina removable walking boot. A localinjection of a corticosteroid may be usedbut is associated with a risk of an injuryto the posterior tibial tendon. Physicaltherapy modalities such as ice, heat, andultrasound may be helpful for providingsymptomatic relief. Orthotics shouldbe prescribed for patients with bio-mechanical abnormalities, especially ifhyperpronation is present.

The indications for surgical de-compression include a failure of non-operative treatment as described aboveand objective evidence of nerve com-pression within the tarsal tunnel. Thebest results of surgery are achieved inpatients with positive electrodiagnostictests, a positive Tinel sign, a space-occupying lesion, and paresthesias in thedistribution of the posterior tibial nerve.The results of surgery have been re-ported to be successful in 50% to 90% ofpatients. The use of a tourniquet isoptional; however, if a tourniquet isused, it should be deflated prior toclosure to ensure that a hematoma doesnot form. Some authors have recom-mended distal decompression of themedial and lateral plantar tunnels1.Unsatisfactory outcomes are associated

with postoperative wound complica-tions such as infection, dehiscence,hematoma formation, incomplete re-lease of the tarsal tunnel, and complexregional pain syndrome.

Posterior Tibial Tendon Dysfunction(Adult-Acquired Flatfoot Deformity)Adult-acquired flatfoot deformity be-gins with tenosynovitis or injury to theposterior tibial tendon, eventually re-sulting in tendon elongation and dys-function. Originally, this condition wasknown as posterior tibial dysfunctionbecause tendon failure occurred as a re-sult of tendon degeneration. As theposterior tibial tendon elongates andbecomes dysfunctional, unopposedperoneus brevis contraction results inhindfoot eversion, causing stretching ofthe unsupported medial ankle ligamentsand soft tissues. The spring ligamentfails, the talus plantar flexes, and themedial longitudinal arch collapses. Asthe forefoot abducts at the talonavicularjoint, the Achilles tendon falls lateral tothe midline and contributes further tohindfoot valgus.

A hypovascular zone begins 2 to4 cm proximal to the insertion of theposterior tibial tendon, rendering thisarea susceptible to tenosynovitis and/orinjury, with overuse being a possible

cause. Patients present with posterome-dial ankle pain and swelling over theposterior tibial tendon and have diffi-culty with stair climbing and withwalking on uneven ground. In laterstages, lateral pain predominates be-cause of fibular impingement. Approx-imately 25% of patients have a history ofa previous medial ankle sprain. Onclinical examination, a pes planovalgusdeformity develops as the tendon elon-gates and soft-tissue swelling is oftenobserved along the course of the poste-rior tibial tendon. Observation of thestanding patient from the rear demon-strates the ‘‘too many toes’’ sign (Fig. 1).The patient should be asked to do asingle-leg heel rise. With the contralat-eral foot off the ground, a normalpatient will stand on the tiptoes, and, inthe process, the heel inverts. If the heeldoes not invert or if the patient is unableto raise the heel off the ground, there islikely dysfunction of the posterior tibialtendon.

Weight-bearing anteroposteriorand lateral ankle and foot radiographs aswell as an axial calcaneal radiographshould be made. Particular attentionshould be paid to the presence ofdisruption of the normal talar-firstmetatarsal angle on both the antero-posterior and lateral radiographs. Al-

Fig. 1

Photograph illustrating the ‘‘too many toes’’ sign on the right foot, as is seen with posterior tibial

tendon degeneration or rupture.

2003



though not necessary for diagnosis,magnetic resonance imaging can be auseful adjunct. Axial magnetic resonanceimages have been reported to be 96% ac-curate for identifying tendon pathology.

Johnson and Strom5 describedthree stages of posterior tibial tendondysfunction, and Myerson6 addeda fourth (Table I). Stage I is character-ized by tenosynovitis, no deformity, andpreservation of posterior tibial tendonstrength. Often, patients note a longhistory of flatfoot deformity. Stage II ischaracterized by tendon dysfunctionand weakness in the presence of a cor-rectable deformity. Stage II has beenfurther subdivided on the basis of theamount of abduction that is present atthe midfoot7. Stage-IIa disease is char-acterized by minimal abduction (<30%peritalar subluxation on a standing

anteroposterior foot radiograph),whereas stage-IIb disease is character-ized by uncoverage of >30% of the talarhead. Stage-III deformity is character-ized by a rigid deformity with lateralpain due to fibular impingement. Pas-sive inversion of the triple joint complexis not possible past the neutral position.Stage-IV disease is characterized by ankleinvolvement secondary to deltoid liga-ment incompetence, although the footdeformity may be either flexible or rigid.

Nonoperative treatment consistsof treatment in a boot, cast, or custom-ized brace such as the Arizona brace,supplemented with nonsteroidal anti-inflammatory drugs or oral steroids.Steroid injections are not recommendedbecause of the risk of tendon rupture.Physical therapy modalities, begun oncethe initial inflammation subsides, in-

clude ultrasound, iontophoresis withDecadron (dexamethasone), cryother-apy, strengthening with progressive re-sistance of all muscle groups about thefoot and ankle, and stretching of theAchilles tendon with the subtalar joint ina neutral position. Twenty-two of thirty-two patients with stage-II posteriortibial tendon dysfunction who weremanaged temporarily with a doubleupright ankle-foot orthosis and werefollowed for an average of 8.6 years wereable to avoid surgical intervention8. Fivepatients continued use of the brace, andan additional five patients underwentsurgery. Alvarez et al.9 reported thatforty-two of forty-seven patients withstage-I and II posterior tibial tendondysfunction were effectively managedwith an orthosis and structured exer-cises. A customized brace such as anarticulating ankle-foot orthosis or Ari-zona brace is also effective for providinglong-term symptomatic relief. Cur-rently, it is unknown if these devicesalter the progression of the disease.

Patients should be managed non-operatively for at least three months.Surgical treatment of stage-I adult-acquired flatfoot deformity includestenosynovectomy as well as possibletendon repair or flexor digitorum lon-gus tendon transfer. If tendon transfer isperformed, a medializing calcaneal os-teotomy should be done concomitantlyin patients with a flatfoot deformity.

The surgical treatment of stage-IIadeformity involves a transfer of theflexor digitorum longus to the midfootand a medial displacement osteotomyof the calcaneus. An Achilles tendonlengthening or a Strayer procedure isusually necessary because the patientdevelops an equinus contracture. Ina series of 129 surgically managedpatients, Myerson et al.10 reported that97% had pain relief, 94% had improvedfunction, and 84% were able to wearshoes without shoe modifications ororthotics. A medial column fusion orCotton osteotomy may be performed inorder to address forefoot varus. Inpatients with stage-IIb deformity, a lat-eral column lengthening calcaneal os-teotomy may be necessary to addressforefoot abduction.

TABLE I Four Stages of Adult-Acquired Flatfoot Deformity*

Stage Deformity Surgical Treatment

I No deformity from adult-acquired flatfoot deformity(may have preexisting flatfoot)

Tenosynovectomy, possible tendontransfer, and/or medial slideosteotomy

IIa Mild/moderate flexibledeformity (minimal abductionthrough talonavicular joint,<30% talonavicularuncoverage)

Tendon transfer, medial slideosteotomy, possible Cotton procedure

IIb Severe flexible deformity(abduction deformity throughtalonavicular joint, >30%talonavicular uncoverage)

Tendon transfer, medial slideosteotomy, and possible lateralcolumn lengthening or hindfootfusion (subtalar or talonavicularand calcaneocuboid fusion). Cottonprocedure or metatarsal-tarsal fusionperformed as needed for elevation ofthe first ray

III Fixed deformity (involving thetriple-joint complex)

Hindfoot fusion, most commonlytriple arthrodesis. Correctionrequires fusion of all three joints

IV Foot deformity and ankledeformity (lateral talar tilt)

Complete correction of foot deformity,possible deltoid reconstruction.For severe arthritis, perform anklefusion or total ankle arthroplasty,including correction of foot deformity

IVa Flexible foot deformity Foot deformity corrected as withstage IIb

IVb Fixed foot deformity Foot deformity corrected as withstage III

*Reproduced, with modification, from: Deland JT. Adult-acquired flatfoot deformity. J AmAcad Orthop Surg. 2008;16:400. Reprinted with permission.

