TIBIALIS POSTERIOR DYSFUNCTION - The Podiatry Institute

CHAPTER 40TIBIALIS POSTERIOR DYSFUNCTION:Conservative Tleatment ConsiderationsMickey D. Stapp, D.P.M.Tibialis posterior dysfunction (TPD) is a relativelycommon disorder encountered in podiatricpractices. It is often misdiagnosed by severalphysicians and/or under-treated prior to thepatients's presentation to the office. Treatment ofearly tibialis posterior pathology is often notinitiated due to the delay in proper diagnosis.Tibialis posterior dysfunction occurs as aninsidious course of repetitive trauma and overuse,resulting in inflammation, degeneration, andeventual failure of the tendon. The sequentialpathologic changes frequently continue until aunilateral, severe flatfoot with marked rearfooteversion and forefoot abduction results.Surgical treatment of TPD has been the mainstayof therapy over the past decades. Recently,conserwative treatment has gained attention as analternative to surgical intervention, for poorsurgical candidates, and as a preoperative treatmenttrial. As with most progressive pathologies,conservative treatment of TpO is most successfulwhen initiated in its early stages. Conserwativetreatment options for early and late stage TPD willbe discussed.ANATOMYThe tibialis posterior muscle originates from thesuperior aspect of the posterior surface of the tibia,the medial aspect of the posterior surface of thefibula, the posterior surface of the interosseousmembrane, and the deep transverse septum. Themuscle lies in the deepest portion of the posteriorcompartment of the 1"g between the flexordigitorum longus and the flexor hallucis longus.The tendon crosses deep to the flexor digitorumlongus tendon as it courses medially. It lies in itsown synovial tendon sheath as it courses posteriorto the medial malleolus in the retromalleolargfoove.The tibialis posterior tendon passes deep tothe flexor retinaculum, which prevents bowstringingof the tendon, and lies superficial to the deltoidligament as it enters the foot. As the tendon passesinferior to the plantar calcaneal navicular ligament,it divides into two slips. The major and more superficialslip inserts into the tuberosity of the navicular.A posteriorly directed slip may insert into thesustentaculum tali of the calcaneus, while a moredistal slip may continue from the navicular, toinseft on the medial cuneiform and occasionallythe base of the first metatarsal. The deeper, smallerslip courses a groove in the undersurface of thenavicular, to insert on the plantar surfaces of thebases of the central three metatarsals and theintermediate cuneiform. There are many describedanomalies and variations of inseftions of thistendon.'-aBIOMECHANICSThe tibialis posterior muscle is the most powerfulsubtalar joint supinator of the foot, and strongsupporter of the medial longitudinal arch.5 Thetibialis posterior tendon is ideally located medial tothe subtalar joint (ST) axis and posterior to theankle joint axis to invert the foot at the ankle. Themuscle also acts as the major antagonist for theperoneus longus and peroneus brevis muscles.a'6The tibialis posterior tendon has two effectivepulleys along its course. The first, at the medialmalleolus, provides an effective angle of pu1l onthe subtalar and ankle joints. The second, at thenavicuiar tuberosity, provides an effective angle ofpull on the oblique midtarsal joint in the supinationdirection.a The tibialis posterior tendon insefiions atthe cuneiform, and the central three metatarsalbases serve to stabilize the lesser tarsus.'The primary site of action of the tibialisposterior tendon is a subject of ongoing debate.The talonavicular and calcaneocuboid 1'oints,6,E thesubtalar joint,a and the "rearfoot",3 have all beencited as sites of primary action. The tibialisposterior tendon most likely functions at all of theabove sites. It is a stance phase muscle thatcontracts from heel contact to iust after heel lift. At

