Extract
The evaluation and treatment of chronic ankle pain can be a challenge. A
detailed history helps one to evaluate any component resulting from prior
trauma or surgery. A careful physical examination should be performed to
assess the bones, joints, ligaments, and tendons of the area for tenderness,
range of motion, strength, and competence when stressed. Studies in addition
to routine radiographs include bone scans, computerized tomography, and
magnetic resonance imaging. There are many nonspecific treatment regimens;
however, an accurate diagnosis is the basis for a specific and effective
treatment regimen.
The evaluation and treatment of chronic ankle pain can be a challenge. A
detailed history helps one to evaluate any component resulting from prior
trauma or surgery. A careful physical examination should be performed to
assess the bones, joints, ligaments, and tendons of the area for tenderness,
range of motion, strength, and competence when stressed. Studies in addition
to routine radiographs include bone scans, computerized tomography, and
magnetic resonance imaging. There are many nonspecific treatment regimens;
however, an accurate diagnosis is the basis for a specific and effective
treatment regimen.
The evaluation of a patient with chronic ankle pain can be difficult and
requires an understanding of the anatomy of the area and the presentation of
the localized and systemic pathology. Patients with osteoporosis or another
metabolic bone disease may present with chronic ankle pain, as may patients
with gout or, rarely, those with a tumor. These causes will not be discussed
in this paper, but they should always be considered as a possible explanation
for chronic ankle pain.
History
It is essential to obtain the patient's history. A traumatic event
immediately preceding the commencement of the pain must be considered to be
the most likely cause of the pain. One must ask oneself whether there could be
an occult fracture or a tendon injury. A partial or complete tendon tear or an
inflamed tendon can present as a subtle, constant problem. Other questions
include: Is the pain exacerbated by weight-bearing or a different phase of
gait—specifically, heel rise? Is there morning pain, such as is noted in
plantar fasciitis or Achilles tendinitis? Are there any systemic diseases,
such as diabetes mellitus, rheumatoid arthritis, gout, or pseudogout?
Previous surgery must be considered as well, and the following questions
should be asked: Is the presenting pain the same as the pain experienced
before the surgery? Did the previous pain resolve following the surgery, with
new pain initiated as a result of, or as a complication of, the surgery? Is
the old pain present, unchanged by the surgery, with the addition of new pain
as a result of the surgery? These possibilities are best explored by detailed
questioning of the patient.
Physical Examination
The physical examination is a critical component of the initial evaluation,
and a routine complete, methodical examination will often reveal the causative
pathology.
Inspection: The first part of the examination is inspection of the
foot. Gross deformity, loss of toes, discoloration, masses, and malalignment
should be noted. Both lower extremities, distal to the knees, should be
carefully inspected.
Gait: The patient's gait should be observed, and any equipment
used, including shoe inserts or modifications, should be noted. Alterations in
the normal heel-to-toe gait pattern as well as in the shoe-wear pattern can
provide information regarding any areas of the foot that are protected by
alteration of the gait pattern.
Neurologic and vascular structures: The initial examination should
include a thorough evaluation of the neurologic and vascular structures. These
are critical structures that can affect both the pain felt by the patient and
the ability of a surgical wound to heal. Peripheral or central neuropathy can
be subtle, as can claudication or thromboembolic disease.
Range of motion, ligamentous integrity, and muscle strength: The
passive motion of all joints is determined first. All ligaments should be
stressed to evaluate competence as well as to look for inflammation. Then,
active dorsiflexion, plantar flexion, inversion, and eversion of the ankle and
toes are evaluated. Weakness or decreased active motion, compared with passive
motion, should be noted. Tendons are checked, by palpation, for tendinitis,
partial tears, or stenosing tenosynovitis. Palpation of all tendons can reveal
tenderness consistent with inflammation and/or partial tears, which not
infrequently involve the peroneal tendons. Posterior tibial tendon strength
should be evaluated with the ankle in plantar flexion and eversion. Tenderness
is consistent with laxity or synovitis, such as is seen in association with
injury to the anterior talofibular ligament.