2004



The surgical treatment of stage-IIIdeformity involves a triple arthrodesis tocorrect the plantar flexed talus and thesubluxated talonavicular joint. If exces-sive heel valgus remains after triplearthrodesis, a medial slide osteotomyof the calcaneus is recommended. AnAchilles tendon lengthening or a Strayerprocedure is usually necessary. Isolatedsubtalar fusion is not recommended ifa rigid forefoot varus deformity ispresent as correction of the forefootvarus deformity can only be accom-plished by including the transverse tarsaljoints in the fusion. Surgical treatmentfor stage-IV deformity involves deltoidligament repair or reconstruction (withuse of tendon graft) to correct talar tilt.If the deformities in the hindfoot andankle are flexible, then the same pro-cedures utilized for a stage-II deformitycan be combined with deltoid recon-struction. For rigid deformities, triplearthrodesis with reconstruction of thedeltoid ligament is recommended. End-stage posterior tibial tendon dysfunctionwith associated ankle joint arthrosisrequires either a pantalar fusion ora triple arthrodesis and total anklereplacement.

Patients with seronegative ar-thropathy (ankylosing spondylitis, pso-riasis, and Reiter syndrome) are also atincreased risk for developing a flatfootdeformity. These patients present withenthesopathy, or inflammation andmaximum tenderness at the tendoninsertion. Patients with rheumatoidarthritis also can develop planovalgusdeformity secondary to tenosynovitisand destruction of the subtalar andtalonavicular joints. When these pa-tients have persistent tenosynovitis, theyshould undergo early surgical treatmentto prevent tendon rupture.

Flexor Hallucis Longus TendinitisFlexor hallucis longus tendinitis isdifferentiated from posterior ankle im-pingement by the presence of postero-medial pain and soft-tissue swellingalong the posteromedial aspect of theankle. The flexor hallucis longus tendondescends from the leg into the footthrough a sulcus, which is bordered bythe posteromedial and posterolateral

tubercles of the talus. The pain may beaggravated by passive toe motion.Gymnasts, dancers, runners, and tennisplayers are prone to developing thiscondition as a result of activities thatrequire repetitive push-off. On physicalexamination, crepitation over the flexorhallucis longus may be present. TheThomason test demonstrates that, inthe presence of functional hallux rig-idus, the patient has normal motion ofthe metatarsophalangeal joint with theankle in plantar flexion, but with theankle in dorsiflexion, passive dorsi-flexion of the metatarsophalangealjoint is reduced11. In chronic cases,triggering may be present if nodules arepresent within the substance of theflexor hallucis longus. Radiographsmay show a symptomatic os trigonumor fractures. Magnetic resonance im-aging may show fluid within the tendonsheath (Fig. 2).

Nonoperative treatment beginswith rest and modified training. A

removable walking boot should beused as necessary. Ice, cryotherapy,ultrasound, and stretching are donenext, before surgery is considered.Local steroid injections are not rec-ommended for the treatment of flexorhallucis longus tendinitis but may beuseful to exclude posterior ankle im-pingement due to an os trigonum.Surgery, if needed, involves a release ofthe flexor hallucis longus sheaththrough a posteromedial approach.After surgery, the patient is placed ina splint for three weeks, after whichmotion and strengthening exercises arebegun.

Posterior Ankle ImpingementThe posterior process of the talus in-cludes the posteromedial and postero-lateral tubercles. The flexor hallucislongus runs between these tubercles andhas a discrete osseous tunnel. In 10% ofthe population, an unfused posterolat-eral process, or os trigonum, is present12.

Fig. 2

T1-weighted axial magnetic resonance image of the ankle,

illustrating fluid surrounding the flexor hallucis longus

tendon, consistent with flexor hallucis longus tenosyno-

vitis. (Reproduced, with modification, from: Recht MP,

Donley BG. Magnetic resonance imaging of the foot and

ankle. J Am Acad Orthop Surg. 2001;9:190. Reprinted

with permission.)

2005



An enlarged posterolateral tubercle isknown as a Stieda process (Fig. 3). Anyof these structures can cause posteriorankle pain with the ankle in plantarflexion. Most commonly, an acuteplantar flexion injury will damage the ostrigonum or the synchondrosis. Asymptomatic Stieda process or synovitisin the flexor hallucis longus can alsocause these symptoms.

The patient with posterior ankleimpingement who does not have flexorhallucis longus tenosynovitis complainsof posterolateral ankle pain. Activitiesthat require repetitive plantar flexion,such as ballet dancing, downhill run-ning, and soccer, are often associatedwith this impingement. The patient hasposterolateral tenderness and pain onthe forced plantar flexion test. Thepatient frequently sprains the anklebecause the foot is placed in an invertedposition to avoid impingement. Thepatient also complains of pain withmotion of the great toe when flexorhallucis longus tendinitis is present. Inaddition to standard foot radiographs,a neutral weight-bearing lateral foot andankle radiograph and a plantar flexionlateral foot and ankle radiograph arebeneficial. A plantar flexion lateralradiograph may show an acute or oldfracture of the trigonal process, thepresence of an os trigonum, or dynamicimpingement (Fig. 4). Computed to-mography is a useful adjunct to rule outan occult fracture of the posterior pro-cess. A normal bone scan eliminates thetrigonal process as a source of pathology.Magnetic resonance imaging is the studyof choice to assess for bone edema andpossible changes in the soft tissues, suchas the flexor hallucis longus.

Icing, nonsteroidal anti-inflammatory drugs, activity modifica-tion, and strapping of the foot tominimize ankle dorsiflexion are oftensuccessful. Immobilization in a remov-able boot limits plantar flexion to avoidthe foot position that causes pain. Injec-tion with lidocaine and steroid may beutilized posterolaterally for both diag-nostic and therapeutic purposes. Afterfour to six weeks of this therapy, phys-iotherapy with stretching and strength-ening exercises is prescribed.

Fig. 3

T2-weighted sagittal magnetic res-

onance image of the ankle, demon-

strating an os trigonum. (Reprinted,

withpermission, from:BerkowitzMJ,

Kim DH. Process and tubercle frac-

tures of the hindfoot. J Am Acad

Orthop Surg. 2005;13:498.)

Fig. 4

Plantar flexion lateral ankle radiograph demonstrating posterior ankle impingement due to a Stieda

process.

2006



If nonoperative treatment fails,surgical excision of the os trigonumand redundant capsule is recom-mended. For isolated posterior ankleimpingement, a posterolateral approachis used. The patient is placed in the proneposition, the sural nerve is identified andprotected, and a more direct approachto the trigonal process is provided. Thelimiting factor in this approach is thatdissection medial to the flexor hallucislongus is not advisable because ofpotential damage to the neurovascularstructures in the vicinity. For patientswith concomitant flexor hallucis longustenosynovitis and posterior impinge-ment, a posteromedial approach isrecommended.

Arthroscopic techniques havebeen described for the treatment ofposterior impingement. Proceduresthat have been performed have in-

cluded excision of an os trigonum,decompression of a prominent poste-rior talar process, tenolysis of the flexorhallucis longus, removal of loose bod-ies, and debridement of posteriorosteochondritis dissecans lesions. Un-controlled case series have demon-strated earlier return to activities, lessmorbidity, and outcomes that com-pared favorably with open lateralapproaches13.

