posterior tibial tendon dysfunction

[Guest guest]

BioMechanics April 2004 P ain Management

PTTD symptoms respond to orthotic intervention

Variable surgical results are refocusing treatment efforts on more

conservative methods.

By: Sheldon S. Lin, MD, Wayne Berberian, MD, and Van Gelderen

One common cause of acquired flat-foot deformity is dysfunction of the

posterior tibial tendon.1-5 Historically, the treatment for PTT

dysfunction has been surgical.4,6,7 However, results from tendon

transfers, osteotomies, and fusions have been variable.8-11 Nonoperative

treatment of this disorder with orthotic management is another way to

minimize hindfoot valgus alignment, lateral calcaneal displacement, and

medial ankle collapse.

Anatomy and pathophysiology

A clear understanding of the normal function of the PTT is necessary

before analyzing its pathology. The tendon originates from the proximal

third of the tibia and the interosseous membrane, courses behind the

medial malleolus, where it changes direction acutely and inserts into

the plantar and medial aspect of the navicular, the plantar aspect of

the three cuneiforms, and the bases of the second, third, and fourth

metatarsals.12 Due to this anatomic position, the PTT serves to plantar

flex as well as to invert the middle part of the foot with an action

that occurs primarily across the transverse tarsal joint. When the

subtalar joint is in an inverted position, the transverse tarsal joint

becomes rigid as the axes of the talonavicular and calcaneocuboid joints

are no longer parallel and diverge.13,14 This biomechanical relationship

allows the gastrocnemius-soleus complex to plantar flex the metatarsal

heads as a rigid lever arm. Therefore, the PTT's role in inverting the

hindfoot and locking the transverse tarsal joint is critical for normal

gait and ambulation.15

The pathophysiology of PTT dysfunction involves both primary and

secondary changes. Initially, loss of longitudinal arch height and an

increasing valgus angulation of the heel occur. Loss of longitudinal

arch height is due to the gastrocnemius-soleus complex acting on the

everted calcaneus and to the peroneus brevis muscle acting unopposed on

the talonavicular joint with a dynamic abduction eversion force. Through

these continued dynamic forces, the medial static constraints of the

longitudinal arch gradually attenuate.16 The increasing valgus

angulation of the heel is probably a result of the loss of strength in

secondary soft tissue supportive structures, including the deltoid

ligament, the talonavicular capsule, and the spring ligament.17 Once

these deformities have occurred, the PTT has significant difficulty

overcoming the soft tissue laxity to correct the position of the foot.18

Secondary changes that may develop over time include an equinus

deformity of the ankle, a fixed horizontal orientation of the subtalar

joint, and a fixed valgus angulation of the heel. The associated

contracture of the Achilles tendon causes more sagittal-plane motion to

occur at the subtalar joint rather than at the tibiotalar joint. As the

deformity progresses, this change eventually causes the calcaneus to

impinge on the fibula, creating pain in the lateral part of the foot and

ankle.17

Clinical presentation

The clinical presentation of patients with PTT dysfunction varies; some

patients with minimal deformity are quite symptomatic, while some with

marked deformities have minimal symptoms. The patient with PTT

dysfunction usually denies any acute traumatic event of any significant

degree. Instead, a majority of patients describe a gradual onset of

deformity. The classic patient is a woman over 40 who presents with a

vague discomfort about the ankle.6,16,19,20 Initially, it may be

difficult for patients to localize the discomfort. Tenderness may be

elicited along the medial aspect of the ankle, especially under stress

with activities. As the tendon dysfunction progresses, patients may

localize or describe mild to moderate tenderness in the medial malleolar

region.12

On physical exam, it is important to look for both early and late signs

of PTT dysfunction. Hinterman and Gachter21 advocated the first

metatarsal rise sign of early PTT dysfunction. This test is performed by

externally rotating the shank of the affected foot with one hand or

passively aligning the heel of that foot into a varus position. The head

of the first metatarsal will rise if there is PTT dysfunction but will

remain on the floor in patients with normal PTT function.12

Funk et al,6 ,19 and and Strom22 are credited with

describing the pathognomonic triad for late PTT dysfunction. First,

19 described the classic foot deformity (consisting of a valgus

alignment of the hindfoot and increased abduction of the forefoot) as

the hallmark of PTT dysfunction. As a result of these deformities a

" flat-foot appearance " develops. Finally, there is the presence of " too

many toes. " 22 This sign is determined by observing the patient from

behind and counting the number of toes viewable on the involved and

uninvolved feet. This triad, in conjunction with the patient's being

unable to perform a single heel rise, is consistent with a diagnosis of

PTT dysfunction.12 While there is no study documenting the progression

of early to late PTT dysfunction, the presence of these deformities

implies its chronicity.

and Strom22 are credited with characterizing the first three

stages of PTT dysfunction (Table1). Recently, Myerson17 described a

stage IV deformity characterized by valgus angulation of the talus and

early degeneration of the ankle joint.