Radiographic evaluation: Good-quality weight-bearing plain
radiographs, including at least anteroposterior, lateral, and oblique views of
the ankle, are essential. Special views of the calcaneus and subtalar joint
are necessary when the symptoms and findings on physical examination suggest
pathological changes in these areas. Bone scans can help to reveal an occult
fracture that is not seen on plain radiographs. Computerized tomography scans
are best for evaluating subtle bone abnormalities and fractures, whereas
magnetic resonance imaging is best for evaluating soft-tissue lesions.
Posterior Tibial Tendon
Disorders involving the posterior tibial tendon are a common cause of
medial ankle pain. The posterior tibial tendon is medial to the axis of the
subtalar joint and serves several functions. It balances the pull of the
peroneal tendons, protects the spring ligament, and inverts and stabilizes the
hindfoot during toe-off.
There are intrinsic and extrinsic causes of disorders involving the
posterior tibial tendon. Intrinsic causes include persistent inflammation,
degeneration in the hypovascular area posterior and distal to the medial
malleolus, and a symptomatic accessory
navicular1.
Degenerative tendinosis can occur without
inflammation2.
Extrinsic causes include steroid injections and traumatic toe
injury3,4.
When the posterior tibial tendon is dysfunctional, the pull of the peroneal
tendons is
unopposed5. The
spring, medial hindfoot, and midfoot ligaments become attenuated, leading to a
progressive foot deformity. There is increased forefoot abduction, calcaneal
valgus with plantar flexion of the talar head, and contracture of the Achilles
tendon—i.e., a flatfoot deformity
(Fig.
1)6,7.
In the ankle, there is a decrease and lateral shift of the tibiotalar contact
area, which may lead to degenerative
changes8.
The physical examination of a patient with a disorder involving the
posterior tibial tendon varies depending on the degree of tendon function.
Specific examination techniques include inversion strength testing
(Fig. 2) and single-limb heel
rise (Fig. 3). Inversion
strength testing is performed with the foot in maximum eversion. In eversion,
the posterior tibial tendon is the only invertor. When the foot reaches the
midline, the anterior tibial tendon also inverts the foot. The tendinitis
often makes the tendon painful to palpation.
Classifications of disorders involving the posterior tibial tendon are
based on tendon function, foot flexibility, position, and radiographic
appearance. Radiographic abnormalities associated with dysfunction of the
posterior tibial tendon include peritalar subluxation, forefoot abduction,
talonavicular joint sag, and collapse of the longitudinal arch. Johnson and
Strom presented the first classification scheme for disorders of the posterior
tibial tendon9
(Table I), which was later
modified by
Myerson10
(Table II).
Nonoperative treatment of disorders of the posterior tibial tendon varies
according to the stage of the disease. Treatment of Stage-I disease includes
immobilization, nonsteroidal anti-inflammatory drugs, and orthotics. Treatment
of Stage II includes immobilization, orthotic support, or a hinged ankle-foot
orthosis. Treatment of Stage III or IV includes a rigid ankle-foot orthosis or
an Arizona
brace11.
Surgical treatment is indicated for a disorder of the posterior tibial
tendon when the patient has persistent symptoms despite nonoperative
treatment. Synovectomy of the posterior tibial tendon has been recommended for
Stage-I disorders12
(Fig. 4). Several different
surgical procedures have been reported for Stage-II disorders, with a transfer
of the flexor digitorum longus used in all of them. Variations of the surgery
include transfer of the flexor digitorum longus with a medial displacement
calcaneal osteotomy with or without a lateral column
lengthening13-16.
Also, transfer of the flexor digitorum longus with repair of the spring
ligament and subtalar fusion has been
recommended17.
Regardless of the procedure, all have reportedly resulted in improvement in
the talo-first metatarsal angle, talonavicular coverage, and medial
cuneiform-to-floor distance.