Achilles Tendinitis andRetrocalcaneal BursitisDisorders of the Achilles tendon andretrocalcaneal bursa are the mostcommon causes of posterior ankle pain.Runners are frequently affected, as arethose who participate in jumpingsports. The Achilles tendon arises fromthe gastrocnemius and soleus musclesand broadly inserts onto the calcaneal

tuberosity. The tendon receives itsvascular supply from proximal muscu-lar branches and distal calcanealbranches. The tendon is protected byan external sheath, the paratenon, andhas an avascular zone approximately2 to 6 cm proximal to its calcanealinsertion due to a watershed zone of itsblood supply. A retrocalcaneal bursa,located anterior to the Achilles tendon,lubricates the anterior aspect of thedistal part of the Achilles tendon.Pathology of the Achilles tendon can bedue to inflammation limited to theparatenon (paratenonitis), intrasub-stance mucoid degeneration and tendonthickening (tendinosis), or insertionalAchilles tendinosis with retrocalcanealbursitis.

Noninsertional Achilles tendonpathology causes pain in the avascularzone (Fig. 5). Predisposing factors for

Fig. 5

Fig. 6

Fig. 5 T2-weighted sagittal magnetic resonance image demonstrating thickening of the Achilles tendon and intrasubstance

degeneration, consistent with chronic tendinosis. (Reprinted, with permission, from: Reddy SS, Pedowitz DI, Parekh SG,

Omar IM, Wapner KL. Surgical treatment for chronic disease and disorders of the Achilles tendon. J Am Acad Orthop Surg.

2009;17:3-14.). Fig. 6 T1-weighted sagittal magnetic resonance image demonstrating insertional Achilles tendinitis and

impingement secondary to a Haglund deformity. (Reprinted, with permission, from: Recht MP, Donley BG. Magnetic

resonance imaging of the foot and ankle. J Am Acad Orthop Surg. 2001;9:191.)

2007



noninsertional Achilles tendinitis in-clude increased age, male sex, excessivehindfoot varus or valgus, and overuse.Patients with insertional Achilles tendi-nosis and retrocalcaneal bursitis presentwith posterosuperior heel pain that isaggravated by shoe wear and activity.Insertional Achilles tendinitis can bea presenting symptom of seronegativearthritis. Swelling, crepitus, and tender-ness are characteristically present inpatients with paratenonitis. Tendernesscan be elicited by squeezing the tendonproximal to its insertion. Fusiformswelling is typical of degenerative ten-dinosis. Patients with insertional Achil-les tendinitis and retrocalcaneal bursitishave tenderness at the calcaneal in-sertion (Fig. 6).

Medial and lateral fullness ofthe retrocalcaneal space is typical ofretrocalcaneal bursitis. In patientswith tendinitis and concomitant bursi-tis, tenderness is present anterior to theAchilles tendon and an enlargement ofthe posterior superior calcaneal process(a Haglund deformity) may be present.Standing anteroposterior and lateral ra-diographs of the foot and ankle should bemade. Haglund deformity, if present, isseen on the lateral radiograph. Ultra-sound has been reported to be sensitiveand specific for confirming noninser-tional Achilles tendinosis14. Magneticresonance imaging is useful for evaluatingboth noninsertional and insertionalAchilles tendinitis as well as paratenonitis.

Nonoperative treatment for non-insertional and insertional Achilles tendi-nitis is nonsteroidal anti-inflammatorydrugs for pain relief, heel lifts, Achillestendon stretching, shoes that do not putpressure on the back of the heel, andactivity modification. Ice, massage, ultra-sound, and iontophoresis can be used.Temporary immobilization in a remov-able boot or night splint or even a short-leg cast can be used if the patient has severepain. Corticosteroid injections are notrecommended because of the risk oftendon rupture. Eccentric calf-musclestrengthening has been recommended asan effective treatment for both insertionaland noninsertional tendinopathy15,16.Prospective randomized studies havedemonstrated that repetitive low-energy

shock-wave therapy was superior toeccentric muscle training for patientswith insertional and noninsertional ten-dinopathy17,18. In one study, kinematicevaluation of runners with noninsertionaltendinopathy demonstrated an increasein eversion of the subtalar joint19. Con-sequently, orthotic devices that controlsubtalar eversion may help this group ofpatients. Another study evaluated theeffectiveness of platelet-rich plasma inpatients with noninsertional tendinop-athy20. This randomized controlled trialevaluated patients who were managedwith eccentric exercises and either salinesolution injections (control) or platelet-rich plasma. The authors found thatplatelet-rich plasma did not result insignificant improvements in terms of painor function compared with the findingsin the group managed with saline solu-tion. Nonoperative treatment of acuteparatenonitis is usually successful, butpatients with chronic symptoms are morelikely to require surgery.

Surgical treatment for Achillestendinitis or paratenonitis is indicatedfor patients in whom symptoms persistdespite supervised nonoperative man-agement for six months.

Tenolysis of the paratenon anddebridement of the degenerative tendonis done for patients with noninsertionaldisease. If >50% of the tendon is in-volved, augmentation with an autoge-nous graft is recommended. Excision ofa Haglund deformity (if present) anddebridement of diseased tendon is donefor patients with insertional disease. If>50% of the tendon insertion is de-brided, augmentation with a flexor hal-lucis longus transfer is recommended.

A compression dressing is appliedafter surgery and is kept on for oneweek, and then the patient is managedwith a cast or a boot for six to eightweeks. The patient should use a heellift for six more weeks and should beginto resume normal activities at threemonths. Maximum medical improve-ment may take six to twelve months,especially in patients with insertionalAchilles tendinitis. Following the surgi-cal treatment of chronic Achilles ten-dinopathy, 86% to 100% of patientshave satisfactory results21-24.

Chronic Lateral InstabilityNine million people sustain anklesprains each year in the United States.Most are due to a plantar flexed in-version injury that leads to compromiseof the anterior talofibular ligament and/or the calcaneofibular ligament. Theseinjuries typically heal uneventfully aftershort-term immobilization, ice, com-pression, and elevation, and early rangeof motion. However, a subset of patientswho sustain an injury of these ligamentsdevelop chronic lateral ankle instabilityand residual symptoms. They have sub-jective complaints of instability withoutradiographic abnormalities but havefunctional instability, complaining ofthe ankle ‘‘giving way.’’ Some havemeasurable hypermobility and objectivefindings of mechanical instability.

Patients complaining of ‘‘givingway’’ typically have a history of a severeankle sprain or recurrent ankle in-version injuries. Pain usually is nota predominant symptom, and, whenpain is present, an associated injuryshould be suspected25-27. Commonlyassociated abnormalities are loosebodies, synovitis, osteochondral in-juries, osteophytes, peroneal tendonpathology, and chondromalacia. Theevaluation should include an examina-tion for malalignment, particularlyhindfoot varus, first-ray plantar flexion,and cavus deformities, which predis-pose to recurrent inversion injuries.Manual anterior drawer and talar tilttests are critical for evaluating theintegrity of the anterior talofibularligament and the calcaneofibular liga-ment, respectively. The involved ankleshould be compared with the contra-lateral ankle to assess for asymmetriclaxity. The involved ankle should also beevaluated for peroneal tendon tender-ness and subluxation.

In addition to standard radio-graphs, stress views can be utilized whenthe clinical examination is equivocal.The anterior drawer stress radiographis the most useful. Radiographic signsof instability include >10 mm of sub-luxation, or 3 mm more than thecontralateral side. On the talar tilt stressradiograph, >10� of varus talar tilt ora side-to-side difference of >3� raises

2008



the possibility of instability. Magneticresonance imaging is not necessary tomake the diagnosis of instability; how-ever, it helps to identify associated intra-articular or periarticular sources ofpain. Strengthening and proprioceptivetraining are the mainstays of physicaltherapy programs and can decreasethe episodes of instability. Bracingand orthotics can be used, especiallyfor patients with varus anklemalalignment.

