Corel Ventura - FLATFOOT

Symptomatic acquired flatfoot is an important or-thopaedic problem, due to progressive loss ofwhole foot function and the increasing problem ofpatient disability. It is a complex entity, involvingthe tibialis posterior tendon, ankle joint, hindfootand midfoot. In most cases the posterior tibial ten-don (PTT) is the root cause of acquired flat foot,

but there are other contributions and many differentfactors have an influence. The clinical picture variesdepending on the stage of the deformity, as well as thetreatment approach. Initially soft tissue procedures,synoviectomy and augmentation of the PTT are advi-sed. In stage 2, lateral column lengthening and calca-neal osteotomy, with soft tissue -tendon transfers (TA,FHL, FDL) are recommended. In stage 3 subtalar, do-uble or triplearthodesis is preferable, while in stage 4pantalar fusion is indicated. In the article more deta-iled etiology, the clinical picture, diagnosis and moda-lities of treatment are presented.

Key words: acquired flat foot, posterior tibial tendondysfunction, treatment

INTRODUCTION

Flat foot, especially the acquired type, is a commoncondition and can be seen in 10-25% of the entire

population, but, as it is usually asymptomatic, it is over-looked and not treated in most cases1. Moreover, in

practice, it is usually misdiagnosed as ankle sprain2.It can be divided into several groups: adult non-Poste-

rior Tibial Tendon Dysfunction (PTTD), adult PTTD flat-foot, flatfoot due to coalition, post-traumatic, neuropathic-Charcot foot. The first type is progression of the juvenileform, while tarsal coalition, post-traumatic, neuropathicflatfoot is not so common. In this paper adult PTTD flat-foot is described, with concern about the other forms,which must be excluded before treatment.

Acquired flatfoot is defined as partial or total loss of thedynamic and static supportive structures of the medialarch of the hindfoot and ankle. Furthermore, in most casesit correlates with tibial posterior insufficiency, i.e. posteri-or tibial tendon dysfunction is the most common cause ofacquired flatfoot among adults. There are other risk fac-tors, such as female gender, age, obesity, diabetes mellitus(DM), hypertension (HT), "overuse syndrome", infla-mmatory arthritis, chronic recurrent tenosynovitis, whichcould have an impact on expression of the acquired flat-foot2,3.

As mentioned, besides the PTT, there are other, less co-mmon, causes of flatfoot: flatfoot due to coalition, neuro-pathy (due to diabetes mellitus, peripheral neuritis), andpost-traumatic. Also, arthritis in the ankle, the talonavicu-lar joint and tarsometatarsal (Lis-franc) joint, as well asinflammatory arthritis, may result in the occurrence offlatfoot2,3.

There are statements that isolated loss of the PT tendonwithout ligamentous disruption will not lead to a progres-sive flatfoot deformity, i.e. the adult acquired flatfoot de-formity cannot be reproduced experimentally by releasingthe tibialis posterior tendon alone4.

"In conclusion, we have shown that, to create flatteningof the plantar arch, there is a need to cut the medial struc-tures, including the spring and plantar ligaments and po-ssibly the plantar fascia."5. This is true. In biomechanicsthe dynamic supporting structures of the arch are: plantaraponeurosis, posterior tibial tendon and plantar intrinsicmusculature, while static supportive structures of the archare: the spring ligament complex, superficial deltoid liga-ment, long and short plantar ligaments, plantar aponeuro-sis. However, in practice, without the dynamic support ofthe PTT the other ligaments and joint capsule becomeweak and flatfoot develops2. The circle of disturbances ofthe foot then completes: PTT elongation leading to springligament and plantar fascia problems (elongation) and del-

. ........................................Current treatment options of acquired flatfoot

Aleksandar R. Leši}1,2, Henry Dushan E. Atkinson3, Slaviša G. Zagorac 2, Marko @. Bumbaširevi}1,2

