Posterior tibial tendon dysfunction

Posterior By Kevin

M. Supple,

Tibia1 Tendon

Dysfunction

Jason R. Hanft, Brian J. Murphy,

Chet J. Janecki,

and Geza F. Kogler Posterior tibia1 tendon dysfunction, a common entity, frequently is unrecognized and inappropriately managed. Acutely, pain and swelling are present over the medial ankle and longitudinal arch. Long-standing inflammation can lead to tendon rupture, resulting in a progressive planovalgus or “flat foot” deformity. Plain radiographs illustrate the changes in bony anatomy associated with chronic posterior tibia1 deficiency, while magnetic resonance imaging scans can identify the three stages of posterior tibia1 tendon pathology. Most cases are amenable to

D

YSFUNCTION OF THE tibialis posterior tendon is common in elderly individuals. Originally associated with progressive foot pain and deformity in patients with rheumatoid arthritis, more recently this entity has been recognized in nonrheumatic populations.1-6 Clinical presentation is often an insidious course of inflammation, degeneration, and finally tendon failure resulting in progressive planovalgus foot deformity. Numerous theories have been devel-

From the Department of Diagnostic Radiology, Magnetic Resonance Imaging Center, Siemens Medical Systems Musculoskeletal MRI Research-Reference Site, Doctors’ Hospital, Coral Gables, FL; the Division of Sports Medicine, Department of Orthopaedics and Rehabilitation, University of Miami School of Medicine, Doctors’ Hospital, Coral Gables, FL; the ProstheticlOrthotic Program, Tamiami Campus, Miami, FL; and the South Miami Foot Health Center, South Miami, FL. Kevin M. Supple, MD: Resident, Division of Sports Medicine, Department of Orthopaedics and Rehabilitation, University of Miami School of Medicine, Doctors'Hospital;Jason R. Hanft, DPM: Practitioner, South Miami Foot Health Center; Brian J. Murphy, MD: Assistant Professor, Depatiment of Diagnostic Radiology, Magnetic Resonance Imaging Center, Siemens Medical Systems Musculoskeletal MRI ResearchReference Site, Doctors’ Hospital; Chet J. Janecki, MD: Assistant Professor, Division of Sports Medicine, Department of Orthopaedics and Rehabilitation, University of Miami School of Medicine, Doctors Hospital; Geza F. Kogler, CO: Instructor, ProstheticlOrthotic Program, Tamiami Campus. Address reprint requests to Kevin M. Supple, MD, Division of Sports Medicine, Depattment of Orthopaedics and Rehabilitation, Doctors’ Hospital, University of Miami School of Medicine, 5000 UniversityDr, Coral Gables, FL 33146. Copyright o 1992 by WB. Saunders Company 0049-0172192/2202-0004$5.00/O

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conservative therapy, including rest and administration of nonsteroidal antiflammatory agents. Often a short period of immobilization in a cast or the use of an orthosis is beneficial. In cases with persistent tenosynovitis, complete tendon rupture, or progressive deformity, surgical intervention is indicated. Copyright 0 1992 by W.B. Saunders Company INDEX WORDS: Tendinitis; tibialis magnetic resonance imaging.

posterior;

oped to explain this tendency for inflammation and rupture.7,s This article outlines the clinical, roentgenographic, magnetic resonance imaging (MRI), and pathoanatomic presentation of posterior tibia1 tendon dysfunction as well as current trends in both conservative and surgical management. ANATOMY

AND BIOMECHANICS

The tibialis posterior muscle arises from the interosseous membrane and adjacent surfaces of the tibia and fibula in the proximal third of the leg. Its wide cross-sectional area and relatively short excursion make it a powerful motor unit. The myotendinous junction occurs over the distal third of the leg, with the tendon then passing behind the medial malleolus. The distal insertion includes a large slip to the tuberosity of the navicular as well as multiple insertions into the cuneiforms and bases of the second, third, and fourth metatarsals. The course of the tendon lies posterior to the axis of the tibiotalar joint and medial to the axis of the subtalar joint, allowing the muscle to act as both a plantar flexor and inverter of the foot. During normal gait the tibialis posterior acts to invert the hind foot, causing the midtarsal joints to become rigid and allowing the gastrocnemius-soleus complex to transmit plantar flexion forces to the metatarsal heads. Loss of tibialis posterior function allows hind foot eversion, unlocking the midtarsal joints and causing plantar flexion forces to act at the talonavicular joint. Chronic loss of the active support of the medial longitu-