Nonoperative treatment

Although the effectiveness of various operative procedures for treatment

of PTT dysfunction has been delineated in the recent literature, little

has been written concerning nonoperative measures. Appropriate

conservative measures are extremely useful as part of the initial

treatment, especially when the presence of factors such as advanced age,

comorbidities that preclude surgery, low activity levels, or the

presence of minimal discomfort make the nonoperative approach more

prudent. Prior to reviewing methods of conservative treatment, a review

of the literature is necessary to comprehend the previous protocols used

for this common clinical diagnosis.

In 1963 23 reported on a series of 52 patients with " chronic

nonspecific tendovaginitis of the tibialis posterior. " Various

conservative measures were used including restriction of activities,

arch supports, foot baths, plaster of paris, calipers with T-strap, and

injection of hydrocortisone. Although most of the patients were relieved

of symptoms, 12 patients (23.1%) failed to improve despite several

months of conservative treatment. Unfortunately, few specific details of

the treatment protocol were discussed and an analysis of these patients

using an outcome or functional scoring system was not provided.

In 1982 Jahss24 reported on a series of 10 relatively sedentary patients

over 52 years of age diagnosed with spontaneous rupture of the PTT. The

first five patients were treated conservatively because Jahss's

contention was that the surgical technique available at that time

(primary tendon repair) was less than optimal. His regimen consisted of

orthotic oxfords with long medial contours, low rubber scaphoids, a

medial heel wedge, and nonsteroidal anti-inflammatory drugs. Minimal

relief was reported with the patients' status remaining stable or

becoming slightly worse. As a result, although Jahss believed all

patients initially should be treated with a conservative course (length

unspecified), he thought it advisable to explore and repair all

suspected PTT tears, except in older patients who are asymptomatic and

relatively sedentary.

Frey and Shereff25 recommended a conservative treatment of rest, ice,

NSAIDs, and a medial-posted orthosis to decrease pronation during the

weight-bearing phase of ambulation for patients with acute PTT

dysfunction. For the young athlete with severe tenosynovitis,

recommendations included immobilization in a nonweight-bearing short leg

cast with the foot in inversion for several weeks. In regards to chronic

tenosynovitis in athletes, Frey and Shereff recommended a protocol of

rest, NSAIDs, and shoe modification, including medial sole and heel

wedges with longitudinal arch support. The treatment concept is to

relieve stress on the posterior tibial tendon by limiting the extent of

excursion.

Mann13 believed the goal of conservative management of patients with PTT

rupture or symptomatic flat foot is to establish support for the medial

longitudinal arch and valgus deformity of the calcaneus. He recommended

the use of an orthosis with a small correction at the arch and

progressive build-up as a patient becomes more tolerant of the pressure

beneath the longitudinal arch. Use of a University of California

Biomechanics Laboratory (UCBL) orthosis was proposed for its ability to

reduce eversion of the calcaneus while establishing some support beneath

the arch.

Recently, Myerson17 described his protocol for the treatment of patients

with PTT dysfunction. For the patients who present with acute

tenosynovitis, an initial protocol consisting of rest, appropriate

NSAIDs, and immobilization was recommended. Myerson recommended

immobilization with a rigid below-the-knee cast or removable boot for

six to eight weeks, during which time ambulation is allowed.

For patients who demonstrate significant improvement with

immobilization, a molded heel and sole shoe wedge, hinged ankle foot

orthosis, or orthotic arch support is used to invert the hindfoot. If

improvement is only mild or moderate, an additional period of

immobilization (in a cast or removable boot) is recommended; otherwise,

a surgical procedure is contemplated. For patients with advanced

disease, a rigid AFO is recommended to immobilize the involved

articulations.

Current treatment options

When choosing an orthosis for the treatment of acquired flat-foot

deformity, the practitioner has several options to choose from,

including the UCBL orthosis, a molded ankle foot orthosis, and the

Arizona brace. The UCBL brace is a thermoplastic in-shoe orthosis

designed to limit subtalar and midfoot motion. If the patient is unable

to tolerate the UCBL brace, an MAFO or an Arizona brace may be used in

patients with a flexible deformity.17 The MAFO is a thermoplastic

orthosis with an articulation at the level of the ankle joint to allow

free dorsiflexion and plantar flexion. Finally, the Arizona brace is a

custom-molded leather and polypropylene orthosis designed by Ernesto

Castro, CPed, of Mesa, AZ, for the nonoperative management of PTT

dysfunction (see figure).