1School of Medicine, University of Belgrade2Clinic for orthopaedic surgery and traumatology, CCS, Belgrade3Departement of trauma and orthopaedics, North MiddlesexUniversity Hospital and London Sports Orthopaedics, London

/STRU^NI RADUDK 616.71-089

DOI:10.2298/ ACI1301021L

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toid ligament insufficiency. Coupling of static and dyna-mic support of the arch is important, as once imbalanceoccurs, flatfoot is mandatory6. These changes happenthrough six stages and the last one is irreversible:

1. Pre-existing flatfoot; 2. Increased gliding resistance of the posterior tibial ten-

don; 3. Increased strain on supportive ligaments and tibialis

posterior with attenuation and rupture of the posterior tib-ial tendon;

4. Sequential rupture of the spring ligament, superficialdeltoid, and interosseous talo-calcaneal ligaments;

5. Valgus of the heel, shortening of the Achilles tendon;6. Degenerative changes in the ankle joint, midfoot and

forefoot.To be able to treat it adequately, one must understand

this pathology and pathogenesis-etiology of the PTT andflatfoot and that will be discussed here.

DYSFUNCTION OF THE TIBIALIS POSTERIORTENDON

Dysfunction of the tibialis posterior tendon is the mostcommon cause of acquired flatfoot in adults. This prob-lem can be very easily overlooked, so this condition wasconsidered in the past as very rare, but PTT dysfunction iscurrently diagnosed in 13-64% of cases of flatfoot1,6. Ithappens mostly in females, aged over 40, as well as in yo-ung males for whom acute trauma is the leading cause ofPTT damage3.

In 1936, Kulowski was the first to report cases with eff-usion into the tendon sheath of tibialis posterior tendon.The first case of posterior tibial rupture was described byKey in 1953, but the initial publication about surgical ex-ploration of PTT ruptures was written by Kettelkamp andAlexander in 19697. In 1974, Goldner inserted either fle-xor digitorum longus or flexor hallucis longus on the spri-ng ligament instead of the ruptured PTT to replace the ti-bial tendon. From that time there have been many publi-cations regarding treatment options for PTT dysfunctionand symptomatic flatfoot1,3,6,8.

RELEVANT ANATOMICAL DATA

Tibialis posterior originates at the proximal one-third ofthe tibia and interosseus membrane (in the deep layer).The tendon (with sheath) passes posterior to the medialmalleolus (fixed by flexor retinaculum)3. It has a multipleinsertion to stabilize the medial and middle column of thefoot. The PTT is inserted: anteriorly on the navicular tube-rosity joint capsule N-C, 1st cuneiform; medially on the2nd cuneiform, 3rd cuneiform, cuboid, PL tendon, 2nd, 3rd,4th and 5th metatarsal bone; and posteriorly on sustenta-culum tali.

The complexity of PTT insertions is confirmation of itsmultiple and significant functions.

Due to its location, tibialis posterior is considered as aplantar flexor as well as an invertor of the hindfoot. It isthe primary stabilizer of the medial longitudinal arch ofthe foot9.

The normal antagonist to the tibialis posterior is the pe-roneus brevis muscle. Thus, dysfunction of the tibialisposterior leads to valgus deformity (hindfoot eversion)and foot abduction (midfoot and forefoot abduction defor-mity), due to predominance of the peroneus muscle1,2.

Tibialis posterior distributes the body weight throughthe all metatarsal bones, supporting the medial arch. Dys-function of the tibialis posterior does not lead to a flat footuntil the supporting structures (spring ligament, plantarfascia, talonavicular, naviculocuneiform ligament and tar-sometarsal capsule) are elongated, but this gradually ha-ppens. Later, hip and spine problems occur.

