TIBIALIS POSTERIOR DYSFUNCTION: Conservative Tleatment Considerations

CHAPTER 40 TIBIALIS POSTERIOR DYSFUNCTION: Conservative Tleatment Considerations

Mickey D. Stapp, D.P.M.

Tibialis posterior dysfunction (TPD) is a relatively ligament as it enters the foot. As the tendon passes common disorder encountered in podiatric inferior to the plantar calcaneal navicular ligament, practices. It is often misdiagnosed by several it divides into two slips. The major and more super- physicians and/or under-treated prior to the ficial slip inserts into the tuberosity of the navicular. patients's presentation to the office. Treatment of A posteriorly directed slip may insert into the early tibialis posterior pathology is often not sustentaculum tali of the calcaneus, while a more initiated due to the delay in proper diagnosis. distal slip may continue from the navicular, to Tibialis posterior dysfunction occurs as an inseft on the medial cuneiform and occasionally insidious course of repetitive trauma and overuse, the base of the first metatarsal. The deeper, smaller resulting in inflammation, degeneration, and slip courses a groove in the undersurface of the eventual failure of the tendon. The sequential navicular, to insert on the plantar surfaces of the pathologic changes frequently continue until a bases of the central three metatarsals and the unilateral, severe flatfoot with marked rearfoot intermediate cuneiform. There are many described eversion and forefoot abduction results. anomalies and variations of inseftions of this Surgical treatment of TPD has been the main- tendon.'-a stay of therapy over the past decades. Recently, conserwative treatment has gained attention as an BIOMECHANICS alternative to surgical intervention, for poor surgical candidates, and as a preoperative treat- The tibialis posterior muscle is the most powerful ment trial. As with most progressive pathologies, subtalar joint supinator of the foot, and strong conservative treatment of TpO is most successful supporter of the medial longitudinal arch.5 The when initiated in its early stages. Conserwative tibialis posterior tendon is ideally located medial to treatment options for early and late stage TPD will the subtalar joint (ST) axis and posterior to the be discussed. ankle joint axis to invert the foot at the ankle. The muscle also acts as the major antagonist for the ANATOMY peroneus longus and peroneus brevis muscles.a'6 The tibialis posterior tendon has two effective The tibialis posterior muscle originates from the pulleys along its course. The first, at the medial superior aspect of the posterior surface of the tibia, malleolus, provides an effective angle of pu1l on the medial aspect of the posterior surface of the the subtalar and ankle joints. The second, at the fibula, the posterior surface of the interosseous navicuiar tuberosity, provides an effective angle of membrane, and the deep transverse septum. The pull on the oblique midtarsal joint in the supination muscle lies in the deepest portion of the posterior direction.a The tibialis posterior tendon insefiions at compartment of the 1"g between the flexor the cuneiform, and the central three metatarsal digitorum longus and the flexor hallucis longus. bases serve to stabilize the lesser tarsus.' The tendon crosses deep to the flexor digitorum The primary site of action of the tibialis longus tendon as it courses medially. It lies in its posterior tendon is a subject of ongoing debate. own synovial tendon sheath as it courses posterior The talonavicular and calcaneocuboid 1'oints,6,E the to the medial malleolus in the retromalleolar subtalar joint,a and the "rearfoot",3 have all been gfoove. cited as sites of primary action. The tibialis The tibialis posterior tendon passes deep to posterior tendon most likely functions at all of the the flexor retinaculum, which prevents bowstring- above sites. It is a stance phase muscle that ing of the tendon, and lies superficial to the deltoid contracts from heel contact to iust after heel lift. At 244 CHAPTER 40 heel contact, the tibialis posterior muscle contracts maximum. If tendon fibers stretch no more than to decelerate subtalar joint pronation and internal 400/o of their length, the original wave pattern of leg rotation. Through midstance phase of gait, it tendon fibers will return. If the tendon fibers are supinates the subtalar joint and externally rotates stretched more than 40o/o of their length, the fibers the leg. It also assists in heel lift by its ankle are stressed and may begin to fatigue and tear.a