Operative treatment is reservedfor those who have had a failure ofnonoperative therapy. More than eightyoperative techniques have been de-scribed for the treatment of chroniclateral ankle instability. Anatomic re-pairs that restore normal anatomy andjoint kinematics are preferred. Themodified Brostrom repair, using theextensor retinaculum to reinforcethe ligament repair, has a high patientsatisfaction rate28-30 (Fig. 7). Patientswith generalized ligamentous laxity donot do as well with the modifiedBrostrom technique, and nonanatomicrepair techniques (e.g., the Evans te-nodesis and the Chrisman-Snook pro-cedure) are better for these patients.Nonanatomic repair procedures restorestability but sacrifice normal joint ki-nematics and subtalar motion in theprocess. Anatomic reconstruction pro-cedures utilizing autogenous tissue(such as hamstring tendons) or allo-grafts are also potential treatment op-tions, without altering normal anklekinematics. A split peroneus brevistendon that is anchored distally at itsinsertion; routed through bone tunnelsin the calcaneus, fibula, and talus; andthen sutured back onto itself can also beused for patients with generalized laxity.Case series have indicated that 83% to100% of patients managed with ana-tomic tenodesis report good or excellentoutcomes31.

Peroneal Tendon PathologyThe peroneus longus muscle originatesfrom the lateral condyle of the tibia andthe head of the fibula. The tendontravels behind the lateral malleolusthrough a tunnel known as the retro-malleolar groove. This groove is bor-

dered by the fibula anteriorly and bya fibrous band known as the superiorperoneal retinaculum posterolaterally.The peroneus longus tendon turnsmedially at the cuboid groove andinserts into the lateral part of the plantaraspect of the first metatarsal and themedial cuneiform. The function of theperoneus longus is to evert the foot andplantar flex the ankle, but it also plantarflexes the first ray and thus serves as anantagonist to the tibialis anteriormuscle.

The peroneus brevis originatesfrom the fibula in the middle third of theleg. It is located anterior and medial tothe peroneus longus at the level of theankle and inserts into the tuberosity ofthe fifth metatarsal and functions toevert and plantar flex the foot. Occa-sionally, there is a low-lying brevismuscle belly, which may becomesymptomatic. In most cases, however,the musculotendinous junctions of bothtendons are located proximal to thesuperior peroneal retinaculum. The osperoneum, present in 20% of thepopulation, is an ossified sesamoid

bone, found at the level of the calca-neocuboid joint, that can becomesymptomatic. A peroneus quartusmuscle, found in the lateral compart-ment in about 20% of the population,originates from the brevis muscle bellyand inserts into the peroneal tubercleof the calcaneus. Patients with thismuscle have a higher risk of peronealtubercle hypertrophy and stenosingtenosynovitis.

Patients with peroneal tendonpathology have persistent swelling alongthe peroneal tendon sheath. Retromal-leolar pain or ankle instability is theusual complaint. When the tendons aresubluxating or dislocating, the patientmay have a snapping sensation. Inpatients who have a history of an acuteinjury, tendon rupture should be sus-pected. The alignment of the hindfootshould be evaluated because a varus heelposition is associated with an increasedrate of peroneal tendon disorders.Eversion strength should be tested. Itshould be remembered that the pero-neus tertius, extensor digitorum longus,and extensor hallucis longus also pro-

Fig. 7

Gould modification of the Brostrom procedure for lateral ankle in-

stability, with the inferior extensor retinaculum being used to reinforce

the ligament repair. (Reprinted, with permission, from: Maffulli N, Ferran

NA. Management of acute and chronic ankle instability. J Am Acad

Orthop Surg. 2008;16:612.)

2009



vide some eversion of the foot. Peronealtendon dislocation or subluxation canbe identified by rotating the ankle to seeif the tendons subluxate anterior to thelateral malleolus.

Weight-bearing anteroposteriorand lateral radiographs of the symp-tomatic ankle should be made. Inaddition, an axial heel radiograph willhelp to demonstrate the peroneal tu-bercle and the retromalleolar groove.Computed tomography scans area valuable adjunct for evaluating osseousabnormalities, such as peroneal tuberclehypertrophy, os peroneum fractures, oran avulsion of the lateral malleolus.Magnetic resonance imaging hasemerged as the imaging modality ofchoice for this condition because het-erogeneity or discontinuity of the tendon,a fluid-filled tendon sheath, marrowedema along the lateral calcaneal wall,a hypertrophied peroneal tubercle, theshape of the posterior part of the fibula,and the integrity of the superior peronealretinaculum can all be evaluated.

Nonoperative treatment of pero-neal tendinitis involves nonsteroidalanti-inflammatory medications, rest,and activity modification. Mild cases oftendinitis can be treated with a lateral

heel wedge. In refractory cases, a shortleg cast or CAM walker can be used forsix weeks. If nonoperative treatment isineffective, an open tenosynovectomyand debridement of any region of thetendon that appears to be degenerated isrecommended. The remaining portionof the tendon is subsequently repaired ina tube-like fashion with use of a running4-0 nylon suture (Fig. 8). If the re-maining portion of the tendon is of in-sufficient size or poor quality, a tenodesisof the diseased tendon to the adjacentperoneal tendon (i.e., peroneus brevisto longus tenodesis) should be done.

Peroneal tendon tears or rupturesare treated operatively, unless the patientis not a candidate for operative treat-ment because of medical comorbidities.In such cases, the patient can bemanaged with a lateral heel wedge. Ifpossible, an acute tendon rupture istreated with an end-to-end repair. If thisis not possible, a transfer of the flexordigitorum longus to the peroneus brevisis a viable option. Operative treatmentof peroneal tendon tears is based on theamount of remaining viable tendon.Primary repair and tubularization isindicated for tears involving <50% ofthe tendon, and tenodesis is indicated

for tears involving >50% of the ten-don32. If both tendons are intact, thetorn tissue is debrided and tubularized.If one tendon is torn and irreparable andthe other is functional, a tenodesis can beperformed with use of the myotendinousjunctions of the tendons. If one tendon istorn and irreparable and the other isnonfunctional, flexor digitorum longustransfer as described above should beconsidered. Hindfoot varus, ankle insta-bility, and osteophyte formation, whichcontribute to peroneal tendon tearing,should also be corrected. In one report,residual symptoms were reported to bepresent in >50% of patients and <50% ofpatients returned to sporting activitiesafter operative repair33.

Peroneal tendon subluxation oc-curs following disruption of the superiorperoneal retinaculum. Eckert and Davisdescribed three grades of injuries to thesuperior peroneal retinaculum34. In gradeI, the superior peroneal retinaculum iselevated from the fibula; in grade II,a fibrocartilaginous ridge is elevated fromthe fibula; and in grade III, a corticalfragment is avulsed with the superiorperoneal retinaculum. Nonoperativetreatment can be attempted for acutegrade-I and III injuries with use of

Fig. 8

Illustration depicting a peroneal tendon tear and repair. (Reprinted, with permission, from: Philbin TM, Landis GS, Smith B. Peroneal tendon

injuries. J Am Acad Orthop Surg. 2009;17:310.)

2010



a short-leg cast for six weeks. If thistreatment fails, the superior peronealretinaculum is reattached surgically afterthe creation of an osseous trough alongthe posterolateral aspect of the fibula. Forpatients with chronic peroneal subluxa-tion, a fibular groove-deepening pro-cedure is indicated. This procedureinvolves raising an osseous flap from theposterolateral corner of the fibula andusing a burr to remove the cancellousbone beneath the flap. The flap is thenreduced and is tamped into place. Thesuperior peroneal retinaculum is thenrepaired over the tendons, which arelocated in the newly-deepened groove. Ina similar fashion, a bone block procedurecan be performed, with a sagittal cut ofthe fibula, translating the more lateralportion posteriorly, and holding thedisplaced fibula with screws35.

