Posterior Tibial Tendon Dysfunction - University of Delaware

Journal of Orthopaedic & Sports Physical Therapy
2OOO;3O(2):68-77

Posterior Tibial Tendon Dysfunction

William M. Geideman, MD
)effrey E. )ohnson, MD

Posterior tibial tendon dysfunction is the most common cause of acquired flatfoot Holmes and MannI7 found that
deformity in adults. Although this term suggests pathology involving only the posterior tibial 60% of patients with rupture of
tendon, the disorder includes a spectrum of pathologic changes involving associatedtendon, the posterior tibial tendon had 1
ligament, and joint structures of the ankle, hindfoot, and midfoot. Early recognition and or more of the following associat-
treatment is the key to prevention of the debilitating, long-termconsequences of this ed conditions: hypertension, obesi-
disorder. Conservative care is possible in the earliest stages, whereas surgical reconstruction ty, diabetes mellitus, previous sur-
and eventually arthrodeses become necessary in the latter stages. The purpose of this article gery or trauma about the medial
is to review the symptoms, physical examination, radiological examination, classification, aspect of the foot, or exposure to
steroids. Local injections of ste-
and treatment of posterior tibial tendon dysfunction. / Orthop Sports Phys Ther 2000;30:68- roids near the posterior tibial ten-
don have also been reported as a
77. cause of

Key Words: flatfoot, pes planovalgus, posterior tibial tendon dysfunction,
tendinitis

HISTORY

osterior tibial tendon dysfunction is the major cause of ac- Most patients present with a his-
quired flatfoot deformity in adults. The later stages of the tory of insidious onset of unilater-
disorder are characterized by increased heel valgus, plantar- al acquired flatfoot deformity, as
flexion of the talus, flattening of the medial longitudinal only 50% can recall a history of
arch, and abduction of the forefoot at Chopart's joint. Poste- some form of ua~ma.~"ymptoms
rior tibial tendon dysfunction includes a broad range of progressive dis- may be present for months or
orders, ranging from tenosynovitis to tendon rupture with or without years. Bilateral posterior tibial ten-
hindfoot collapse to a fixed, rigid, flatfoot deformity. don dysfunction is rare.
The causes of posterior tibial tendon dysfunction are varied. They in-
clude age-related degeneration or overuse with attenuation, chronic re- Early symptoms include pain
current tenosynovitis, inflammatory arthritides,';"' and, infrequently, and swelling along the medial foot
acute traumatic rupture.1J.21.3A4n association with seronegative spondy- and ankle, pain in the plantar me-
loarthropathy (ie, Reiter's syndrome, ankylosing spondylitis, and psoriat- dial arch, and occasionally pain ra-
ic arthritis) was found in one series in 47 of 76 patientsJ2 Most r u p diating into the medial proximal
tures are the result of an intrinsic abnormality of the tendon. There is a calf. Patients find standing on
zone of hypovascularity in the region of the medial malleolus that is the their toes painful and difficult.
most common site of rupture,'" but this does not explain the reason for Over time, patients note a gradual
rupture proximal to the malleolus or at the navicular insertion. worsening of their condition, with
The prevalence of rupture is increased in middle-aged, obese wom- progressive collapse of the medial
en.ll.lY27.3I3t is uncommon to see ruptures in young patients, except for longitudinal arch. With the devel-
opment of severe hindfoot valgus,
acute tra~maticrupture^.".".^'.^!'^^^ they may perceive that they are
walking on their medial ankle.
Chief resident, Department of Orthopaedic Surgery, WashingtonUniversity School of Medicine, St They frequently report abnormal
Louis, Mo. wear of the sole of their shoe.
Walking increases the pain, and
Chief,Foot and Ankle Service, and Associate professor, Department of Orthopaedic Sur-ger.y, Wash- they note earlier fatigue and a de-
ington University School of Medicine, St, louis, Mo. crease in their e n d ~ r a n c e . ' ~
Send correspondence to William M. Geideman, 10651 Steppington Drive, Apt 5052, Dallas, TX
75230. E-mail: [email protected]

FIGURE 1. (A) Stage I posterior tibial tendon dysfunction. Note swelling posterior to the medial malleolus. (B)Single limb heel rise. Patient with stage

1 disease is able to perform this with normal inversion of the heel on the right.