Seminars in Arthritis andRheumatism, Vol22, No 2 (October), 1992: pp 106-l 13

107

POSTERIOR TIBIAL TENDON DYSFUNCTION

dinal arch causes the ligamentous supporting structures to gradually elongate, resulting in a progressive flat foot deformity. CLINICAL PRESENTATION

Presentations can be divided roughly into two groups. The first are patients typically in their fifth and sixth decades who present with the insidious onset of medial ankle or longitudinal arch pain. They frequently describe a progressive flattening of the arch. In some instances a specific injury or sensation of “giving way” on the medial side of the foot is described, but symptoms usually have been present for months to years. The second group tends to be younger and often give a history of some type of repetitive or high-stress activity (eg, dancing, running) preceding the onset of clinical symptoms. In the acute stages, a localized area of pain, swelling, or increased warmth is often found over the course of the tendon from just distal to the medial malleolus to the navicular insertion. This represents the tenosynovitis associated with the early stages of tibialis posterior tendon dysfunction. Pain and weakness upon resisted foot inversion will be noted on motor testing, and in cases of complete rupture the tendon will not be palpable. The hallmark of long-standing tendon rupture is loss of the longitudinal arch through concurrent development of hindfoot

Fig 1:

Posterior view of

feet-normal affected Note valgus

foot on left,

foot

increased (A)

on right. hindfoot

of the affected

right foot. Also note increased forefoot abduction of the right foot, evidenced by “too many toes” showing lateral to the ankle.

valgus and forefoot abduction. Hindfoot valgus can best be appreciated from a posterior view of the weight-bearing foot (Fig 1). Additionally, on posterior viewing, the “too many toes” sign will show more toes visible lateral to the heel area of the affected side, evidencing increased forefoot abduction. The “single heel rise” test provides a functional assessment of the tibialis posterior. With tendon rupture, the patient is unable to invert the hindfoot and to rise up onto the ball of the foot. ETIOLOGY

Numerous theories attempt to explain the inflammatory and degenerative process found in posterior tibia1 tendons.1-3,7y9J0The role of rheumatic conditions, including rheumatoid arthritis and systemic lupus erythematosus, in producing tenosynovitis is well documented.11J2 For those cases unrelated to connective tissue disease, it is believed that a traumatic or mechanical process leads to tenosynovitis. For some acute presentations, the tendinitis is essentially an “overuse injury” in which repetitive trauma produces microtears that fail to heal fully and ultimately elicit an inflammatory response. Some authors believe that compression or constriction of the tendon beneath the flexor retinaculum mechanically degenerates the tendon. Others suggest that the sharp angled turn behind the

SUPPLE

108

malleolus creates excessive frictional forces. Recently an area of hypovascularity has been identified in the posterior tibia1 tendon just distal to the malleolus. Most likely some combination of trauma and predisposing mechanical factors initiates the inflammatory cycle. The inflammation and subsequent swelling of the tendon in its surrounding sheath create a stenosing tenosynovitis that further contributes to tendon degeneration. DIAGNOSTIC