Occult Fractures of the HindfootProcess and tubercle fractures of thehindfoot can be difficult to diagnose andtreat. These injuries are often misdiag-nosed as a sprain of the ankle or foot,leading to a delay in diagnosis andsuboptimal outcomes36. Prompt diag-nosis requires a high index of suspicionand a thorough knowledge of the anat-omy of the hindfoot. Specialized radio-graphs as well as computed tomographyand magnetic resonance imaging may beneeded to confirm the diagnosis. Frac-tures of the anterior process of thecalcaneus occur with inversion of theplantar flexed ankle and are the result ofan avulsion injury of the bifurcate liga-ment. Tenderness is usually reproducedin an area 2 cm anterior and 1 cm inferiorto the anterior talofibular ligament.This fracture is typically not visualizedon standard anteroposterior radiographsof the foot and ankle. An obliqueradiograph of the foot with the x-raybeam directed 10� to 25� superior andposterior to the midfoot is necessary. Thisprojects the anterior process away fromthe talar neck and enables optimalvisualization of the fracture. As anadjunct, multiplanar computed tomog-raphy imaging with fine 1-mm cuts canbe done to provide a more accuratedelineation of displacement and fragmentsize, which influence treatment decisions.

For fracture fragments that are<1 cm in size and are displaced by<2 mm, a below-the-knee, non-weight-bearing cast can be applied for a pe-riod of six weeks, followed by transitionto a removable walking boot andprogressive weight-bearing. Open re-duction and internal fixation is recom-mended for fractures that are >1 cm insize and are displaced by >2 mm withintra-articular involvement37.

Lateral talar process fractures typ-ically occur after a fall or motor-vehicleaccident, but they also occur in associa-tion with snowboarding injuries. Ap-proximately 2000 lateral talar processfractures occur annually in these ath-letes38. The lateral talar process is avulsedby the lateral talocalcaneal ligamentwith an inversion injury. Another mech-anism is an eversion moment that isapplied to a dorsiflexed, axially-loadedfoot, causing compression and frac-ture of the lateral talar process. Carefulpalpation just anterior and inferior to thelateral malleolus can elicit pain, whichshould raise suspicion for this injury.Lateral talar process fractures usually canbe visualized on routine radiographs,although subtle fragments just distal tothe lateral malleolus may be difficult to

appreciate (Fig. 9). The amount ofdisplacement and the extent of articularinvolvement of the posterior facet ofthe subtalar joint are seen on a thin-cutcomputed tomography scan39.

Fracture fragments that are <1 cmin size and are displaced by <2 mm aretreated nonoperatively. Displaced frac-tures are best treated with open reductionand internal fixation or primary excision,with excision favored in scenarios inwhich the fracture is comminuted. If openreduction and internal fixation is feasible,fixation is typically done with mini-fragment screws or Kirschner wires38.

Sinus Tarsi SyndromeSinus tarsi syndrome is associated withpersistent lateral ankle pain directlyover the sinus tarsi. It is usuallya result of an inversion injury, and thepatient may complain of a feeling ofinstability. Several theories have beenadvocated to explain the source of pain,including interosseous ligament injury;hypertrophy of the synovium; orhypertrophy of the fat, resulting inimpingement of the neural plexus. Thediagnosis is one of exclusion and isconfirmed on the basis of pain reliefafter an injection of local anesthetic

Fig. 9

Anteroposterior ankle radiograph demonstrating a fracture of

the lateral talar process. (Reprinted, with permission, from:

Berkowitz MJ, Kim DH. Process and tubercle fractures of the

hindfoot. J Am Acad Orthop Surg. 2005;13:496.)

2011



into the sinus tarsi. Radiographs dem-onstrate normal findings and serve toeliminate other causes of pain, such asoccult fractures or subtalar arthritis.Magnetic resonance imaging maydemonstrate nonspecific inflammationin the sinus tarsi, sinus tarsi fat alter-ations, chronic synovitis and synovialthickening, interosseous talocalcanealligament tears, cervical ligament tears, ora ganglion cyst40. Nonoperative treatmentis similar to that for chronic lateralankle instability. Injections, diagnosticand therapeutic, have been reportedto be successful in approximately two-thirds of patients. Open and arthro-scopic debridement of the contents ofthe sinus tarsi have been described41.

Osteochondral Lesions of theTalar DomeOsteochondral lesions involving the talardome were originally thought to besecondary to ischemia; however, mostauthors currently think that they are dueto trauma. Various names have beenused to describe osteochondral lesionsinvolving the talar dome, includingosteochondritis dissecans, transchondralfracture, and osteochondral fracture. Thetalus has a decreased capacity for repairbecause of its limited blood supply, andthe sequelae of osteochondral talar injuryinclude joint degeneration and limitedrange of motion at the ankle.

Osteochondral lesions of the talusare frequently associated with moreobvious traumatic injuries of the foot andankle. Diagnosis of talar dome injury isoften delayed. In some series, as many as28% of osteochondral injuries of thetalus were associated with other fracturesinvolving the foot and ankle, mostfrequently the malleoli. Osteochondrallesions of the talus can occur as the resultof a single traumatic episode or as theresult of repetitive microtrauma, such asrecurrent lateral ankle sprains.

Several schemes exist for theclassification of osteochondral lesionsof the talus on the basis of radiographs,computed tomography, magnetic reso-nance imaging, and arthroscopic find-ings42-44 (Table II). In patients withchronic ankle pain and a history ofinjury, clinical suspicion for an osteo-

chondral lesion should be high. Radio-graphic evaluation is the initial imagingmodality of choice; however, false-negative radiographs are not uncommon.Any osteochondral lesions that areidentified with use of standard radio-graphs should be further evaluated withuse of computed tomography, whichprovides a more complete delineation ofthe integrity of the subchondral bone.Magnetic resonance imaging is a usefuladjunct for patients without any radio-graphic abnormality (Fig. 10). Thesuperiority of magnetic resonance im-aging for visualizing the surface of thearticular cartilage and edema of the talusmakes it the study of choice for theevaluation of suspected stage-I osteo-chondral lesions. The treatment ofosteochondral lesions of the talus isbased on the stage of the lesion. Castimmobilization for twelve to sixteenweeks with progressive weight-bearingto full weight-bearing at the end ofimmobilization is recommended forstage-I or II lesions. Patients witha stage-I or II lesion that remains painfulfor one year and those with a stage-III orIV lesion are candidates for surgery.Surgery can involve debridement andlavage, marrow-stimulating procedures,or restorative techniques. Arthroscopicdebridement of the lesion and tech-

niques that induce healing by stimula-tion of underlying marrow aresuccessful in approximately 80% ofpatients43. Lesions measuring >1.5 cm2

do not respond well to these techniques.Restoration of the articular surfacewith osteochondral autografts hasbeen successful for the treatmentof lesions measuring <1 cm2 (Fig. 11)45.The major disadvantage of using anautograft is donor-site morbidity.Osteochondral allografts have beenutilized for larger lesions; however, thelong-term outcomes remain uncertain.Autologous chondrocyte implantation isa promising technique and has been usedfor patients who remain symptomaticafter previous surgery46. The location ofthe lesion dictates the appropriate surgi-cal approach and may require the useof osteotomies in order to optimizevisualization. Indications for performingthese procedures include a lesion witha diameter of >1 cm and a depth of atleast 5 mm that cannot be repairedprimarily. Autologous chondrocyte im-plantation into the talus has demon-strated some encouraging results inpreliminary studies46.