244 CHAPTER 40heel contact, the tibialis posterior muscle contractsto decelerate subtalar joint pronation and internalleg rotation. Through midstance phase of gait, itsupinates the subtalar joint and externally rotatesthe leg. It also assists in heel lift by its anklejoint plantar flexion force, and by allowing thegastrocnemius-soleus complex to lift the heel whilethe tibialis posterior tendon stabilizes therearfoot.aPATHOLOGYDifferent classification systems have beendeveloped to describe the associated pathologywith TPD. Funk et al.E identified four types oflesions in 19 patients with the clinical diagnosis oftibialis posterior dysfunction that underwentsurgical exploration. Group I consisted of ar,,ulsionof the tendon at the insertion; Group II consisted oftendons with mid-substance ruptures; Group IIIconsisted of tendons with an in-continuity tear; andGroup IV consisted of tendons with tenosynovitisonly and no tear.Johnson and Strome proposed a stagingsystem. Stage I demonstrates normal tendon lengthwith mild weakness on single heel rise, and nosignificant rearfoot deformity. Stage II demonstratesan elongated tendon, increased pain, "too manytoes sign," marked weakness and difficulty withsingle heel rise, and a flexible valgus position ofthe rearfoot. Stage III shows elongation of thetendon, rigid valgus of the rearfoot, pain now overthe sinus tarsi, no rearfoot inversion on single heelrise or inability to rise on the ball of the foot, andsevere flatfoot with "too many toes sign."Mann'o suggested that the mechanism for theprogressive unilateral flatfoot results from aweakening of the tibialis posterior muscle, whichgives the peroneus brevis muscle a much greatermechanical advantage to pronate the foot. Thispersistent pronation, along with a loss ofligamentous support, eventually collapses the arch,everts the rearfoot, and abducts the forefoot.The pathologic changes that occur with TPDinclude rupture, hypertrophy, degeneration, cysticchanges, and tenosynovitis." The physiologic andpathologic changes occur within the tendon as aresult of microtears, inflammation, and rupture thatensues as a consequence of repetitive loading.During normal activity, a tendon probably does notexceed a tensile load of 25o/o of its physiologicmaximum. If tendon fibers stretch no more than400/o of their length, the original wave pattern oftendon fibers will return. If the tendon fibers arestretched more than 40o/o of their length, the fibersare stressed and may begin to fatigue and tear.aIf the overuse and/or abnormal biomechanicsof the tibialis posterior tendon continues, and thetendon lengthens or ruptures, the plantar ligamentsof the midtarsal joint may also fail. The talus willplantarflex and adduct and the talar head willbecome prominent between the calcaneus and thenavicular. The calcaneus will evert and theunopposed peroneus muscles will abduct theforefoot. Eventually, the adult, unilateral, acquiredflatfoot with forefoot abduction, flexor substitutionstabilization , and an apropulsive gait develops.1e,i2ETIOLOGYThere are multiple causative factors of TPD. Systemiccauses include the arthritides, systemic lupuserythematosus, sero-negative spondyloartrhopathies,and collagen diseases.6Mueller also described and classified 1oca1etiologies as lollows:Type I, Direct: direct injury to the tendon,resulting in dysfunction.Type II, Pathologic rupture: tendon degenerationassociated with systemic conditions suchas rheumatoid arthritis.rupture: etiologyType III, Idiopathicunknown.Type IV, Functional rupture: the tibialisposterior tendon is intact but not functioningwell.The concept of functional rupture isimpofiant. Abnormalities of function that result in apronated foot may predispose a patient to TPD.The majority of TPD patients have an intact tendonthat may be hypertrophic, but functions as if thereis a complete rupture of the tendon. The loss offunction of the tendon is presumed to occur fromthe tendon healing in a lengthened position. Thehypertrophy occurs from scarring in the healingprocess of the tendon.'3Iatrogenic causes of TPD may include tendontrauma secondary to surgery at the medial ankleregion, or repetitive steroid injections into the

