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Tibialis posterior tendon rupturea cause of rheumatoid flat foot.

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441
BRIEF REPORT
TIBIALIS POSTERIOR TENDON RUPTURE: A CAUSE OF
RHEUMATOID FLAT FOOT
DANIEL J. DOWNEY, PETER A. SIMKIN, LAURENCE A. MACK, MICHAEL L. RICHARDSON,
RAY F. KILCOYNE, and SIGVARD T. HANSEN
Flat foot, a major cause of foot pain and disability, may result from rupture of the tibialis posterior
tendon. We describe 2 patients with rheumatoid arthritis who developed flat feet secondary to surgically confirmed tendon rupture, and we discuss the anatomy and
diagnosis of this condition. In the second patient, we also
present the results of tendon imaging with both magnetic resonance and ultrasound.
Flat foot is a common disabling deformity in
chronic rheumatoid arthritis (RA), where it has been
reported in up to 46% of patients (1). The pathogenesis
of this problem has not been explored, although it has
been attributed to “softening of ligaments” that support the longitudinal arch of the foot (2). A more
probable cause for this correctable problem, particularly in the unilateral setting, is rupture of the tibialis
posterior tendon. This may result from tenosynovitis
From the Departments of Medicine, Radiology, and Orthopaedics, University of Washington, Seattle.
Supported in part by National Institute of Arthritis and
Musculoskeletal and Skin Diseases grant ROI-I-AR-3281I and by
Clinical Research Center and Western Washington Chapter grants
from the Arthritis Foundation.
Daniel J . Downey, MD: Department of Medicine (current
address: Department of Orthopaedics and Rehabilitation, University
of New Mexico Medical Center, Albuquerque); Peter A. Simkin,
MD: Department of Medicine; Laurence A. Mack, MD: Department
of Radiology; Michael L. Richardson, MD: Department of Radiology;
Ray F. Kilcoyne, MD: Department of Radiology (current address:
Department of Radiology, VA Medical Center, San Antonio, Texas);
Sigvard T. Hansen, MD: Department of Orthopaedics.
Address reprint requests to Peter A. Simkin, MD, Department of Medicine, Division of Rheumatology, RG-28, University of
Washington, Seattle, WA 9819s.
Submitted for publication May 15, 1987; accepted in revised
form August 28, 1987.
Arthritis and Rheumatism, Vol. 31, No. 3 (March 1988)
similar to that which causes extensor tendon rupture in
the rheumatoid hand.
We present the cases of 2 patients. The first
patient, with classic RA, had an early diagnosis and
successful repair of tibialis posterior tendon rupture.
The second patient, with probable RA, had a late
diagnosis and developed a disabling deformity. In the
second patient, the tendon was examined by both
magnetic resonance imaging (MRI) and ultrasound.
CASE REPORTS
Patient 1. The patient, a 55-year-old woman
with classic rheumatoid disease, came to the University Hospital arthritis clinic for a routine followup
visit. Ten days earlier she had felt and heard a “pop”
accompanied by a stabbing pain under the left medial
malleolus as she stepped into a shower. Subsequently, she felt considerable pain at this site, but did
not recognize swelling or hematoma. She also described a dull aching discomfort under her foot during
weight bearing, which felt “like my arch is falling
down.” Examination revealed prominent tenderness
below the malleolus, weakness in inversion, and some
sag in the medial longitudinal arch on weight bearing.
The patient had a 9-year history of seropositive
RA, manifested by subcutaneous nodules and symmetric synovitis most prominent in the metacarpophalangeal (MCP) joints, wrists, knees, and forefeet. She
also had longstanding “ankle” involvement, but the
flexor tendon sheaths behind the medial malleolus had
not been considered a particular problem area. At
presentation, her medications were 5 mg of prednisone
every morning, 4 aspirin tablets 4 times a day, and 250
mg of chloroquine a day.
442
Figure 1. Posterior view of the feet of patient 2, demonstrating
valgus heel deformity and collapsed longitudinal arch resulting from
tibialis posterior tendon rupture in the left foot.