In the final stages, the planovalgus deformity pro- should be palpated from above the medial malleolus
gresses. Pain will shift laterally because of calcaneofib to its insertion onto the navicular to assess its integri-
ular or lateral subtalar impingement, and medial ty and to assess any pain or swelling from tenosynovi-
pain frequently will d i ~ a p p e a r . ~ ~ tis. Lateral tenderness in the subfibular or sinus tarsi
region indicates calcaneofibular abutment or subtalar
PHYSICAL EXAMINATION arthritis.

Early in the development of posterior tibial tendon Another useful test for recognizing early posterior
dysfunction, swelling and fullness in the posterome- tibial tendon dysfunction is the first metatarsal rise
dial ankle is common. With an established flatfoot sign. This test is performed by externally rotating the
deformity, the involved foot will be abducted and will shank of the affected foot with 1 hand or passively
have lost the longitudinal arch. When viewing the aligning the heel of the affected foot into a varus po-
standing patient from behind, the examiner will note sition with the patient standing, full weight bearing on
the increased hindfoot valgus and the appearance of both feet. The head of the first metatarsal will rise in
the "too many toes sign." This sign, originally de- the presence of posterior tibial tendon dysfunction
scribed by Johnson,"' indicates that with advanced and will remain on the floor if posterior tibial tendon
forefoot abduction, more toes will be visible on the function is normal.'"his is caused by the loss of pos-
affected side laterally. terior tibial tendon function, resulting in flattening of
the medial longitudinal arch and the consequent
The single limb heel rise tesf"' is a sensitive indica- elongation of the supporting plantar medial ligamen-
tor of posterior tibial tendon dysfunction. This is per- tous structures, in particular the caspsuloligamentous
formed by asking patients to stand near a wall, gently complex of the first metatarsalcuneiform joint. This
balancing themselves with their arms forward and allows the gastrocnemius-soleuscomplex to act at the
their hands resting on the wall. Patients then flex level of the first metatarsal head and cause dorsiflex-
the knee of one leg, lifting the opposite foot off the ion with weight bearing and external rotation of the
ground, and then attempt to rise up onto the ball of shank of the foot or passive heel varus.
the affected foot. With posterior tibial tendon dys-
function, inversion of the heel is weak or absent, and The strength of the tendon is evaluated by asking
either the heel remains in valgus or the patient is the patient to attempt to invert the foot from a plan-
unable to rise onto the forefoot. If able to perform tarflexed and everted position. This position isolates
this test, the patient may note medial ankle pain. Re- the posterior tibial tendon, neutralizing the synergistic
petitive heel rises may reveal a subtle weakness of the inversion from the anterior tibialis m~scle.'"~The
tendon."4 contralateral foot also should be tested in a similar
fashion to determine the strength of the patient's
With the patient seated, the posterior tibial tendon nonimpaired ankle and to help identify a partial tear

J Orthop Sports Phys Ther-Volume 30. N~unber2. Febnvaly 2000

70 J Orthop Sports Phys Ther .Voh~me30 -Number 2 - February 2000

FIGURE 2. Continued.

based on comparative ~eakness.~It' is important to PATHOLOGICANATOMY
palpate the posterior tibial tendon behind the medial
malleolus to feel it actively contract during inversion. With attenuation or rupture of the posterior tibial
An active, palpable contraction in a patient with an tendon, the medial longitudinal arch of the foot col-
acquired flatfoot deformity puts the diagnosis of pos- l a p s e ~a,n~d there is a relative internal rotation of
terior tibial tendon rupture in doubt; tendonitis or the tibia and talus. The subtalar joint everts, causing
partial rupture of the posterior tibial tendon or r u p the heel to assume a valgus position and the foot to
ture of the spring or deltoid ligament then may be abduct at the talonavicular joint. A compensatory
the cause of flatfoot deformityJJ forefoot varus deformity ensues. As the heel assumes
an increased valgus alignment, the Achilles tendon
Motion of the ankle and subtalar joints should also becomes positioned lateral to the axis of rotation of
be evaluated. Ankle motion is usually normal, where- the subtalar joint. Over time, the shortened position
as subtalar motion becomes more limited as the dys- of the hindfoot results in an Achilles tendon contrac-
function progresses. The subtalar joint may become ture. As the deformity progresses, the fibula abuts
fixed in valgus in cases of long-standing deformityaJ4 against the lateral wall of the calcaneus, causing pain
The amount of passive hindfoot inversion is an im- in the lateral hindfoot.
portant variable in the selection of treatment and
therefore should be assessed a c ~ u r a t e l y . ~ ~ CLASSIFICATION