246 CHAPTER 40physician the best and most accurate infonnation. Ifa true rupture is suspected, with a palpable defectalong the tendon course, an MRI will show theextent and exact location of the rupture. In a"functional rupture," an MRI typically showshypertrophy and effusion about the affectedtendon. Perhaps the best advantage of the MRI is inplanning a soft tissue procedure to address the TPD.If the surgeon plans a procedure that relies on theintegrity of the tibialis posterior tendon, a preoperativeMRI would be most beneficial.'3 Recently,ultrasound has been reported to be a promisingmethod of evaluating rupture of the TPD.CONSERVATTVE TREATMENTConservative treatment of TPD is seldom reported.There are many patients with this clinical disorderlhat are poor surgical candidates. Morbid obesity,peripheral vascular disease, cardiac disease,advanced age, and high-risk deep venousthrombosis patients are only some examples ofpoor operative candidates. Other patients may electfor nonsurgical treatment modalities. It is generallyaccepted that the late stage tibialis posteriordysfunctional foot with secondary structuralchanges is best addressed with surgery.Conseruative treatment is best utilized for the earlyto midstage TPD patient with no structural changes.It is often necessary to attempt some conservativemeans of treatment before proceeding with surgicalintervention. Lastly, conservative treatmentmodalities are the only treatment modalities at thephysician's disposal for some patients.In Stage I TPD as described by Johnson andStrom, the patient may have purely a peritendinitischaracterized by amber synovial fluid and synovialproliferation. This stage may also present withlongitudinal split tears, bulbous enlargement, anddegeneration of the tendon.e It is this stage thata perceptive practitioner will make an earlydiagnosis. The Stage I patient presents with painalong the medial ankle and arch, possible edemaand calor along the tendon course, and pain withattempts at single leg toe rise test.Stage I TPD operative patients should betreated conserwatively for three to sk months.Relative rest, ice, compression, nonsteroidalanti-inflammatory medications, and ofthoses orshoe modifications should be initiated. Often, thepatient best benefits from immobilization on initialpresentation combined with a nonsteroidal antiinflammatorymedication. In patients withperitendinitis, without clinical signs of weakness,complete resolution of symptoms is possible, in theauthor's experience, ulllizing a removable walkingcast and anti-inflammatory medication for three tosix months. A custom-molded functional orthoticdevice can be utllized in conjunction with theremovable walking cast for added suppolt of thelongitudinal arch. This same orthotic device is thencontinued after discontinuance of the walking castand return to normal shoes. Continued weightbearing is preferable as the stress encouragestendon repair by helping to organize new collagenfibers in the direction of the stress.{ Steroidinjections in and around the tendon should beavoided.Stage I non-operative patients can often bemaintained comfortably with custom fabricatedfunctional foot orthoses. B1ake4'20,21 has writtenextensively on the use of orthoses rather thansurgical intervention for TPD and flatfeet. Orthoticcontrol will decrease the length of time the tibialisposterior muscle fires, reduce rearfoot eversion andresulting load on the muscle-tendon complex, andal1ow for better function of the foot. This will allowfor enhanced healing of the tibialis posteriormuscle-tendon.' After the "tendinitis" has resolved,formal physical therapy can be initiated forrestrengthening.In Stage II TPD, the tendon shows markeddegeneration, enlargement, and multiple longitudinaltears.e The patient exhibits increased pain,difficulry with ambulation, inability to performsingle leg toe rise test, and "too many toes" sign.Conselative treatment for operative patients inthis stage, should be carried out as previouslydescribed for Stage I patients. Howevet,conserwative trial can be shofiened in light ofalready existent muscle weakness. NonoperativeStage II TPD patients may also be managed longterm with the use of functional orthotic devices. Ifthe forefoot abductron and/or forefoot varusis severe, a custom molded shoe should beconsidered.Stage III TPD is marked by rigid flatfootdeformity. The structural changes associated withloss of tibialis posterior tendon integrity havebecome fixed with coexisting degenerativearthrosis. These patients present with pain in themedial and lateral ankle, apropulsive gait, positive