Anterior Ankle ImpingementAnterior ankle impingement can be dueto soft-tissue or osseous lesions and

TABLE II Classifications of Osteochondral Lesions of the Talus

Radiographic classification (Berndt and Harty42)

Stage I: small area of compression of the subchondral bone

Stage II: osteochondral fracture that is partially detached

Stage III: complete detachment from the underlying bed without displacement

Stage IV: complete detachment with displacement resulting in a loose body

Computed tomography classification (Ferkel and Hommen43)

Stage I: cystic lesion within talar dome with intact roof on all views

Stage II-A: cystic lesion with communication to talar dome surface

Stage II-B: open articular surface lesion with overlying nondisplaced fragment

Stage III: nondisplaced lesion with lucency

Stage IV: displaced fragment

Magnetic resonance imaging classification (Anderson et al.44)

Stage I: subchondral compression with marrow edema; normal radiographs and positiveuptake on bone scintigraphy

Stage II-A: subchondral cyst

Stage II-B: incomplete fragment separation

Stage III: unattached, nondisplaced fragment with synovial fluid around the fragment

Stage IV: displaced fragment

2012



typically is related to the superior portionof the anterior talofibular ligament orthe distal portion of the anteroinferiortibiofibular ligament47. Redundant in-jured synovial or ligamentous tissuecauses joint irritation. Repetitive exag-gerated ankle dorsiflexion can lead tosoft-tissue impingement, and soccer andbasketball players are particularly proneto developing anterior tibiotalar bonespurs, which result in osseous impinge-ment. Patients complain of anterior pain,stiffness, and swelling. Walking uphill ispainful, whereas downhill walking ismore comfortable. The hallmark of thephysical examination is painful limita-tion of passive dorsiflexion and anteriorankle tenderness. The osseous bone spursare seen on a lateral ankle radiograph,whereas magnetic resonance imaging isuseful for seeing the soft-tissue lesions(Fig. 12). Nonoperative treatment in-cludes rest, ice, anti-inflammatorymedications, and physiotherapy. Anintra-articular injection of a local anes-thetic and steroid can be diagnostic andtherapeutic. Patients often experiencesymptomatic relief with a small heel lift.Patients who fail to respond to conser-vative treatment benefit from arthro-scopic debridement of soft-tissue lesions.Osseous lesions can be treated with

arthroscopic or open methods, depend-ing on the size and location of the lesionas well as the skill of the surgeon48.

Nerve Entrapment at the Levelof the AnkleThe deep peroneal nerve and the anteriortibial artery are deep to the extensor

hallucis longus and the extensor digito-rum brevis. Approximately 1 cm proxi-mal to the ankle joint, the nervebranches into a medial motor branchand a lateral sensory branch. The nervecan be compressed by the superiorextensor retinaculum, the inferior ex-tensor retinaculum, and the extensorhallucis brevis muscle49. Proximal com-pression by the superior retinaculumcauses sensory changes and clawing ofthe toes. Distal compression by theinferior retinaculum or the extensorhallucis brevis muscle causes isolatedsensory deficits.

Patients complain of burninganterior ankle and dorsal foot pain andmay have a history of trauma orrecurrent ankle sprains. Paresthesias inthe first dorsal web space may bepresent. An injection of local anesthetic1 cm proximal to the site of nervecompression should improve or allevi-ate symptoms. The site of nerve com-pression is determined by the presenceof a positive Tinel sign, which re-produces the symptoms and distalparesthesias in the distribution of thenerve. If the injection does not relievethe symptoms, nerve compression isunlikely. Radiographs may demonstrateosteophytes as the source of entrap-

Fig. 10

T1-weighted coronal magnetic resonance image of the ankle,

demonstrating an osteochondral lesion of the medial part of

the talus. (Reprinted, with permission, from: Schachter AK,

Chen AL, Reddy PD, Tejwani NC. Osteochondral lesions of the

talus. J Am Acad Orthop Surg. 2005;13:154.)

Fig. 11

Autologous osteochondral transplant for the treatment of an osteochondral

lesion of the talus. (Reprinted, with permission, from: Schachter AK, Chen AL,

Reddy PD, Tejwani NC. Osteochondral lesions of the talus. J Am Acad Orthop

Surg. 2005;13:156.)

2013



ment, and space-occupying lesionssuch as ganglion cysts can be seen beston magnetic resonance imaging. Elec-trodiagnostic testing can determine thelocation of the lesion, including com-pression more proximally in the leg orin the lumbar spine.

The superficial peroneal nerveis a pure sensory nerve that becomessuperficial in the distal third of the leg,approximately 10 cm proximal to the tipof the fibula. It then continues in thesubcutaneous layer and branches intothe medial dorsal cutaneous nerve andthe intermediate dorsal cutaneousnerve, 6 to 7 cm proximal to themalleolus. Entrapment typically occurswhere the nerve becomes subcutaneous,and symptoms rarely radiate proximalto the site of nerve compression. Nerveinjury or entrapment can occur inpatients with inversion injury as thenerve gets tethered where its exits thefascia50. Iatrogenic entrapment can oc-cur after open reduction and internalfixation of fibular fractures and place-ment of lateral ankle arthroscopic por-tals51,52. Occasionally, space-occupyingmasses such as ganglion cysts or fracturecallus will entrap the nerve. Patientspresent with pain radiating across theankle and the dorsum of the foot.

Tenderness or a Tinel sign is typicallypresent 10 cm proximal to the tip of thedistal part of the fibula. Pain is repro-duced with several provocative maneu-vers, such as foot plantar flexion andinversion, which places the nerve undercompression and tightens the fascia.When the foot is dorsiflexed andeverted, the nerve is under tension andbecomes more sensitive to percussion.The motor and reflex examinationreveals normal findings. Ankle stabilityshould be assessed, as instability canplace intermittent tension on thesuperficial peroneal nerve. Proximalcauses of nerve irritation, includingcompression at the fibular neck andlumbar pathology, must be considered.The differential diagnosis should alsoinclude exertional compartment syn-drome, especially if the patient de-scribes exacerbation of symptomswith activity. A diagnostic injectionof local anesthetic just proximal to thesite of entrapment helps to confirmthe diagnosis.

The lateral sural nerve originatesfrom the common peroneal branchof the sciatic nerve. It innervates thelateral part of the proximal third ofthe leg. The medial sural nerve origi-nates from the posterior tibial branch

of the sciatic nerve and is subfascial.It innervates the posterolateral partof the proximal half of the calf. Thesetwo branches meet in the lower third ofthe calf to form the common suralnerve, which runs along the lateralborder of the Achilles tendon, next tothe short saphenous vein. It thentravels subcutaneously, inferior to theperoneal tendon sheath at the ankle,toward the fifth metatarsal tuberosity,and provides sensation to the lateralaspect of the fifth toe and the fourthweb space. Entrapment can occur afterclosed and operative treatment offractures, which cause subsequentscarring in the region of the fifthmetatarsal or ankle. Space-occupyinglesions can also lead to compressionof the nerve.

Patients present with paresthesiasin the cutaneous distribution of thesural nerve and have a history of traumaor recurrent ankle sprains. Examinationof the entire course of the nerve isnecessary, and local tenderness withpercussion can identify any areas ofimpingement. More proximal causes ofnerve irritation should be considered.Specifically, S1 nerve-root irritation cancause paresthesias in the lateral aspectof the foot. However, if the S1 nerve

Fig. 12

Lateral radiograph of the ankle, demonstrating anterior osseous ankle impingement.

2014



root is involved, gastrocnemius-soleusweakness and abnormal ankle reflex aretypical accompanying findings. In pa-tients with isolated sural nerve entrap-ment, neither of these findings shouldbe seen.

Entrapment of the saphenousnerve over the medial aspect of theanterior part of the ankle is anothersource of chronic pain. Patients com-plain of numbness along the medialborder of the foot and pain exacerbatedby tight-fitting shoes, particularly withankle straps. Iatrogenic injury can occurduring placement of a medial arthro-scopic portal or during open reductionand internal fixation of a medial mal-leolar fracture.

Radiographs reveal normal find-ings. Magnetic resonance imaging isuseful for identifying a space-occupyinglesion. Electromyography and nerveconduction velocity studies help toassess for a more proximal cause ofnerve compression.