joint plantar flexion force, and by allowing the If the overuse and/or abnormal biomechanics gastrocnemius-soleus complex to lift the heel while of the tibialis posterior tendon continues, and the the tibialis posterior tendon stabilizes the tendon lengthens or ruptures, the plantar ligaments rearfoot.a of the midtarsal joint may also fail. The talus will plantarflex and adduct and the talar head will PATHOLOGY become prominent between the calcaneus and the navicular. The calcaneus will evert and the Different classification systems have been unopposed peroneus muscles will abduct the developed to describe the associated pathology forefoot. Eventually, the adult, unilateral, acquired with TPD. Funk et al.E identified four types of flatfoot with forefoot abduction, flexor substitution lesions in 19 patients with the clinical diagnosis of stabilization , and an apropulsive gait develops.1e,i2 tibialis posterior dysfunction that underwent surgical exploration. Group I consisted of ar,,ulsion ETIOLOGY of the tendon at the insertion; Group II consisted of tendons with mid-substance ruptures; Group III There are multiple causative factors of TPD. Systemic consisted of tendons with an in-continuity tear; and causes include the arthritides, systemic lupus Group IV consisted of tendons with tenosynovitis erythematosus, sero-negative spondyloartrhopathies, only and no tear. and collagen diseases.6 and Strome proposed a staging Johnson Mueller also described and classified 1oca1 system. Stage I demonstrates normal tendon length etiologies as lollows: with mild weakness on single heel rise, and no significant rearfoot deformity. Stage II demonstrates Type I, Direct: direct injury to the tendon, an elongated tendon, increased pain, "too many resulting in dysfunction. toes sign," marked weakness and difficulty with Type II, Pathologic rupture: tendon degenera- position single heel rise, and a flexible valgus of tion associated with systemic conditions such the the rearfoot. Stage III shows elongation of as rheumatoid arthritis. tendon, rigid valgus of the rearfoot, pain now over the sinus tarsi, no rearfoot inversion on single heel Type III, Idiopathic rupture: etiology rise or inability to rise on the ball of the foot, and unknown. severe flatfoot with "too many toes sign." Type IV, Functional rupture: the tibialis Mann'o suggested that the mechanism for the posterior tendon is intact but not functioning progressive unilateral flatfoot results from a well. weakening of the tibialis posterior muscle, which gives the peroneus brevis muscle a much greater The concept of functional rupture is mechanical advantage to pronate the foot. This impofiant. Abnormalities of function that result in a persistent pronation, along with a loss of pronated foot may predispose a patient to TPD. ligamentous support, eventually collapses the arch, The majority of TPD patients have an intact tendon everts the rearfoot, and abducts the forefoot. that may be hypertrophic, but functions as if there The pathologic changes that occur with TPD is a complete rupture of the tendon. The loss of include rupture, hypertrophy, degeneration, cystic function of the tendon is presumed to occur from changes, and tenosynovitis." The physiologic and the tendon healing in a lengthened position. The pathologic changes occur within the tendon as a hypertrophy occurs from scarring in the healing result of microtears, inflammation, and rupture that process of the tendon.'3 ensues as a consequence of repetitive loading. Iatrogenic causes of TPD may include tendon During normal activity, a tendon probably does not trauma secondary to surgery at the medial ankle exceed a tensile load of 25o/o of its physiologic region, or repetitive steroid injections into the CHAPTER 40 245 tendon or tendon sheath. Steroid injections into continued inflammation leads to degeneration, and around the tibialis posterior tendon are hypertrophy, and eventual "functional rupture" of cautioned against by many authors.','2 1a,'5 Mueller, the tibialis posterior tendon. As this occurs, muscle in his 7984 report of 25 cases of ruptures and weakness is noted. lacerations of the tibialis posterior tendon, used Banks and McGlamry describe manual muscle steroid injections along the tendon, but with little testing of the tibialis posterior tendon by exerting relief.'6 Ford and DeBender reported on 15 various an abductory force to the patient's supinated foot ruptured tendons in 13 patients injected with a against resistance. Normally, a patient should be steroid in or about