IMAGING

Plain radiographs identify the osseous changes that occur with the pes planovalgus deformity, and bilateral studies are essential for comparison. Generally there is an increase in the talocalcaneal angle on both anteroposterior (AI’) and lateral views, caused by the progressive valgus attitude of the calcaneus and plantar flexion of the talus. The lateral view may also show a naviculocuneiform “sag” and an increase in the talar first metatarsal angle (normal angle, 0”; > 15”, severe flat foot). Additionally, on the AP view an increase in forefoot abduction may be noted (Figure 2A and B). Computed tomography (CT) scanning and MRI are both sensitive modalities for identifying tendon abnormalities. CT scans show excellent bony anatomy but have limited soft tissue contrast resolution. MRI has superior soft tissue contrast resolution and provides greater anatomic tendon detail. For MRI, both ankles are symmetrically secured within a cylindrical surface coil (knee coil) and are imaged simultaneously to allow left and right comparison. Sagittal Tlweighted images and axial Tl-weighted, dualecho (proton density and T2-weighted), and gradient-echo images are obtained. Coronal imaging infrequently adds additional information. The normal posterior tibialis tendon has low signal intensity (black) on all pulse sequences without focal regions of increased or decreased caliber. Normal thinning of the tendon is present as the tendon courses around the medial malleolus on axial images. Small amounts of fluid in the tendon sheath can be seen normally on T2-weighted and gradient-echo images, but larger amounts usually indicate tendinitis. Based on MRI and surgical findings, three stages of posterior tibia1 tendon pathology have

ET AL

been classifiedi3J4 (Figure 3A-C). Type 1 corresponds to focal tendon degeneration with the development of longitudinal splits, edema, hemorrhage, and scar formation. These events are visualized as increased heterogeneity of the tendon on CT scan and MRI. Tendon size is usually increased compared with the contralatera1 ankle and is best seen on axial images. As degeneration progresses, more tendon fibers rupture and the tendon undergoes attenuation and stretching, producing the type 2 partial rupture. The tendon generally appears thinned in these cases. Type 3 is a complete rupture with no continuity between tendon ends. TREATMENT

Nonoperative

Considering the spectrum of tibialis posterior tendon dysfunction, there are necessarily a variety of therapeutic interventions. For patients seen within the first few weeks of symptom onset, traditional conservative measures are appropriate; rest and antiinflammatory medications are the mainstays of initial therapy. In some cases, shoe modifications that increase hindfoot varus are beneficial. This can be accomplished with a 3/16 medial heel lift. Alternatively, a UCBL (University of California, Berkeley Laboratory) orthotic can be used, which provides support of the medial arch through control of the hindfoot (Fig 4A). The goal is to place the heel into more varus while avoiding increased pressure over the course of the posterior tibia1 tendon. For patients with more severe pain, swelling, and synovitis refractory to initial nonoperative measures, immobilization for approximately 4 weeks in a short leg cast with the foot maintained in a slightly inverted and plantar flexed position is appropriate. Although controversial, some authors recommend the use of a peritendinous steroid injection. It is important to ensure placement of the injectable within the tendon sheath, rather than intratendinous, to help avoid the potential complication of tendon rupture. In cases with persistent symptoms or established tendon rupture with early progressive deformity and for chronic cases in patients who are not surgical candidates, a combined UCBL/ AFO (ankle/foot orthosis) improves forefoot

109

POSTERIOR TIBIAL TENDON DYSFUNCTION

Fig 2:

(A) AP view of bony anatomy-affected

drawn down the longitudinal

normal right foot, the second metatarsal and calcaneous (normal talocalcaneal posterior

has allowed

second metatarsal

foot on left, normal foot on right. Lines have been

axes of the calcaneous

the calcaneous

(A),

talus (B), and second metatarsal

(c). On the

axis bisects the hindfoot angle formed by the axis of the talus

angle, 15” to 35”). On the affected left side, rupture of the tibialis and forefoot

to rotate from beneath the talus such that the

axis does not bisect the hindfoot angle, causing the hindfoot angle to widen. (B)

Lateral view of bony anatomy (normal foot, upper left). The longitudinal axes of the talus (A) navicular (6) are colinear. Also note the normal relationship between the axes of the talus calcaneous (15” to 50”). In the affected foot on the lower right, the talus falls into plantar flexion, increasing the talocalcaneal angle. Also note the divergence of the talar and navicular axes talonavicular “sag”).

and and thus (the

110

SUPPLE ET AL

(A) Type I tibialis posterior

Fig 3:

ture. (Orientation reader

standing

toward

the

weighted

for reading at the

supine

image

patient’s

patient.)

tendon

rup-

MRls is with the feet,

Proton

looking density-

(TR = 2100, TE = 20) shows

increased size of the abnormal

left tendon (open

white

the normal

arrow)

tendon

compared

(black arrow).

weighted

image

with

(6) Type

right

II rupture.