Nonoperative treatment of allnerve entrapments involves the avoid-ance of tight-fitting shoes, the adminis-tration of anti-inflammatory medications,and physical therapy modalities tohelp to modulate the pain. Supportiveankle bracing and a lateral heel wedgehelp to prevent inversion of the ankle.Occasionally, medications such as ga-bapentin or tricyclic antidepressantshelp to alleviate symptoms.

Surgery, consisting of neurolysis,removal of osteophytes, and excisionof any soft-tissue masses, is consideredif nonoperative treatment fails. Thedecompression should start proximallyat a point where the normal anatomyof the nerve can be visualized. Therelease should be carried out distal tothe site of the positive Tinel sign.Meticulous hemostasis should beachieved prior to closure to preventhematoma formation and additionalnerve entrapment. In recurrentcases, excision of the nerve and bury-ing of the stump can help. Thesaphenous, lateral sural, medial sural,and superficial peroneal nerves do notprovide sensation to the plantar aspectof the foot and can be sacrificed ifnecessary.

Complex Regional Pain SyndromeA full discourse on the diagnosis andtreatment of complex regional painsyndrome is beyond the scope of thisinstructional course lecture. This di-agnosis should be considered forpatients with chronic ankle pain that isnot consistent with the conditionsdescribed. Type-I complex regionalpain syndrome develops after a nox-ious stimulating event such as a crushinjury, fracture, or sprain. The symp-toms typically do not follow thedistribution of a single, specific nerve.Type-II complex regional pain syn-drome develops after injury toa specific nerve, such as laceration.Complex regional pain syndrome ismore common in females and patientswho smoke, and it has been reportedto occur in 1% of fractures and up to5% of patients with peripheral nerveinjuries. The stages of complex re-gional pain syndrome include an acutephase (zero to three months), a dys-trophic phase (three to six months),and an atrophic stage. Early recogni-tion and treatment are paramount inorder to achieve successful treatment.Burning pain, cold intolerance, tem-perature changes, swelling, allodynia(pain from a stimulus that does notnormally cause pain), and dysesthesias(unpleasant abnormal sensations) arecommon. Characteristic physicalfindings include discoloration of theskin (redness, cyanosis, mottling),altered skin temperature (hot or cold),edema, decreased range of motion,atrophy (late), abnormal sweatingpatterns, loss of hair, and abnormalnail growth. The kick-off sign hasrecently been described53. Thirty-ninepatients with complex regional painsyndrome, while sitting on the exam-ination table, held the affected ex-tremity with the knee extended againstgravity. When the leg was pushed backto a relaxed and suspended position,the thirty-nine patients eventually in-voluntarily resumed the extended po-sition. This position in which thepatients held the legs was termed the‘‘kick-off ’’ position sign. Synovialthickening and equinovarus contrac-tures characterize the late stage of

complex regional pain syndrome.Osteopenia secondary to disuse andincreased blood flow is a commonradiographic finding. Diffuse uptakeon the delayed images of a technetiumbone scan is characteristically seen,with a specificity of 75% to 98% for thediagnosis of complex regional pain syn-drome54. A referral to a comprehensivepain-management team that uses acombination of medication and physicaltherapy is recommended. Recalcitrantcases may benefit from sympatheticblockade and spinal cord stimulation. Inpatients with complex regional painsyndrome who require surgery, pre-operative consultation with a pain ser-vice is recommended. These patientsmay benefit from regional anesthesiawith indwelling catheters to minimizepostoperative pain.

SummaryChronic ankle pain is a common pre-senting complaint in orthopaedic sur-gery. A careful history and physicalexamination are paramount in orderto arrive at the correct diagnosis.Ancillary imaging testing may helpconfirm the diagnosis. The clinicianshould recognize that both intra-articular and extra-articular pain gener-ators can be responsible for the sub-jective complaints.

Dane K. Wukich, MDDominic A. Tuason, MDUPMC Comprehensive Foot and Ankle Center,University of Pittsburgh School of Medicine,2100 Jane Street Suite 7300,Pittsburgh,PA 15203.E-mail address for D.K. Wukich:[email protected] address for D.A.Tuason: [email protected]

Printed with permission of the AmericanAcademy of Orthopaedic Surgeons. Thisarticle, as well as other lectures presented atthe Academy’s Annual Meeting, will beavailable in February 2011 in InstructionalCourse Lectures, Volume 60. The completevolume can be ordered online atwww.aaos.org, or by calling 800-626-6726(8 A.M.-5 P.M., Central time).

2015



References

1. Dellon AL. The four medial ankle tunnels: a criti-cal review of perceptions of tarsal tunnel syndromeand neuropathy. Neurosurg Clin N Am. 2008;19:629-48, vii.

2. Rosson GD, Larson AR, Williams EH, Dellon AL.Tibial nerve decompression in patients withtarsal tunnel syndrome: pressures in the tarsal,medial plantar, and lateral plantar tunnels.Plast Reconstr Surg. 2009;124:1202-10.

3. Kinoshita M, Okuda R, Morikawa J, Jotoku T, AbeM. The dorsiflexion-eversion test for diagnosis oftarsal tunnel syndrome. J Bone Joint Surg Am.2001;83:1835-9.

4. Patel AT, Gaines K, Malamut R, Park TA, Toro DR,Holland N; American Association of Neuromuscularand Electrodiagnostic Medicine. Usefulness of elec-trodiagnostic techniques in the evaluation of sus-pected tarsal tunnel syndrome: an evidence-basedreview. Muscle Nerve. 2005;32:236-40.

5. Johnson KA, Strom DE. Tibialis posterior tendondysfunction. Clin Orthop Relat Res. 1989;239:196-206.

6. Myerson MS. Adult acquired flatfoot deformity:treatment of dysfunction of the posterior tibial tendon.Instr Course Lect. 1997;46:393-405.

7. Deland JT. Adult-acquired flatfoot deformity. J AmAcad Orthop Surg. 2008;16:399-406.

8. Lin JL, Balbas J, Richardson EG. Results of non-surgical treatment of stage II posterior tibial tendondysfunction: a 7- to 10-year followup. Foot Ankle Int.2008;29:781-6.

9. Alvarez RG, Marini A, Schmitt C, Saltzman CL.Stage I and II posterior tibial tendon dysfunctiontreated by a structured nonoperative managementprotocol: an orthosis and exercise program. FootAnkle Int. 2006;27:2-8.

10. Myerson MS, Badekas A, Schon LC. Treat-ment of stage II posterior tibial tendon deficiencywith flexor digitorum longus tendon transfer andcalcaneal osteotomy. Foot Ankle Int. 2004;25:445-50.

11. Hamilton WG, Geppert MJ, Thompson FM. Painin the posterior aspect of the ankle in dancers. Dif-ferential diagnosis and operative treatment. J BoneJoint Surg Am. 1996;78:1491-500.

12. Chao W. Os trigonum. Foot Ankle Clin. 2004;9:787-96, vii.

13. Scholten PE, Sierevelt IN, van Dijk CN. Hindfootendoscopy for posterior ankle impingement. J BoneJoint Surg Am. 2008;90:2665-72.

14. Mitchell AW, Lee JC, Healy JC. The use ofultrasound in the assessment and treatment ofAchilles tendinosis. J Bone Joint Surg Br.2009;91:1405-9.

15. Fahlstrom M, Jonsson P, Lorentzon R, AlfredsonH. Chronic Achilles tendon pain treated with eccentriccalf-muscle training. Knee Surg Sports TraumatolArthrosc. 2003;11:327-33.

16. Ohberg L, Lorentzon R, Alfredson H. Eccentrictraining in patients with chronic Achilles tendinosis:normalised tendon structure and decreased thick-ness at follow up. Br J Sports Med. 2004;38:8-11.