Biomechanical analysis

The Arizona brace extends proximally to the midshaft of the tibia and

distally to the metatarsal heads. Once properly fitted, the low-profile

brace can be inserted inside a patient's shoe for daily wear.26 The

brace works by minimizing hindfoot valgus alignment, lateral calcaneal

displacement, and medial ankle collapse. When casting the mold for the

brace, the calcaneus is reduced to its proper anatomic alignment

underneath the tibia and talus. The brace maintains this relationship by

three-point fixation, similar to a well-molded cast.26

Imhauser et al27 found, when comparing the unbraced cadaveric flat foot

to the braced cadaveric flat foot, the Arizona brace completely restored

the height of the longitudinal arch and the height of the navicular, but

it did not restore talar height or calcaneal angle.

In terms of hindfoot parameters, the brace did not significantly

increase calcaneal or talar dorsiflexion. Similarly, the brace did not

effectively invert the calcaneus with respect to the tibia.27 The

authors hypothesized this may be because of the rigid plastic support

that is molded around the medial and lateral aspects of the tibia and

extends under the plantar surface of the foot; the rigid structure may

also interfere with functional activities, such as walking.

When compared to the Arizona brace, the UCBL orthosis was found to be

superior in reducing calcaneal angle and correcting hindfoot parameters.

Imhauser et al27 found that the UCBL brace significantly restored all

parameters of the arch, including calcaneal angle, inclination of the

first metatarsal, and increased talar, navicular, and arch heights.

Moreover, the UCBL brace significantly corrected two out of three

hindfoot parameters: dorsiflexion of the talus at the ankle joint and

inversion of the calcaneus with respect to the tibia.27

These results were supported by Mereday et al,28 who found the UCBL

brace had an immediate effect on arch parameters, including a reduction

in calcaneal eversion by an average of 7.9 degrees and an increase in

arch height of 11.2 degrees . Talar alignment in plantar/dorsiflexion is

vital because the talus acts to distribute body weight to the heel and

forefoot. Therefore, improper talar alignment will cause altered weight

distribution and abnormally high stress on the medial calcaneal

ligaments and tarsal articulations.28

Clinical results

Chao et al29 have reported on the success of bracing in a series of 52

patients diagnosed with PTT dysfunction treated during a four-year

period with either an MAFO or a UCBL brace with medial posting.

Forty-nine patients were included in the study; three were lost to

follow-up, and one died of unrelated causes. In patients with flexible

deformities who had less than 10 degrees residual forefoot varus with

the heel in a neutral position and who were not obese (13 feet total), a

UCBL brace with medial posting was used; all other patients (40 feet)

were treated with an MAFO. A functional scoring system was devised based

on pain, limp, use of assistance devices, distance of ambulation, and

patient satisfaction.5

With a mean follow-up period of 20.3 months (range eight to 60 months),

67% of the patients demonstrated good to excellent results based on the

functional scoring system.5 Critical evaluation of the two groups

revealed 10 of the 13 feet (77%) treated with a UCBL shoe insert with

medial posting and 23 of 40 feet (57.5%) treated with an MAFO

demonstrated good to excellent results. The average length of daily

orthosis use was approximately 12.3 hours (range 1.5 to 16 hours). The

number of modifications made on the orthosis ranged from zero to four,

with an average of one modification per patient.12 Of the 33 patients

classified as having " good to excellent results, " six discontinued their

use of the orthosis at the latest follow-up because of complete

resolution of symptoms.12

Augustin et al26 recently published one series analyzing the efficacy of

the Arizona brace. The study followed Myerson's protocol17 for the

treatment of 21 patients (27 ankles) with PTT dysfunction, including an

initial trial of rest, NSAIDs, and immobilization with a rigid below

knee cast or removable boot for six to eight weeks. After obtaining

informed consent, the patients were asked to fill out two

questionnaires. The first questionnaire was the Foot Function Index

(FFI)30 which uses an analog visual scale to evaluate the patient's own

perception of function, pain, and disability before wearing the brace.

Within each of these categories, several questions pertain to the

particular topic; these are averaged and a percentage score is obtained

for function, pain, and disability.