A clinically very important part in the tibialis posterioris the hypovascularised zone in the retromaleolar groove.The hypovascular zone begins 40mm proximal to the na-vicular and extends 14 mm proximally7. It is a commonsite for pathological features. This is the weak point of thePTT, responsible for PTT dysfunction and the consequent

TABLE 1

CLASSIFICATION BASED ON MRI

Type MRI

Type IOne or two fine longitudinal splits, withoutevidence of transubstance degenration

Type IIThe tendon is narrowed with longitudinalsplits and evidence of intramural degeneration

Type III

Diffuse swelling of the tnedon with uniformdegeneration. A few strands can be intact ofthe tendon is completely replaced by scartissue

TABLE 2

CLASSIFICATION ACCORDING TO THE CLINICALSIGNS -JOHNSON-STROME13

Stage Clinical Presentation

Stage IMedial foot and ankle pain, swelling, mildweakness, tendon lenght is normal

Stage II

A flesible panovalgus foot. Medial or lateralpain or both. The "too many toes sign" andsingle limb heel rise are present. The tendonis elondated and functionally incompetent

Stage IIIAll the signs of stage II are present, the pesplanovalgus deformity is fixed. Lateral Painat the calcaneal -fibular contact

Stage IV

End stage, valug tilt of the talus in the anklemortise leads to lateral tiobiotaladegenration, osteoarthritis of the ankle, withlimited ability to walk

Stage IV was added to the original Johnson-Srome classificationlater by Mayerson

22 A.R. Le{i} et al. ACI Vol. LX

instability of the medial and middle columnae of the foot1.Clinically it presents as valgus and flat foot6.

PATHOGENESIS AND PATHOLOGICAL ANATOMY

Our understanding of the pathogenesis of PTT dysfunc-tion is still controversial. Dysfunction of the PTT leads tocollapse of the medial longitudinal arch of the foot andrelative internal rotation of the tibia and talus. Eversion ofthe subtalar joint occurs causing the valgus position of theheel and abduction of the foot at the talonavicular joint.The Achilles tendon moves laterally and this position

leads to shortening and lateral impingement of the lateral-fibular maleolus on the calcaneus.

Basically, the classic triad of PTT insufficiency is pre-sented in valgus heel position, collapse of the medial lon-gitudinal arch and forefoot abduction, but only in the fou-rth stage of PTT disorder1,3.

AETIOLOGY

Several causes of PTT dysfunction have been proposed.Among them the most frequent are degenerative changes,which could lead to rupture8. Thus, obesity, pes planusand hypovascularity have been considered as significantrisk factors for the development of PPT dysfunction10.Rheumatoid arthritis can lead to the valgus deformity ofthe forefoot, with synovial inflammation and joint carti-lage destruction. This can also cause rupture of the PTT asa consequence of tendon synovitis1.

Congenital equinus of the foot with overload of the PTTcan lead to this lesion. Also, the role of the accessory na-vicular bone and talocalcaneal coalition has been discu-ssed in the etiology of PTT dysfunction1,3.

CLASSIFICATION

There are various classifications of PTT dysfunction,according to etiology, magnetic resonance imaging (MRI)findings or stage of disease.

Muller classified the etiological factors into four groups:Type 1- Direct injury, Type 2- Pathological rupture, Type3- Idiopathic rupture, Type 4- Functional rupture. A newclassification of PTT dysfunction has been proposed ac-cording to the MRI finding (Table 1), while one based onthe clinical expression-presentation, the classical John-son-Strome classification, is still widely employed6 (Ta-ble 2). The Johnson-Strome classification is useful, sinceit determines prognosis and treatment options.

DIAGNOSIS

Diagnosis of PTT dysfunction is based on clinical fin-dings: unilateral progressive hindfoot valgus deformity,associated with pain and swelling behind the medial ma-lleolus2. The pain is aggravated during walking. It is morecommon among female patients, aged over 40 years. Instage II there is loss of function and shape of the foot. Instage III the deformities are fixed. In stage IV, accordingto Johnson-Strome, the pain is more pronounced on thelateral than on the medial side, which are characteristicsfor the initial phases. The patients may have a sense of in-stability, may limp and the deformities become visible.On examination, from the posterior view planovalgus(flatfoot), flattening of the medial longitudinal arch andforefoot abduction deformity are obvious, and the singlerise test is positive, as well as the "too many toes sign"3.The first MT head sign and Achilles tendon shortening areevident.