BRIEF REPORTS
Surgical exploration confirmed the clinical diagnosis of complete rupture of the posterior tibial
tendon. Fraying and distraction of the torn ends precluded primary repair. Therefore, the flexor digitorum
longus tendon was cut and anastomosed to the distal
stump. The proximal end of the torn posterior tibial
tendon was also sutured to the flexor digitorurn tendon
at a level above and behind the medial malleolus.
The subsequent disease course of this patient
was complicated in the same year by the acute rupture
and successful repair of extensor tendons 3 , 4 , and 5 in
her right hand and, 2 years later, by the presumed
rupture of the right extensor carpi radialis. For more
than 10 years, however, she has sustained excellent,
pain-free function and a normal longitudinal arch in the
left foot.
Patient 2. The patient, a 65-year-old woman,
presented to the University Hospital with a 3-year
history of pain and swelling in the medial aspect of her
left hindfoot. One-and-a-half years prior to presentation, she was descending a flight of stairs when she felt
and heard a pop below her medial malleolus. She
immediately felt an increase in pain, which was evalu-
Figure 2. Magnetic resonance images in the sagittal plane of both feet of patient 2. Heel is to right and midfoot to left for each foot. Open arrows
designate the navicular (top arrow), the medial malleolus (left arrow), and the plantar fascia (lower arrow) . The tibialis posterior tendon (closed
arrow) is present in the right foot (right image) but is absent in the left foot (left image).
BRIEF REPORTS
443
Figure 3. Static ultrasound images obtained beneath medial maleoli of both feet of patient 2. The tibialis posterior tendon is normally found
between the skin (superior surface) and the echogenic medial malleolus (open arrows). In the right foot (right image), the tendon (closed arrows)
is visible in its sheath, whereas the left foot (left image) reveals only a fluid density in the area of the sheath. Dynamic testing further emphasized
these findings, with obvious tendon motion in the right foot and no tendon movement in the left. Soft tissue swelling is notable above the left
tendon sheath.
ated in a local emergency room. Results of radiographs
were normal, and the patient was released with a diagnosis of possible stress fracture. Subsequently, she noticed a progressive flattening of her left foot and an
inability to walk without “ankle” pain. Despite the use
of a double upright brace, she was unable to return to her
work as a nurse. In the 2 months prior to presentation,
she had also developed pain in her left knee and hip.
Her medical history revealed morning stiffness
and intermittent symmetric wrist, MCP, proximal interphalangeal (PIP), and distal interphalangeal (DIP) joint
swelling and pain of many years duration. She also had
right shoulder pain, which was treated with repeated
glucocorticosteroid injections over an approximate 2year period. A review of her physiologic systems and
medical history included no findings of dermatologic,
pulmonary, renal, or other systemic disease.
Examination of her left foot and ankle revealed a
heel in valgus deformity, a collapsed, but mobile, longitudinal arch (Figure l), swelling and mild tenderness
beneath the medial malleous, and an inability to invert
the foot forcefully while in plantar flexion. The tibialis
posterior tendon was palpable in the right foot, but not
in the left. Additional findings included Heberden’s
nodes at the DIP joints, soft tender nodules, bilaterally,
at the second through fifth PIP joints, and swelling at
the right second and third MCP joints. The Westergren
erythrocyte sedimentation rate was 12 mdhour. A test
for rheumatoid factor gave a negative result, but the
antinuclear antibody titer was 1:160 with a speckled
pattern. Test results for anti-SS-A, anti-DNA, and
anti-extractable nuclear antigens were negative.
Plain radiographs of the left ankle bearing
weight showed marked osteopenia, a valgus heel calcaneal angle, and anterior and inferior displacement of
the talar head. Radiographs of the hands revealed
changes indicative of interphalangeal osteoarthritis.