CHAPTER 40 247single leg toe rise test with inability to lift the heel,and rigid pes planus with accompanying rearfooteversion, forefoot abduction, and often forefootvarus. No conserwative treatment will benefit theoperative patient. The patient will best benefit froma stabilizing, realigning arthrodesis procedure. Thedifficulty arises in this group of patients that do notdesire surgical interuention or are poor surgicalcandidates. Ankle-foot orthoses have been successftrllyused in these cases.",'3 Lee and associates usedthe ankle-foot orthoses combined with a UCBL(University of California Biomechanics Laborator])ofthotic device successfully in 53 tlbialis posteriortendon ruptures.23 Custom-molded shoes can alsobe used in this group of patients with accommodationsfor coexisting equinus and forefoot varus.la Adouble upright brace altached to a custom-moldedshoe has proven effective in maintainingambulation in patients with gross end stagedeformities of TPD.CONCLUSIONTibialis posterior dysfunction is a disablingcondition for many patients. Even though earlysurgical interuention may be the best treatment formany patients, conserative therapy may be theonly consideration in some patients. Patients withearly signs of TPD can be treated successfully withshort courses of conservative care, followed byphysical therapy. End-stage TPD patients can alsobe managed at a comfortable level with aggressiveconservative care.1.23561q10.11.1.2t3.14.15.rc.lt.18.1.92021.2223REFERENCESValmassy RL, Marozsan J: Tibialis posterior dysftrnction: treatmentwith functional foot ofihoses, literature reviet', and presentationof case studies. Louer Extremi\) 3:185-194, 1995.Draves DJ: Anatom! of tbe Louer Extremiry) Baltimore, MD:\7i11iams & Wilkins; 7986: 268-210.Kaye RA., Jahss MH: Foot fellows review. tibialis posterior: areview of anatomy ancl biomechanics in relation to support of themedial longitudinal arch. Foot Ankle 71214-247, 7997.Blake Rl, Andeson K, Ferguson H: Posterior tibial tendinitis: aliterature review with case repofis. J Am Pocl Med,4ssoc 84:141-1,49, 1991.Root M, Y/eed .J, Orien W: Normal and Abnormal Functictn of tbeFootLos Angeles, CA: Clinical Biomechanics Corporation: 1977.Mueller TJ: Acquired flatfoot secondary to tibialis posteriordysfi-rnction: biomechanical aspects. J Foot Surg 30:2-17, 1997.'WernickJ, Cusack J, Wernick E: Spontaneous lupture of theposterior tibial tendon: a cooselvative approach. Curent Pocltlcd. )une-)uly. I I ls. 1o8o.Funk DA, Cass JR, Johnson KA: Acquired adult flatfoot seconclaryto posterior tibial tendon pathology. /BoneJoint Surg 68A:95-102,1986.Johnson I{-A, Strom DE: Tibialis posterior tendon dysfunction. ClinOthop 239:796-206, 1989.Mann RA, Thompson FM: Rupture of the posterior tibial tendoncausing flatfoot. J BoneJoint Sutg 67A:556-i61,, 1,985.Goldner JL, Keats PK, Bassett FH, et al: Progressive talipesequinovar-us due to trauma or degeneration of the posterior tibialtendon and n-redial plantar ligaments. Ortbop Clin 5:39-51, 7974.Mendicino SS, Quinn M: Tibialis posterior dysfunction: anoveruiew with a surgical case report using a flexor tendontransfer. J Foot Surg 28:154-1,57 , 7989.Mahan KT: Tibialis posterior dysfunction: an overwiew. In YickersNS, ed. Recor'tsttuctiue Surgery of the Foot and Ankle, Update 96,Tucker, Gar Podiatry Institute Publishing; 1996:3-6.Banks AS, McGlamry ED: Tibialis posterior tendon rupture. /,42Pod Med Assoc 77:770-176, 1987.Johnson I(A: Tibialis posterior tendon rlrpture. Clin Or"thop 777:140-147,1983.Mueller TJ: Ruptures and lacerations of the tibialis posteriortendon. J Am Pod Assoc 71:109'779, 1984.Ford LT, DeBenderJ: Tendon rupture after local steroid injection.So Mecl J 7 2:827 -830, 1979.Kannus P, Jozsa L: Hisotopathological changes precedingspontaneolrs rupture of a tendon. J Bone Joint Surg 73A:1,507-752i. 1.991..Frey C, Shereff M, Greenridge N: Vascularity of the postedortihial tcntlon. .l Bone.loint Jr{g -2A: 8E'i-888. 1940.Blake RL, Ferguson H: Foot orthosis for the severe flatfoot insports. .J Am Pod Metl Assoc 81: 549-5i5, 1991.Blake RL: Athletic injuries: orthoses versus surgery. InJay RM, ed.Cw'rent Theraplt in Podiatric Surgety. Philadelphia, PA: BCDeckerrl3T-142: 1989.Marzano R: The Shorter Cure for Tibialis Posterior Dysfunction.Biomechanics 4t 43 45, 1,995.Lee TH, Chao $0, Wapner KL: Choosing Orthoses OverSurgery:Using Orthoses, Nonsurgical Treatment of Posterior TibialTendon Dysfr:nction Can Be Successfal. Biomecbanics 4: 27-29,1995.