the tendon.17 able to resist such a force, and the examiner should Other, more physiologic etiologies, have been not be able to overpower the tendon. With an described and continue to be investigated. Kannus inflamed or ruptured tendon, the patient will be and Jozsa'* studied tendons from 891 patients and unable to maintain the supinated position and can concluded that spontaneous rupture occurred in often easily be overpowered.'a tendons showing degenerative changes. It is Johnson describes a single leg toe rise test. theorized that these degenerative changes occur in The patient is asked to stand only on the affected TPD from the long-standing inflammation within exffemity. He or she is then asked to attempt to rise and around the tibialis posterior tendon. on the ball of the affected foot. The tibialis Frey'e has described a zone of hypovascularity posterior tendon must be used to bring the rearfoot within the tibialis posterior tendon located into a locked position so that the gasctrocnemius- posterior and distal to the medial malleolus. This soleus complex car, plantarflex at the ankle and area of hypovascularity and the degenerative rise on the ball of the foot. A normal test will changes seen in overuse and abnormal functioning demonstrate ability to rise on to the ball of the foot of the tibialis posterior tendon, may be the with simultaneous inversion of the rearfoot. A predisposing factor for TPD and rupture.'3 positive test will show continued rearfoot valgus Mann'3 reported an unusually high incidence with no inversion noted and little or no ability to of os tibiale externum in TPD. Normally, 70o/o to rise on the ball of the foot.15 Both of these tests will 750/0, this author has described an incidence of reproduce the pain that the patient experiences if 50% in TPD. He suggests that the mechanical the tendon remains intact, but not functioning. disadvantage caused by the insertion of the tendon In late stages of TPD evidenced by such fibers onto the ossicle may be a contributing factor described muscle weakness, loss of the long- in developing TPD in many patients. itudinal arch is usually present. The heel will be in a valgus position and the forefoot is usually CLINICAI PRESENTATION abducted. The "too many toes" sign may be AND DIAGNOSIS present, in which more than the normal number of toes will be noted laterally when the affected foot Initially, patients presenting with tibialis posterior is viewed from the posterior position.'5 symptomatology complain of medial arch or medial Radiographs may show signs consistent with talocalcaneal ankle pain. Their complaints may be associated pronation, including an increased with swelling and localized warmth posterior and angle, diminished articulation of the talonavicular inferior to the medial malleolus. Pain on palpation joint, anteriorly displaced c.vma line, and the lateral along the course of the posterior tibialis tendon is process of the talus abutting the floor of the sinus usually present from the posterior medial malleolus tarsi. If present for an extended period of time, to the insefiion into the navicular. degenerative changes of the medial column, joints In the early stage of TPD, pain aggravated by midtarsal, subtalar, and ankle may be noted. weight bearing, may be the only presenting factor. A valgus alignment of the talus within the ankle Pain is usually noted with palpation along the mortise may also occur. course of the tendon. In this early stage, no clinical The diagnosis of TPD is usually made based weakness or associated change in foot structure on the history and clinical signs and symptoms may be noted. As the problem continues, or goes described previously. Tenography, CT scans, and untreated, the inflammatory cycle progresses. MRI have all been utilized to aid in the diagnosis. Localized edema and calor may now be seen. The Of these diagnostic modalities, MRI offers the 246 CHAPTER 40