Sagittal, TI-weighted MRI results are shown for both
ankles in Figure 2. In the right foot, the tibialis
posterior tendon was observed lying beneath the medial malleolus to its navicular insertion, whereas in the
left foot the tendon was not visible. Although this
BRIEF REPORTS
444
finding was strongly suggestive of a diagnosis of tendon rupture, the diagnosis was not established because
a partial volume artifact could not be ruled out.
Ultrasound images are shown in Figure 3. The right
tibialis posterior tendon was seen adjacent to the
medial malleolus, where it moved with normal motion
of the foot, but the left tendon was not visible on either
static or dynamic images. In addition, an apparent
fluid density was present within the left tendon sheath.
At surgical exploration, only a thin band of scar
tissue was found in the thickened left tibialis posterior
tendon sheath. Triple arthrodesis was performed and
the mildly hypertrophic flexor digitorum communis
tendon was then transferred to the distal attachment of
the tibialis posterior. This procedure was elected over
tendon transfer alone because of progressive arch
collapse. The patient, 4 months postsurgery, is now
ambulating, bearing full weight on the left lower extremity with minimal discomfort, and is considering
going back to work as a nurse.
DISCUSSION
The tibialis posterior tendon acts dynamically
to support the longitudinal arch of the foot (3). This
occurs in concert with the keystone function of the
navicular bone at the top of the arch and the truss-like
action of the plantar calcaneonavicular, or spring
ligament, beneath the arch. The tibialis posterior muscle originates on the posterior surfaces of the tibia,
fibula, and interosseous membrane, and gives rise in
the distal leg to its tendon, which runs beneath the
medial malleolus and talar head to insert chiefly into
the tuberosity of the navicular. Other important insertions, less commonly recognized, are the first and
second cuneiforms and metatarsal bases (4). When the
tibialis posterior tendon fails, the head of the talus is
destabilized in its relation to the navicular and, when
loaded, slips anteriorly, medially, and inferiorly in
respect to the calcaneus. This progresses with time as
the spring ligament becomes irreversibly stretched
out. The result is seen clinically as a flat foot and
valgus heel.
Rupture of the tibialis posterior tendon, like
other tendons, is most likely to occur if the tendon is
pathologically weakened (5). Repeated steroid injections and decreased blood supply may contribute to
tendon weakening and rupture, but the most common
predisposing factor is chronic tenosynovitis (6). Tenosynovitis, in turn, may be caused by trauma or by
various rheumatic conditions, including RA, systemic
lupus erythematosus, gout, and gonococcal infection
(778).
The early diagnosis of rupture of the tibialis
posterior tendon is frequently missed, as it was in our
second patient. Mann and Thompsons’ series of 19
nonrheumatoid patients with this condition included
only 2 who were referred with the correct diagnosis,
and the average time between tendon rupture and
referral was 43 months (9). This series demonstrates
that physicians do not consider this diagnosis with
sufficient frequency.
In the acute stage, tendon rupture may not
cause obvious deformity and can easily be confused
with minor trauma. The history of a pop or snap is
helpful in the diagnosis; however, such a history may
be absent, especially when the tear is partial rather
than complete. On examination, tenderness and swelling are usually found beneath the medial malleolus.
More important to the diagnosis of tendon rupture is
loss of forceful inversion. This is best detected in full
plantar flexion, where the tibialis anterior and long toe
flexors contribute minimally to inversion. The tibialis
posterior tendon will not be palpable during this test if
it has been completely ruptured. Alternatively, tendon
function may be assessed by examining the heel from
behind for normal inversion during tiptoe stance.
The diagnosis of a ruptured tibialis posterior
tendon may be considerably more difficult in the
presence of RA. Many patients with this disease
regularly experience hindfoot pain, swelling, and tenderness. The flexor tendon sheath is but one of several
areas commonly involved by chronic inflammation,
and tenosynovitis is rarely considered a significant
problem, per se. Concurrent, painful disease in the
metatarsophalangeal joints may preclude the “tiptoe”
test position and may lead to a shuffling gait. When
these problems worsen, both patient and physician
will usually attribute the change to a local flare in the
underlying disease. We believe that these features of
RA (frequently combined with inadequate understanding of the relevant foot mechanics) have led to underrecognition of tibialis posterior tendon rupture as a
cause of rheumatoid flat foot.