Long-standing hindfoot valgus is often associated Johnson and Strom"' described the clinical stages
with an Achilles tendon c o n t r a ~ t u r eT. ~his is as- of posterior tibial tendon dysfunction. In stage I (Fig-
sessed by dorsiflexing the ankle while holding the ure I ) , the length of the tendon is normal, although
hindfoot in subtalar neutral position and the knee in mild degeneration is present. There is medial foot
extension. and ankle pain, swelling, and mild weakness, but no
deformity. The single limb heel rise is painful, but
The relationship of the forefoot to the hindfoot normal. A flexible planovalgus foot characterizes
should be assessed because as the hindfoot valgus stage I1 (Figures 2 and 3). The tendon is ruptured
worsens, the forefoot and midfoot assume a compen- o r functionally incompetent and shows more ad-
satory supinated position that may become fixed. vanced degeneration. The "too many toes sign" is
This forefoot supination is evident as a forefoot varus
posture. This, too, will affect selection of treatment,
as well as the design of any foot o r t h o s i ~ . ~ ~ . ~ ~

FIGURE 2. (A) Stage I1 posterior tibial tendon dysfunction. Note the "too many toes sign" on the left foot with more toes seen laterally when viewing
the patient from behind. Also, note the hindfoot valgus, which is more pronouncedon the left side than the right. (B)Lateral radiograph of the same
patient. Note the plantarflexedpositionof the talar head. (C)Postoperativephotographof the same patientafter a calcanealosteotomy with medialization.
Note the correction of the hindfoot valgus. (D) Postoperative radiograph showing 2-screw fixation of the calcaneal osteotomy and the improvedpitch
of the talus.

J Orthop Sports Phys TheroVohme SO Number 29 Febn~aly2000 71

FIGURE 3. (A) Stage II posterior tibia1 tendon dysfunction. Again, note the hindfoot valgus and the "too many toes sign." (B) and (CI Patient treated
with a short articulated AFO with correction of the hindfoot valgus.

72 1 Orthop Sport5 Phys Ther.Volume 30. Number 2. Febnran 2000

FIGURE 4. (A) Stage Ill posterior tibia1 tendon dysfunction. Note the medial hindfoot fullness and iixed valgus position. (BIPreoperative lateral radiograph

showing severe transverse tarsal joint collapse and osteoarthritis of the subtalar and talonavicularjoints. (C) Postoperative lateral radiograph aiter triple
arthrodesis showing much improved midfoot and hindioot alignment.

present, indicating secondary deformity of the mid- acteristic radiographic changes occur. With increas-
f~ot.~"he patient will be unable to perform a single ing deformity, the anteroposterior view of the foot
limb heel rise, but the hindfoot remains flexible. In will show lateral subluxation of the talonavicular joint
stage 111 (Figure 4), all the signs of stage I1 are pres- as the navicular rotates laterally on the talus, uncov-
ent except that some component of the hindfoot de- ering the talar head."','".:'!' There is an increase in the
formity is fixed. In advanced disease, there may be talo-first metatarsal angle, as well as an increase in
lateral abutment pain at the calcaneal-fibular articula- the divergence of the talus and calcaneus.'!' The lat-
tion. Stage IV (Figure 5 ) . alluded to by Johnson and eral view reveals a plantarflexion deformity of the ta-
Strom's article and later added to their classification lus, a decrease in the lateral talocalcaneal angle, the
by Myerson,J4involves valgus tilt of the talus in the collapse of the longitudinal arch, a variable increase
ankle mortise leading to lateral tibiotalar degenera- in the talo-first metatarsal angle, and sag at the talon-
tion.Zl.J4 avicular, naviculocuneiform, or metatarsalcuneiform
joints.2" decrease in the distance from the medial
RADIOGRAPHIC EVALUATION cuneiform to the floor compared with the contralat-
era1 foot also has been de~cribed.~:'
Anteroposterior and lateral weight bearing radio-
graphs of both feet, as well as radiographs of the an- With advanced deformity, narrowing of the talon-
kle with the patient weight bearing should be o b avicular and subtalarjoints may be seen."' Anterior-
tained. Early in the disease, radiographs may reveal posterior radiographs of the ankles with the patient
normal findings or show minimal changes of angular standing may reveal tibiotalar arthritis, talar tilt, and
deformity. As the clinical deformity progresses, char- calcaneofibular impingement in severe deformities.