X-rays are helpful. Weight bearing X-rays are more sen-sitive. Both lateral and anterior-posterior (AP) view aremandatory3. X-rays can reveal dorsolateral subluxation ofthe navicular bone (i.e. limited talar head coverage), in-

FIGURE 1:

SCHEMATIC PRESENTATION OF TENDON TRANS-FER AND AUGMENTATION OF THE CAPSULE OFTHE TALONAVICULAR JOINT

FIGURE 2:

SHEMATIC PRESENTATION FOR MEDIAL CAL-CANEAL OSTEOTOMY

Br. 1 Current treatment options of acquired flatfoot 23

creased calcaneocuboid, talonavicular, talar-first metatar-sal angle, decreased calcaneal pitch (normally 20-25 de-grees), dorsolateral peritalar subluxation and hallux va-lgus deformity. The absence or presence of degenerativechanges in ankle and foot joints must be assessed2,3,6. Softtissue-edema, partial or complete PTT and other tissuesare best seen with MRI but ultrasound examination is ea-sier and cheaper.

TREATMENT

This depends mainly on the stage of progression of theflatfoot and it can be non-surgical and/or surgical.

Non-surgical treatment

It is generally considered that non-surgical treatment isinsufficient in the treatment of PTT and acquired flat foot,but several studies have shown that such treatment withthe use of orthosis can be a reasonable alternative optionto surgical treatment initially, especially in stage I andII14,15,16,17. It is not suitable for fixed deformities and inlater stages of the condition.

Non-operative treatment consists of: rest, use of crut-ches, cast immobilization, orthoses, modification of foot-wear, short walking cast, ankle-foot-orthoses (AFO) andbraces. The aim is to correct the flexible deformity. Medi-cal treatment using NSAID suppresses pain. The goals ofnon-operative treatment are elimination of clinical symp-toms, improvement of hindfoot alignment and preventionof progressive foot deformity. However, non-operativetreatment is of limited value and is reserved for the firststage of PTT deformity, although it is advisable to startwith conservative treatment.

Surgical treatment

Generally, surgical treatment is indicated when conser-vative treatment has failed after a period of 3 to 6 months.However, in the preoperative stage the exact etiologymust be discovered, e.g diabetes, rheumatic or neurologi-cal diseases, tarsal coalition. Also any associated defor-mities and contracture of the gastrocnemius muscle mustbe evaluated. The point of strongest pain, flexibility of the

FIGURE 2B:

POSTOPERATIVE X-RAY AFTER THE CALCANEALOSTEOTOMY AND MEDIAL DISPLACEMENT FIXEDBY THE TWO CANULLATED SCREWS -LATERALVIEW

FIGURE 2C:

POSTOPERATIVE X-RAY AFTER THE CALCANEALOSTEOTOMY AND MEDIAL DISPLACEMENT FIXEDBY THE TWO CANULLATED SCREWS- AP VIEW

FIGURE 2A:

PREOPERATIVE X-RAY OF THE FLAT FOOT


foot and the integrity of the medial arch must be deter-mined.

Surgical treatment can be divided into two main groups:soft tissue procedures (sinoviectomies, tendon repair, ten-don reattachment, reinforcement, tendon transfer) and bo-ne surgery (osteotomies, arthroeresis, arthrodeses). Accor-ding to some authors, 80% of operated patients have a pa-inless foot2.