Both a higher index of suspicion and better
diagnostic tools will be needed to establish the incidence of this complication. Patients with rheumatoid
synovitis of the dorsal wrist and the digital extensor
tendon sheaths are regularly admonished to report any
loss of extensor function in the hand. The practice of
stressing this advice ensues from widespread recogni-
BRIEF REPORTS
tion of possible tendon rupture at this site, the serious
consequences of such rupture, and the ability of the
lesion to be surgically corrected. Since tibialis posterior tendon rupture also has serious sequelae which
may be prevented by appropriate surgery (9,10), we
believe that RA patients with swelling and tenderness
behind and beneath the medial malleolus should be
advised to report any acute symptoms in this location,
as well as new aching pain under the arch on weight
bearing. Such patients then should be evaluated to
assess the integrity of the tibialis posterior tendon.
When physical findings are equivocal, as they will be
in many RA patients, tendon imaging provides a
promising diagnostic aid.
Tendon imaging techniques, however, are currently imperfect. Tenography involves the probing and
injection of contrast material into the posterior tibial
tendon sheath. If the tendon and sheath are torn or
scarred, the contrast material will not fill the sheath.
This finding may be difficult to distinguish from an
inadequate injection. Alternatively, the study results
may appear falsely normal if the contrast material is
inadvertently injected into the adjacent tendon sheath
of the flexor digitorum communis (11). These shortcomings of tenography have led to a search for better
imaging tools. MRI and ultrasound are the most promising techniques.
Magnetic resonance imaging progressively has
been gaining wider application in the musculoskeletal
system. MRI has been used successfully in the diagnosis of knee ligament tears (12), and is beginning to be
used for traumatic tendon injuries (13). In our second
patient, MRI showed an apparent defect in the left
tibialis posterior tendon near its insertion site on the
navicular (Figure 2). This finding was confirmed at
surgery, but there was question at the time of MRI as
to whether a partial volume artifact or true tendon
defect existed. This concern arose because the angled
course of the tibialis posterior tendon places it in more
than one radiographic plane. Consecutive slices of
good definition are necessary to distinguish between a
tangential, partial volume section of a normal tendon
and attenuation or rupture of the tendon in disease. In
our study, as in usual MRI practice, the images were
stepped rather than consecutive. This may have been
the reason that this expensive test provided only an
equivocal radiologic diagnosis. Until these technical
problems are resolved, MRI is best restricted to investigational imaging of the posterior tibialis tendon.
Ultrasound imaging avoids the economic and
partial-volume defect difficulties of MRI, and is also
445
more widely available. This technique is currently
used in both static and dynamic testing to accurately
diagnose rotator cuff tears (14). It is also applied in
veterinary medicine for imaging the tendons and ligaments of extremities in race horses (15). Our initial
results with ultrasound are promising because on both
static and dynamic testing, the abnormal ankle clearly
lacked a discernible tendon.
We have described 2 patients with RA who developed tibialis posterior tendon ruptures secondary to
chronic tenosynovitis. A prompt diagnosis led to a
successful long-term repair in the first patient, but in the
second patient delayed diagnosis led to debilitating painful flat foot. In the foot, as in the hand, tendon ruptures
should be recognized as a cause of severe disability in
RA. A high index of suspicion will lead to early diagnosis
and prevention of progressive deformity. In our second
patient, who underwent both MRI and ultrasound imaging, ultrasound was the more helpful.
Acknowledgments. We thank Limy Simkin for typing
this manuscript and Mart Mannik for reviewing it.
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446
Progressive talipes equinovalgus due to trauma or degeneration of the posterior tibia1 tendon and medial
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BRIEF REPORTS
13. Ehman RL, Berquist TH: Magnetic resonance imaging
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