Magnetic resonance (MR) imaging is the method

J Orthop Sports Phys Ther*Voliime 30 Number 2. February 2000

cally demonstrated on short-tau inversion recovery
(STIR) images.%

Ultrasound evaluation of the posterior tibial ten-
don is currently under investigation. Diagnostic ultra-
sound can detect changes in tendon size, the pres-
ence of fluid, and any intratendinous echogenic
changes, thereby differentiating intratendinous and
peritendinous structural changes. In addition, it is
cheaper and faster than MR imaging, although signif-
icant skill and experience by the ultrasonographer is
required to obtain the maximum amount of informa-
tion from this t e ~ h n i q u e . ~ . ~

DIFFERENTIAL DIAGNOSIS

FIGURE 5. Anteroposterior ankle radiograph of stage IV disease dernon- The majority of adult acquired flatfoot deformities
strating severe hindfoot valgus with osteoarthrosis and valgus tilt of the are the result of posterior tibial tendon dysfunction,
tibio-talar joint. but several conditions have a similar clinical presen-
tati~n.'~:'A~ttenuation or rupture of the calcaneona-
of choice to evaluate pathologic conditions of the vicular (spring) ligament complex including the tal-
onavicular capsule will have a similar clinical presen-
posterior tibial however, some contro- tation as posterior tibial tendon dysfunction. A
strong voluntary contraction of the posterior tibial
versy exists over the exact role of MR imaging in the tendon on manual testing supports the diagnosis of
spring ligament pathology.
treatment plan of patients with posterior tibial ten-
Degenerative arthritis of the ankle joint with valgus
don dysfunction. '7344.JJ talar tilt places the hindfoot in marked valgus with
midfoot pronation and leads to a flatfoot def~rmity.'~
Conti et alqeveloped a classification scheme of Standing anterior-posterior radiographs of the ankle
will rule out degenerative arthritis as a cause of adult
tears of the posterior tibial tendon based on MR im- acquired flat foot deformity.

aging. The classification takes into account structural Arthritis of the talonavicular joint, spontaneous or
after trauma, causes forefoot abduction deformity,
features and abnormal signals within the substance collapse of the midfoot, and prominent callus forma-
tion on the plantar-medial aspect of the foot.'J
of the tendon. In a type I tear, the MR image shows
Posttraumatic tarsometatarsal (Lisfranc) joint ar-
1 or 2 fine, longitudinal splits in the tendon, often thritis can present as an acquired flatfoot deformity.
Usually the first, second, and third tarsometatarsal ar-
on the undersurface, without patterns of degenera- ticulations are involved, and patients have painful os-
teophyte formation on the dorsal midfoot and pro-
tion. T1 weighted images reveal a homogeneous gressive abduction and dorsiflexion of the forefoot
on presentati~n.'~
black signal throughout the tendon. Type I1 tears are
Inflammatory arthritis of the hindfoot, usually sec-
characterized by wider longitudinal tendon splits and ondary to rheumatoid disease, can cause valgus tilt at
the ankle or subtalar joint instability. Lacerations of
intramural degeneration. These are seen as gray ar- the posterior tibial tendon, although uncommon,
have caused an acquired
eas within the normally uniform black tendon. The
Neuroarthropathy, such as diabetes, as well as oth-
tendon also may show variable diameter on selected er peripheral neuropathies, may cause an acquired
flatfoot deformity.'"
cuts where a bulbous section may be distal to an at-
TREATMENT
tenuated portion. Type I11 tears are notable for more
Treatment is based on an accurate staging of the
diffuse swelling and uniform degeneration of the disease with both nonsurgical and surgical treatments
designed to correct the abnormalities particular to
tendon. A few tendon strands may remain, or the that stage of disease and to prevent progression to
the next stage.
tendon may be replaced entirely with scar tissue.

Complete ruptures with tendon gap are most graphi-

J Orthop Sports P h y Ther-Volume SOeNumber 29Febnlary 2000

FIGURE 6. A University of California, Berkeley Laboratories (UCBL)orthosis with medial posting.