The second questionnaire used was the Medical Outcomes Survey (MOS)

36-item short-form health survey (SF-36).31 Based on multiple choice

responses, this evaluates the patient's overall perception of his/her

health and function as well as pain level.

Finally, all patients were examined by a physician before dispensing of

the brace and were scored according to the AOFAS (American Orthopaedic

Foot & Ankle Society) Hindfoot Score System.32 A maximum score is 100;

points are deducted for the use of assistive devices, pain, difficulty

walking distances over uneven terrain, and decreasing motion in the

hindfoot and midfoot joints. Hours per day of brace use and the use of

NSAIDs before and after beginning brace use were documented as well.26

Disease classification was according to the criteria of and

Strom.22 In this study, six patients had stage I disease (seven ankles),

12 patients had stage II disease (15 ankles), and five patients had

stage III disease (five ankles). Mean follow-up was 12 months (range

three to 19 months). Each patient wore the brace for an average of 10

hours/day (range 0 to 14 hours/day). The average age of the patients was

57.3 years (range 34 to 81 years).26 Two patients were dropped from the

study. One had continuing pain while wearing the brace and was

dissatisfied with her results. She subsequently underwent surgery by a

physician in another part of the country but was unavailable for

follow-up questioning. The other patient had severe peripheral vascular

disease that was diagnosed after she had been fitted for the brace.

Because of her potential risk, the patient was advised by her vascular

surgeon to discontinue brace wear.26

After using the Arizona brace, clinical evaluation of patients was done

using the AOFAS Hindfoot Score System, the FFI, and the SF-36

questionnaire. AOFAS Hindfoot Scores increased from 37.7 before the use

of the brace to 76 after brace use (p < 0.001). Changes in FFI scores

were significant in all categories: activity, 58.6 versus 85.2 (p <

0.05); pain, 34 versus 70.7 (p < 0.0005); and function, 28.3 versus 67.7

(p < 0.005) before and after brace use, respectively. All patients

reported at least a moderate improvement in pain and function with the

exception of the two who had stage II disease.

The SF-36 questionnaire analyzes patient perception in nine areas:

physical function, social function, physical role function, emotional

role function, mental health, fatigue/energy, pain, health perception,

and change in health perception. Of the nine measured categories, there

was statistical significance in all measured areas (p < 0.05), except

for change in health perception (p = 0.2168). All patients who had stage

I or stage II disease showed pain relief that was referable to the brace

and demonstrated an improvement on all three clinical measurement

instruments used in the study. Moreover, three out of five (60%)

patients who had stage III disease had relief of symptoms that was

referable to the brace.26 The authors concluded that the Arizona brace

may be a useful adjunct in treating patients who cannot tolerate a rigid

AFO.

Conclusion

Nonoperative treatment of posterior tibial tendon dysfunction can be

successful, especially if initiated in the early stages of disease. The

goal of treatment is to maintain and immobilize the initial deformity

and prevent additional progression of the flat-foot deformity.5 The

practitioner has a variety of treatment options for PTT dysfunction,

including the UCBL brace, MAFO, and the Arizona brace. Significant

relief of symptoms in 90% of patients treated with the Arizona brace

compared to previously reported rates of 77% with the UCBL brace and

57.5% with an MAFO suggests potential therapeutic advantages the Arizona

AFO brace may have. Future research in this area should include a

randomized comparison of the available bracing options.

Sheldon Lin, MD, and Wayne Berberian, MD, are assistant professors of

orthopedics at New Jersey Medical School. Van Gelderen is a

third-year medical student at the same institution.

References

1. Beals TC, Pomeroy GC, Manoll A. Posterior tibial tendon

insufficiency: diagnosis and treatment. J Am Acad Ortho Surg

1999;7(2):215-221.

2. Contl SF. Posterior tibial tendon problems in athletes. Ortho Clin

North Am 1994;25(1):109-121.

3. Henceroth II WD, Deyerie WM. The acquired unilateral flatfoot in the

adult: some causative factors. Foot Ankle 1982;2(4):304-308.

4. Mann RA. Acquired flatfoot in adults. Clin Orthop 1983;(181):46-51.

5. Wapner KL, Chao W. Nonoperative treatment of posterior tibial tendon

dysfunction. Clin Orthop 1999;(365):39-45.

6. Funk DA, Cass JR, KA. Acquired adult flat foot secondary to

posterior tibial tendon pathology. J Bone Joint Surg Am

1986;68-A(1):95-102.

7. Horton GA, Olney BW. Triple arthrodesis with lateral column

lengthening for treatment of severe planovalgus deformity. Foot Ankle

Int 1995;16(7):395-400.