Surgical techniques

1. Synoviectomia, decompression, tenolysisIndicated in seronegative inflammatory disorders, with-

out structural changes, synoviectomy can be performed inthe isolated, initial phases8. Besides sinoviectomy, ne-

crotic parts of the tendon can be removed and side-to-sidetenodesis with Flexor Digitorum Longus (FDL) can beadded3,7. This procedure is commonly associated withflexor digitorum longus transposition and elongation ofthe gastrocnemius muscle1. The Flexor Hallucis Longus(FHL) can be used to transfer and repair the spring liga-ment. According to Kitaoka, these soft tissue proceduresdo not stop evolution of the disease and they are ineffec-tive in most cases.

2. Transposition of the tendon-tendon transfer (Figure 1)The goal of this procedure is to counteract PTT hypo-

function, if elasticity of the PTT remains normal. It can bedone with tenodesis of flexor digitorum longus to the in-jured PTT, through a posteromedial approach, with care-ful exploration of the deltoid ligament, which can be re-

FIGURE 4A

PREOPERATIVE X-RAY OF THE FLAT FOOT

FIGURE 4B,C:

POSTOPERATIVE X-RAY WITH THE IMPLANTEDSCREW IN SINUS TARSI-ARTHOERESIS PROCE-DURE

FIGURE 3:

SCHEMATIC PRESENTATION OF THE LATERALCOLUMN LENGTHENING WITH ILIAC CRESTGRAFT,FIXED WITH THE PLATE AND SCREWS


paired or substituted with the plantaris tendon. Anotheroption is to do a partial FDL transfer to the navicular boneor medial cuneiform bone6,18. Cobb and later Helal pro-posed anterior tibial tendon tendodesis in the case of ine-ffective PTT. Additionally, tightening of the talonavicularjoint capsule is advised1. Elongation of the Achilles ten-don (AT) is sometimes advocated. This procedure allowsnormal hindfoot movement, but a disadvantage is limitedcorrection of the deformity6,8.

3. Medial calcaneal osteotomy with flexor transposition(Figure 2)

Compared with the above mentioned procedures, thistype of surgical treatment allows deformity correction.Medial "sliding"-translation osteotomy of the calcaneusprevents valgus deformity through medicalization of themechanical axis (Figure 2a,b,c). The approach is lateraloblique (under 45°) behind the peroneal tendons. Calca-neus must be moved medially by 1cm and fixed with two(6.5 mm) spongious screws). In addition, cast immobili-zation for 6 weeks can be applied. This procedure is donein conjunction with tenosinoviectomy or/and tendon tran-sfer, as well as eventual Achilles tendon lengthening.

4. Lateral column lengtheningThis type of procedure was first described by Evans

(opening wedge osteotomy of the calcaneus with insertionof bone graft)19. It is indicated in the second stage of thedisease, when the deformity is flexible and the PTT is freeand insufficient. It can be done through a lateral incisionover the calcanocuboid joint (Figure 3).

Nowadays, percutaneous placement of a device for enla-rgement of sinus tarsi is popular in correction of flatfoot(Figure 4a,b,c), while arthoeresis indicated for the 2nd sta-ge of flatfoot disorder.

5. Single, double and triple arthrodesesThese procedures are used in rigid deformities with as-

sociated inflammatory and degenerative arthritis, i.e. instage III deformity (Figure 5).

Single arthrodesis could be: subtalar, talonavicular orcalcaneocuboid.

Double or triple arthrodesis is recommended for stageIV of flatfoot deformity. Double arthrodesis includes:subtalar + talonavicular or talonavicular + calcaneocuboid

Triple arthrodesis involves: subtalar + talonavicular +calcaneocuboid (Figure 6a,b,c,d)

Triple arthrodesis is done through two incisions:- a medial approach presents the talonavicular joint, bet-

ween tibialis anterior and posterior tendons and arthrode-sis is fixed with a compression screw.