physician the best and most accurate infonnation. If presentation combined with a nonsteroidal anti- a true rupture is suspected, with a palpable defect inflammatory medication. In patients with along the tendon course, an MRI will show the peritendinitis, without clinical signs of weakness, extent and exact location of the rupture. In a complete resolution of symptoms is possible, in the "functional rupture," an MRI typically shows author's experience, ulllizing a removable walking hypertrophy and effusion about the affected cast and anti-inflammatory medication for three to tendon. Perhaps the best advantage of the MRI is in six months. A custom-molded functional orthotic planning a soft tissue procedure to address the TPD. device can be utllized in conjunction with the If the surgeon plans a procedure that relies on the removable walking cast for added suppolt of the integrity of the tibialis posterior tendon, a pre- longitudinal arch. This same orthotic device is then operative MRI would be most beneficial.'3 Recently, continued after discontinuance of the walking cast ultrasound has been reported to be a promising and return to normal shoes. Continued weight method of evaluating rupture of the TPD. bearing is preferable as the stress encourages tendon repair by helping to organize new collagen CONSERVATTVE TREATMENT fibers in the direction of the stress.{ Steroid injections in and around the tendon should be Conservative treatment of TPD is seldom reported. avoided. There are many patients with this clinical disorder Stage I non-operative patients can often be lhat are poor surgical candidates. Morbid obesity, maintained comfortably with custom fabricated peripheral vascular disease, cardiac disease, functional foot orthoses. B1ake4'20,21 has written advanced age, and high-risk deep venous extensively on the use of orthoses rather than thrombosis patients are only some examples of surgical intervention for TPD and flatfeet. Orthotic poor operative candidates. Other patients may elect control will decrease the length of time the tibialis for nonsurgical treatment modalities. It is generally posterior muscle fires, reduce rearfoot eversion and accepted that the late stage tibialis posterior resulting load on the muscle-tendon complex, and dysfunctional foot with secondary structural al1ow for better function of the foot. This will allow changes is best addressed with surgery. for enhanced healing of the tibialis posterior Conseruative treatment is best utilized for the early muscle-tendon.' After the "tendinitis" has resolved, to midstage TPD patient with no structural changes. formal physical therapy can be initiated for It is often necessary to attempt some conservative restrengthening. means of treatment before proceeding with surgical In Stage II TPD, the tendon shows marked intervention. Lastly, conservative treatment degeneration, enlargement, and multiple long- modalities are the only treatment modalities at the itudinal tears.e The patient exhibits increased pain, physician's disposal for some patients. difficulry with ambulation, inability to perform In Stage I TPD as described by Johnson and single leg toe rise test, and "too many toes" sign. Strom, the patient may have purely a peritendinitis Conselative treatment for operative patients in characterized by amber synovial fluid and synovial this stage, should be carried out as previously proliferation. This stage may also present with described for Stage I patients. Howevet, longitudinal split tears, bulbous enlargement, and conserwative trial can be shofiened in light of degeneration of the tendon.e It is this stage that already existent muscle weakness. Nonoperative a perceptive practitioner will make an early Stage II TPD patients may also be managed long diagnosis. The Stage I patient presents with pain term with the use of functional orthotic devices. If along the medial ankle and arch, possible edema the forefoot abductron and/or forefoot varus and calor along the tendon course, and pain with is severe, a custom molded shoe should be attempts at single leg toe rise test. considered. Stage I TPD operative patients should be Stage III TPD is marked by rigid flatfoot treated conserwatively for three to sk months. deformity. The structural changes associated with Relative rest, ice, compression, nonsteroidal loss of tibialis posterior tendon integrity have anti-inflammatory medications, and ofthoses or become fixed with coexisting degenerative shoe modifications should be initiated. Often, the arthrosis. These patients present with pain in the patient best benefits from immobilization on initial medial and lateral ankle, apropulsive gait, positive CHAPTER 40 247 single leg toe rise test with inability to lift the heel, REFERENCES and rigid pes planus with accompanying rearfoot eversion, forefoot abduction, and often forefoot 1. Valmassy RL, Marozsan J: Tibialis posterior dysftrnction: treatment with functional foot ofihoses, literature reviet', and presentation varus. No conserwative treatment will benefit the of case studies. Louer Extremi\) 3:185-194, 1995. operative patient. 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