8. JE, Cohen BE, DiGiovanni BF, Lamdan R. Subtalar arthrodesis

with flexor digitorum longus transfer and spring ligament repair for

treatment of posterior tibial tendon insufficiency. Foot Ankle Int 2000;

21(9): 722-729.

9. Conti SF, Wong YS. Osteolysis of structural autograft after

calcaneocuboid distraction arthrodesis for stage two posterior tibial

tendon dysfunction. Foot Ankle Int 2002; 23(6):521-529.

10. Coetzee JC, Hansen ST. Surgical management of severe deformity

resulting from posterior tibial tendon dysfunction. Foot Ankle Int 2001;

22(12):944-949.

11. Myerson MS, Corrigan J. Treatment of posterior tibial tendon

dysfunction with flexor digitorum longus tendon transfer and calcaneal

osteotomy. Orthopedics 1996; 19(5):383-388.

12. Lin S, Lee T, Chao W, Wapner K. Nonoperative treatment of patients

with posterior tibial tendinitis. Foot Ankle Clin 1996;1:261-277.

13. Mann RA. Biomechanical approach to the treatment of foot problems.

Foot Ankle 1982;2(4):205-212.

14. Mann RA. Biomechanics of the foot. Inst Course Lect 1982;31:167-180.

15. Ambagtsheer JB. The function of muscle of lower leg in relation to

movement of the tarsus: An experimental study in human subjects. Acta

Orthop Scand Suppl 1978;172:1-196.

16. Mann RA, FM. Rupture of the posterior tibial tendon causing

flatfoot: surgical treatment. J Bone Joint Surg 1985;67-A(4):556-561.

17. Myerson MS. Adult acquired flatfoot deformity: treatment of

dysfunction of the posterior tibial tendon. J Bone Joint Surg

1996;78-A:780-792.

18. Niki H, Ching RP, Kiser P, Sangeorzan BJ. The effect of posterior

tibial tendon dysfunction on hindfoot kinematics. Foot Ankle Int

2001;22(4):292-300.

19. KA. Tibialis posterior tendon rupture. Clin Orthop

1983;(177):140-147.

20. Myerson M. Posterior tibial tendon insufficiency. In: Myerson M, ed.

Current therapy in foot and ankle surgery. St. Louis: Mosby-Year Book,

1993:123-135.

21. Hinterman B, Gachter A. The first metatarsal rise sign: a simple

sensitive sign of tibialis posterior tendon dysfunction. Foot Ankle Int

1996;17(4):236-241.

22. KA, Strom DE. Tibialis posterior tendon dysfunction. Clin

Orthop 1989;(239):196-206.

23. R. Chronic non-specific tendovaginitis of the tibialis

posterior. J Bone Joint Surg 1963;45-B:542-545.

24. Jahss MH. Spontaneous rupture of the tibialis posterior tendon:

clinical findings, tenographic studies, and a new technique of repair.

Foot Ankle 1982;3(3):158-166.

25. Frey CC, Shereff MJ. Tendon injuries about the ankle in athletes.

Clin Sports Med 1988;7(1):103-118.

26. Augustin JF, Lin SS, Berberian WS, JE. Nonoperative

treatment of adult acquired flat foot with the Arizona brace. Foot Ankle

Clin 2003;8(3):491-502.

27. Imhauser CW, Abidi NA, el DZ, et al. Biomechanical evaluation

of the efficacy of external stabilizers in the conservative treatment of

acquired flatfoot deformity. Foot Ankle Int 2002;23(8):727-737.

28. Mereday C, Dolan CM, Lusskin R. Evaluation of the University of

California Biomechanics Laboratory shoe insert in " flexible " pes planus.

Clin Orth Rel Res 1972;82:45-58.

29. Chao W, Wapner KL, Lee TH, et al. Nonoperative management of

posterior tibial tendon dysfunction. Foot Ankle Int 1996;17(12):736-741.

30. Budiman-Mak E, Conrad KJ, Roach KE. Foot Function Index: a measure

of foot pain and disability. J Clin Epidem 1991;44(6):561-570.

31. Ware JE Jr, Sherbourne CD. The MOS 36-item short-form health survey

(SF-36). I. Conceptual framework and item selection. Med Care

1992;30(6):473-483.

32. Kitaoka HB, IJ, Adelaar RS, et al. Clinical rating systems

for the ankle-hindfoot, midfoot, hallux, and lesser toes. Foot Ankle Int

1994;15(7):349-353.

© 1996- 2004 CMP Media LLC, a United Business Media company