- the "olierov" incision allows approach to the calcane-ocuboid joint, subtalar joint and lateral part of the talo-navicular joint (with meticuolus preservation of the suralnerve and superficial peroneal nerve branches). The ten-don of extensor digitorum brevis must be moved distally,the sinus tarsi should be cleaned with a drill, the subtalar

FIGURE 5:

SCHEMATIC PRESENTATION OF THE TRIPLE ARTH-RODESIS IN THE TREATMENT OF THE ACQUIREDFLATFOOT

FIGURE 6A:

PREOPERATIVE X-RAY OF THE FLAT FOOT,LATERAL VIEW

FIGURE 6B:

PREOPERATIVE X-RAY OF THE FLATFOOT, AP VIEW


and calcaneocuboidal joints must be fixed with screws.Rarely bone grafts must be used.

Treatment according to the stages of the condition. Thenature of the deformity determines the type of surgicalprocedure:

In stage I conservative measures, tendon debridement,synoviectomies (and sometimes calcaneal osteotomycould be done)2. In stage II tendon transfer is performedin combination with corrective osteotomies. The mechani-cal deformity should be corrected by calcaneal osteotomyand be augmented by arthroeresis or lateral lengthening.PTT is augmented by splitting the anterior tibial tendon or

FDL.2 Achilles tendon lengthening or castrocnemius re-section could be done20.

In stage III correction is obtained through subtalar, cal-caneocuboid and talonavicular articulations20.

Stage IV. Due to the degenerative changes in the anklejoint, the salvage procedure is pantalar arthrodesis (ankle,subtalar, calcaneocuboid and talonavicular) or total anklereplacement, supramaleolar osteotomy2.

CONCLUSION

Adult acquired flatfoot is a condition represented by acascade of soft and articular tissue failures leading to dys-function of the foot and ankle during everyday activities.The main cause of this condition is PTT dysfunction andunderlaying comorbidities. Intervention with ankle footorthoses has become the usual standard of treatment be-fore surgical intervention. In later stages with a painfulfoot surgical treatment re-mains the gold standard fortreatment and the type of pro-cedure depends on the stageof disease.

SA@ETAK

Simptomatsko ste~eno ravno stopalo predstavlja va‘anortopedski problem, zbog progresivnog gubitka funkcijestopala i pogoršanja pacijentovog funcionalnog stanja.Ovo je kompleksan entitet, uklju~uje tetivu tibialis poste-rior, sko~ni zglob, zadnji i srednji deo stopala. U najve-}em broju slu~ajeva tetiva tibialis posterior je uzrok ste-~enog ravnog stopala, ali postoje i drugi uzroci i uticaj os-talih faktora. Klini~ka slika varira u zavisnosti od stepenadeformiteta, kao i pristup le~enju. Inicijalno se savetujumekotkivne procedure, sinovoiektomije, oja~anje tetivem. tibialis posterior. U II stadijumu se savetuje produ‘e-nje lateralne kolumne i kalkanealna osteotomija, sa tetiv-nim transpozicijama (TA, FHL, FDL). U stadijumu III sesavetuje subtalarna, dvostruka ili tripla artrodeza, dok je ustadijumu IV indikovana pantalarna artrodeza. U ovomradu su prikazani etiologija, klini~ka slika, dijagnoza i na-~ini le~enja ste~enog ravnog stopala usled lezije tetive m.tibialisa posteriora.

Klju~ne re~i: ste~eno ravno stopalo, disfunkcijam.tibialisa posterior, le~enje

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FIGURE 6 c:

POSTOPERATIVE X-RAY AFTER TRIPLE ARTHRODE-SIS FOR THE FLAT FOOT -LATERAL VIEW

FIGURE 6d:

POSTOPERATIVE X-RAY AFTER TRIPLE ARTHRODE-SIS FOR THE FLAT FOOT- ANTEROPOSTERIOR VIEW


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Acknowledgments: The paper is supported by grant No 175075,Ministry of Science Republic of Serbia


Corel Ventura - FLATFOOT

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