The goals of nonoperative treatment include the average 30-month follow-up, 16 of 19 patients report-
elimination of clinical symptoms, improvement of ed feeling "much better" after this procedure and
hindfoot alignment, and the prevention of progres- 74% had complete relief of pain. This repair may be
sive foot deformity. For stage I disease, nonsurgical reenforced by means of a side-tu-side tenodesis to
treatment should be tried for at least 3 to 4 months. the adjacent flexor digitorum longus tendon.'JR+'
A short walking cast or removable cast boot immobi-
lization is indicated for patients with acute tenosyno- In stage I1 disease, nonsurgical treatment involves
v i t i ~ . ~ ~I.fJs'y.m~p~toms are improved after immobili- an initial period of cast or removable cast boot im-
zation, then a custom orthotic or ankle foot orthosis mobilization or, in subacute cases, an AFO. Long-
(AFO) may be fitted to the patient. The orthotic term nonsurgical treatment requires more rigid s u p
should be a full-length, semirigid, totalcontact insert port of the foot and ankle. This may be accom-
with medial posting. The primary function of the or- plished with an AFO, corrective total contact insert,
thotic is to provide arch support and correct the o r a University of California, Berkeley Laboratories
flexible component of the deformity. Physical thera- orthosis (UCBL) (Figure 6).3 The UCBL functions to
py for Achilles tendon stretching and posterior tibia1 place the hindfoot in neutral and limit the motion
tendon strengthening is also b e n e f i ~ i a l . "N~ ~on~ste- of the subtalar joint. Many designs of AFO have been
roidal antiinflammatory medicine may decrease pain described for treatment of the flexible flatfoot defor-
and associated swelling. mity including a 1-piece molded polypropylene AFO,
a short articulated AFO (Figure 3), a short lace-up
Surgical treatment should be undertaken only af- leather (Figure 7), and a plastic AFO, as well as the
ter failure of nonsurgical measures. Surgically, a syn- traditional double upright AFO with T-strap. These
ovectomy will remove any hypertrophic tenosynovi- all function to limit subtalar motion. In addition,
um. If a necrotic portion of the tendon is encoun- shoe modifications such a medial flare, wedge, or sta-
tered, as evidenced by discoloration, attenuation, and bilizer may be
longitudinal rents, this area may be excised and the
remaining tendon repaired in an end-toend fash- Surgical treatment of patients with stage I1 disease
i ~ n . ~ " na study by Teasdall and Johnson4%th an is controversial. There are many described proce-
dures, each with only short-term follow-up and all

J Orthop Sports Phys Ther-Volume SOeNumber 2.Febnla1-y 2000

placement may be a p p r ~ p r i a t eO. ~th~er options for
treatment include a lateral column lengthening to
recreate the medial longitudinal arch performed
through the calcaneal neck, as described by Evans,
or through the calcaneocuboid joint with subsequent
f u s i ~ n . ~L. "en~g~thening through the calcaneal neck
in adults has led to calcaneocuboid joint overload
and early arthro~is.L~a' teral column lengthening
may be performed alone or with a medial displace
ment calcaneal osteotomy, thereby addressing both
the pes planus deformity and the valgus deforming
force of the Achilles t e n d ~ n . ~ '

Stage I11 disease (fixed deformity) is not passively
correctable, and therefore, any nonoperative treat-
ment will need to accommodate the deformity. Cus-
tom foot orthotics, shoes, and AFOs, may help allevi-
ate pain and slow progression. Because the deformity
is not passively correctable, tendon reconstruction
alone is not helpful, and to correct the deformity, a
subtalar or triple arthrodesis usually is performed. In
stage IV, the tibiotalar joint is involved. Treatment
thus involves a tibiotalocalcaneal, pantalar fusion, or
hindfoot arthrodesis combined with bracing.

CONCLUSION

FIGURE 7. Short leather lace up ankle-iootorthosis(AFO)with copolymer Accurate diagnosis requires a high index of suspi-
reinforcement medial and lateral for added support. cion and an understanding of the physical signs,
symptoms, and natural history of the acquired flat-
foot deformity. Physicians must accurately stage the
extent of the disease, as treatment depends on the
stage and the response to nonsurgical therapy.

with nearly equivalent outcomes. It is not within the

scope of this article to discuss each of these treat- REFERENCES
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