(TR = 600, TE =

thinning of the left tibialis posterior

Tl-

16) shows tendon (ar-

row). (C) Type Ill rupture. Proton density-weighted image (TR = 2200, TE = 25) shows tendon below the medial malleolus row).

Normal

flexor

hallucis

absent

(straight

longus tendon

aris

present (curved arrow).

adduction and heel varus (Fig 4B). This helps reestablish the longitudinal arch while avoiding direct support beneath the arch. Surgical

Some patients have persistent significant tenosynovitis despite aggressive conservative management. Because continued inflammation about the tendon promotes degeneration, tenosynovectomy is warranted to prevent further damage.3J5 The tendon is exposed from the musculotendinous junction to the distal insertion, and the tenosynovium is removed. The tendon is then

carefully inspected for evidence of degeneration or attenuation. If no attenuation exists, the wound is closed and the foot is immobilized in a short leg cast to maintain a position of plantar flexion, inversion, and forefoot adduction for approximately 1 month. This is followed by the use of a UCBL/AFO or custom-molded splint for approximately 4 months. It is essential for these patients to use sturdy footwear with adequate arch support to prevent recurrence. Isolated fraying or longitudinal tears in the tendon frequently can be debrided or repaired and a similar postoperative plan followed.

POSTERIOR TIBIAL TENDON DYSFUNCTION

Fig 4:

(A) UCBL orthotic. (B) Combined UCBL/

AFO orthotic.

In those cases with marked tendon attenuation or frank tendon rupture, surgical management depends upon the location of the rupture, the duration of symptoms, and the associated deformities. Surgical techniques include primary repair, tendon transfer, and arthrodesis. It must be emphasized that tendon repair and transfer are feasible only in flexible feet, and rigid deformities refractory to conservative care typically require arthrodesis. For avulsions of the bony insertion or tendon ruptures just proximal to this point, primary

111

reattachment through a drill hole in the navicular is performed (Fig 5A). A Bunnell-type nonabsorbable suture is placed through the distal stump and then threaded through the bone tunnel and secured. Additional suturing to the soft tissues about the original insertion is performed to augment the strength and anatomic accuracy of the repair. Although primary repair alone may prove adequate, reinforcement with the flexor digitorum longus has been advocated. This technique involves side-to-side tenodesis of the tendons as well as bringing the divided distal end of the flexor digitorum up through the bone tunnel. For cases of severe attenuation or complete midsubstance rupture of the tibialis posterior tendon, flexor digitorum longus tendon transfer is used as described above (Fig 5B and C). In those with long-standing rupture, the tibialis posterior may be so fibrotic that it is no longer capable of providing tendon excursion and contractile function. In this situation, proximal tenodesis is not performed because it would tether rather than assist the transferred flexor digitorum. After division of the flexor digitorum for tendon transfer, the foot intrinsics and short digital flexors are capable of providing functional lesser toe flexion power. Consequently, tenodesis of the distal long flexor stump to the flexor hallucis is not routinely performed.lG In feet with long-standing tibialis posterior deficiency, severe, rigid planovalgus deformity can result. Here the challenge is to provide symptomatic relief and improved mechanical function through realignment of the bony anatomy. Multiple combinations of arthrodeses have been used with various measures of success.15-17 If the deformity arises primarily from subluxation of the calcaneus beneath the talus while other midfoot bony relationships are maintained, a simple subtalar arthrodesis is advocated. For deformities occurring at both the subtalar and transtarsal joints, triple arthrodesis (subtalar, calcaneocuboid, and talonavicular) provides the necessary degree of correction. Fusions performed before the development of marked arthrosis in the neighboring joints give better symptomatic relief.

Fig 5:

(A) Diagram of surgical reattachment

of the tibialis posterior through a drill hole in the navicular.

In this instance, the tendon avulsed from its bony attachment.