17. Rompe JD, Furia J, Maffulli N. Eccentric loadingcompared with shock wave treatment for chronicinsertional Achilles tendinopathy. A randomized,controlled trial. J Bone Joint Surg Am. 2008;90:52-61.

18. Rompe JD, Furia J, Maffulli N. Eccentric loadingversus eccentric loading plus shock-wave treat-ment for midportion Achilles tendinopathy: a ran-domized controlled trial. Am J Sports Med. 2009;37:463-70.

19. Ryan M, Grau S, Krauss I, Maiwald C, Taunton J,Horstmann T. Kinematic analysis of runners withAchilles mid-portion tendinopathy. Foot Ankle Int.2009;30:1190-5.

20. de Vos RJ, Weir A, van Schie HT, Bierma-ZeinstraSM, Verhaar JA, Weinans H, Tol JL. Platelet-richplasma injection for chronic Achilles tendinopathy:a randomized controlled trial. JAMA. 2010;303:144-9.

21. Den Hartog BD. Flexor hallucis longus transfer forchronic Achilles tendonosis. Foot Ankle Int.2003;24:233-7.

22. Martin RL, Manning CM, Carcia CR, Conti SF. Anoutcome study of chronic Achilles tendinosis afterexcision of the Achilles tendon and flexor hallucislongus tendon transfer. Foot Ankle Int. 2005;26:691-7.

23. Will RE, Galey SM. Outcome of single incisionflexor hallucis longus transfer for chronic Achillestendinopathy. Foot Ankle Int. 2009;30:315-7.

24. Saxena A. Results of chronic Achilles tendinop-athy surgery on elite and nonelite track athletes. FootAnkle Int. 2003;24:712-20.

25. DiGiovanni BF, Fraga CJ, Cohen BE, Shereff MJ.Associated injuries found in chronic lateral ankleinstability. Foot Ankle Int. 2000;21:809-15.

26. Komenda GA, Ferkel RD. Arthroscopic findingsassociated with the unstable ankle. Foot Ankle Int.1999;20:708-13.

27. Sugimoto K, Takakura Y, Okahashi K, Samoto N,Kawate K, Iwai M. Chondral injuries of the ankle withrecurrent lateral instability: an arthroscopic study.J Bone Joint Surg Am. 2009;91:99-106.

28. Krips R, Brandsson S, Swensson C, van Dijk CN,Karlsson J. Anatomical reconstruction and Evanstenodesis of the lateral ligaments of the ankle.Clinical and radiological findings after follow-up for15 to 30 years. J Bone Joint Surg Br. 2002;84:232-6.

29. Li X, Killie H, Guerrero P, Busconi BD. Anatomicalreconstruction for chronic lateral ankle instability inthe high-demand athlete: functional outcomes afterthe modified Brostrom repair using suture anchors.Am J Sports Med. 2009;37:488-94.

30. Messer TM, Cummins CA, Ahn J, Kelikian AS.Outcome of the modified Brostrom procedure forchronic lateral ankle instability using suture anchors.Foot Ankle Int. 2000;21:996-1003.

31. DiGiovanni CW, Brodsky A. Current concepts:lateral ankle instability. Foot Ankle Int. 2006;27:854-66.

32. Heckman DS, Reddy S, Pedowitz D, Wapner KL,Parekh SG. Operative treatment for peronealtendon disorders. J Bone Joint Surg Am. 2008;90:404-18.

33. Steel MW, DeOrio JK. Peroneal tendon tears:return to sports after operative treatment. Foot AnkleInt. 2007;28:49-54.

34. Eckert WR, Davis EA Jr. Acute rupture of theperoneal retinaculum. J Bone Joint Surg Am. 1976;58:670-2.

35. Selmani E, Gjata V, Gjika E. Current conceptsreview: peroneal tendon disorders. Foot Ankle Int.2006;27:221-8.

36. Chan GM, Yoshida D. Fracture of the lateralprocess of the talus associated with snowboarding.Ann Emerg Med. 2003;41:854-8.

37. Sanders RW, Clare MP. Fractures of the calca-neus. In: Coughlin MJ, Mann RA, Saltzman CL, editors.Surgery of the foot and ankle. 8th ed, vol 2.Philadelphia: Elsevier; 2007. p 2058-60.

38. von Knoch F, Reckord U, von Knoch M, Sommer C.Fracture of the lateral process of the talus in snow-boarders. J Bone Joint Surg Br. 2007;89:772-7.

39. Bonvin F, Montet X, Copercini M, Martinoli C,Bianchi S. Imaging of fractures of the lateral processof the talus, a frequently missed diagnosis. Eur JRadiol. 2003;47:64-70.

40. Lee KB, Bai LB, Park JG, Song EK, Lee JJ. Efficacyof MRI versus arthroscopy for evaluation of sinus tarsisyndrome. Foot Ankle Int. 2008;29:1111-6.

41. Frey C, Feder KS, DiGiovanni C. Arthroscopicevaluation of the subtalar joint: does sinus tarsisyndrome exist? Foot Ankle Int. 1999;20:185-91.

42. Berndt AL, Harty M. Transchondral fractures(osteochondritis dissecans) of the talus. J Bone JointSurg Am. 1959;41:988-1020.

43. Ferkel RD, Hommen JP. Arthroscopy of the ankleand foot. In: Coughlin MJ, Mann RA, Saltzman CL,editors. Surgery of the foot and ankle. 8th ed, vol 2.Philadelphia: Elsevier; 2007. p 1641-1726.

44. Anderson IF, Crichton KJ, Grattan-Smith T,Cooper RA, Brazier D. Osteochondral fractures of thedome of the talus. J Bone Joint Surg Am. 1989;71:1143-52.

45. Valderrabano V, Leumann A, Rasch H, Egelhof T,Hintermann B, Pagenstert G. Knee-to-ankle mosaic-plasty for the treatment of osteochondral lesions ofthe ankle joint. Am J Sports Med. 2009;37 Suppl1:105S-11S.

46. Whittaker JP, Smith G, Makwana N, Roberts S,Harrison PE, Laing P, Richardson JB. Early results ofautologous chondrocyte implantation in the talus.J Bone Joint Surg Br. 2005;87:179-83.

47. Stetson WB, Ferkel RD. Ankle arthroscopy: II.Indications and results. J Am Acad Orthop Surg.1996;4:24-34.

48. Urguden M, Soyuncu Y, Ozdemir H, Sekban H,Akyildiz FF, Aydin AT. Arthroscopic treatment ofanterolateral soft tissue impingement of the ankle:evaluation of factors affecting outcome. Arthroscopy.2005;21:317-22.

49. Liu Z, Zhou J, Zhao L. Anterior tarsal tunnelsyndrome. J Bone Joint Surg Br. 1991;73:470-3.

50. O’Neill PJ, Parks BG, Walsh R, Simmons LM,Miller SD. Excursion and strain of the superficialperoneal nerve during inversion ankle sprain. J BoneJoint Surg Am. 2007;89:979-86.

51. Ucerler H, Ikiz AA. The variations of the sensorybranches of the superficial peroneal nerve course andits clinical importance. Foot Ankle Int. 2005;26:942-6.

52. Ferkel RD, Small HN, Gittins JE. Complications infoot and ankle arthroscopy. Clin Orthop Relat Res.2001;391:89-104.

53. Trevino SG, Panchbhavi VK, Castro-Aragon O,Rowell M, Jo J. The "kick-off" position: a new sign forearly diagnosis of complex regional pain syndrome inthe leg. Foot Ankle Int. 2007;28:92-5.

54. Hogan CJ, Hurwitz SR. Treatment of complexregional pain syndrome of the lower extremity. J AmAcad Orthop Surg. 2002;10:281-9.

2016



Documents

Diagnosis and Treatment of Chronic Ankle Pain€¦ · The PDF of the article you requested follows this cover page. € This is an enhanced PDF from The Journal of Bone and Joint