The repair has been augmented

transfer of the flexor digitorum longus through the drill hole, as well as a side-to-side tibialis posterior to the flexor digitorum tibialis posterior and flexor digitorum

longus. Inset: Close-up view of the navicular tunnel with the longus sutured in place. (B) Diagram of midsubstance

tibialis posterior. A primary repair of the tibialis posterior is performed and the repair is augmented

by transfer

navicular. (C) Diagram of attritional substance. Here the flexor digitorum

by

tenodesis of the

of the flexor digitorum

using nonabsorbable

longus through

tear of suture,

a drill hole in the

rupture of the tibialis posterior with a segmental

loss of tendon

longus is transferred through a drill hole in the navicular and the

distal stump of the tibialis posterior is used to augment the repair. Tenodesis of the proximal end of the tibialis posterior to the flexor digitorum longus is performed only if the tibialis posterior muscle retains contractile function. If the muscle is fibrotic, proximal tenodesis is not performed.

CONCLUSION

Improved understanding of the natural history and clinical presentation of tibialis posterior dysfunction has helped generate rational treatment. Failure to respond to conservative therapy after 3 to 4 months indicates the need for more aggressive interventions, including surgery. Early recognition and appropriate management of posterior tibia1 tendon dysfunction can

reduce or eliminate symptoms and help avoid late complications such as tendon rupture and hindfoot dissociation. REFERENCES 1. Mann RA, Thompson FM: Rupture of the posterior tibia1 tendon causing flat foot. J Bone Joint Surg 67A:556561,1985 2. Johnson KA: Tibialis posterior tendon rupture. CORR 177:140-147, 1983

POSTERIOR TIBIAL TENDON DYSFUNCTION

3. Funk DA, Cass JR, Johnson KA: Acquired adult flat foot secondary to posterior tibia1 tendon pathology. J Bone Joint Surg 68A:95-102,1986 4. Kettlekamp DB, Alexander HH: Spontaneous rupture of the posterior tibia1 tendon. J Bone Joint Surg 51A:759764,1969 5. Key JA: Partial rupture of the tendon of the posterior tibia1 muscle. J Bone Joint Surg 35A:1006-1008,1953 6. Goldner JL, Keats PK, Bassett FH, et al: Progressive talipes equinovalgus due to trauma or degeneration of the posterior tibia1 tendon and medial plantar ligaments. Orthop Clin North Am 5:139-151,1974 7. Frey C, Shereff M, Greenidge N: Vascularity of the posterior tibia1 tendon. J Bone Joint Surg 72A:884-888,199O 8. Banks AS, McGlamry ED: Tibialis posterior tendon ruptures. J Am Pod Med Assoc 77:170-176,1987 9. Cozen L: Posterior tibia1 tenosynovitis secondary to foot strain. CORR 42:101-102, 1965 10. Jahss MH: Spontaneous ruptures of the tibialis posterior tendon: Clinical findings, tenographic studies, and a new technique of repair. Foot Ankle 3:158-166, 1982 11. Downey DJ, Simkin PA, Mack LA, et al: Tibialis

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posterior tendon rupture: A cause of rheumatoid flat foot. Arthritis Rheum 31:441-446,1988 12. Cruickshank B: Lesions of joints and tendon sheaths in systemic lupus erythematosus. Ann Rheum Dis 18:111119,1959 13. Rosenberg SF, Cheung Y, Jahss MH, et al: Rupture of posterior tibia1 tendon: CT and MR imaging with surgical correlation. Radiology 169:229-235, 1988 14. Alexander IJ, Johnson KA, Berquist TH: Magnetic resonance imaging in the diagnosis of disruption of the posterior tibia1 tendon. Foot Ankle 8:144-147,1987 15. Holmes GB, Cracchiolo A, Goldner LJ, et al: Current practices in the management of posterior tibia1 tendon rupture. Cont Orthop 20:79-108,199O 16. Johnson KA: Tibialis posterior tendon dysfunction, in Surgery of the Foot and Ankle. New York, NY, Raven, 1989, pp 221-244 17. Simmons ED, Sullivan JA, Thomas WH: Treatment of posterior tibia1 tendon insufficiency with talonavicular fusions. Presented at AOA Foot and Ankle Society Annual Meeting, New Orleans, LA, February 1990