The effects of medial displacement calcaneal osteotomies and lateral column
lengthening have been investigated in biomechanical studies. A medial
displacement osteotomy can correct the arch in three
planes18 and can
decrease the strain on the spring ligament by decreasing its functional
length19. It can
also decrease the strain on the proximal deltoid ligament, thereby protecting
the spring
ligament20. It has
been postulated that the osteotomy also protects against additional
deformation caused by the Achilles
tendon21 and that
the lateral column lengthening corrects the deformity without overloading or
unloading the spring ligament. Most patients have reported satisfactory
results after these procedures, but triple arthrodesis remains an excellent
option, especially in a geriatric
patient22,23.
Flexor Hallucis Longus
The flexor hallucis longus passes from lateral to medial through a
fibro-osseous tunnel posterior to the medial malleolus and a groove in the
calcaneus. This fibro-osseous tunnel acts as a pulley. Disorders of the flexor
hallucis longus tendon are common in ballet dancers, athletes, and others who
perform activities involving an extreme range of ankle motion. These
activities may produce inflammation within the fibro-osseous tunnel, leading
to a painful stenosing tenosynovitis.
A disorder of the flexor hallucis longus is diagnosed on the basis of the
history and the findings of a physical examination. There is usually recurrent
posterior medial ankle pain, with a history of triggering and/or crepitus. In
ballet dancers, this is often exacerbated in the en pointe position.
The pain can be reproduced by active flexion of the great toe against
resistance. Radiographs are used to look for posterior impingement and os
trigonum syndrome.
Nonoperative treatment includes rest, nonsteroidal anti-inflammatory drugs,
physical therapy, and immobilization. Lidocaine injections within the flexor
hallucis longus sheath have been utilized to facilitate disruption of
adhesions, and pain relief has been
reported24.
Surgical treatment involves débriding the flexor hallucis longus
tendon with resection of any nodules or thickenings and repair of any tears.
An associated os trigonum is excised, and the pulley system is reconstructed.
Hamilton et al. noted that amateur dancers fared worse than did professional
dancers25. Kolettis
et al. found that all of their patients returned to dancing, and most returned
to full activity without
restrictions26.
Tarsal Tunnel Syndrome
Tarsal tunnel syndrome is pain in the foot due to compression of the tibial
nerve at the ankle. The tibial nerve passes behind the medial malleolus in the
tarsal tunnel. It is bounded by the flexor retinaculum medially and the
posterior process of the talus and the calcaneus laterally. The tibial nerve
divides into the medial plantar, lateral plantar, and medial calcaneal
branches. The branching of the nerve is variable, but the majority of the
branching occurs within the tarsal
tunnel27,28.
Tarsal tunnel syndrome is usually an idiopathic entrapment neuropathy of
the posterior tibial nerve and its terminal branches. Other causes of tarsal
tunnel syndrome include trauma, varicosities, fibrosis, and heel
valgus29.
Patients often describe tingling, burning, or numbness along the plantar
aspect of the foot, and, in one series, fifteen (71%) of twenty-one patients
were noted to have altered sensation to pinprick or
touch29. Percussion
along the nerve often reproduces the symptoms. In one
series29,
electrodiagnostic studies revealed positive findings in nineteen (90%) of
twenty-one patients, and, in a second series, they supported the diagnosis in
eighteen (82%) of twenty-two
patients30. A
negative result on electrodiagnostic studies does not exclude the diagnosis of
tarsal tunnel syndrome, which is made on the basis of a combination of the
history (pain, paresthesias, and numbness), findings on physical examination
(a positive Tinel or nerve compression test), and results of electrodiagnostic
studies.
When there is no evidence of a space-occupying lesion within the tunnel
compressing the nerve, nonoperative treatment includes nonsteroidal
anti-inflammatory or neuroleptic drugs, orthotics, physical therapy, and
immobilization. Failure of nonoperative management or evidence of a
space-occupying lesion is an indication for surgical intervention, which
consists of tarsal tunnel release and excision of any space-occupying
lesion.
Surgery should be recommended with caution, as a recent
review28 revealed a
perioperative complication rate of
30%30. Furthermore,
the results of revision surgery are not encouraging, with Skalley et al.
reporting that only five of thirteen feet did well after revision
surgery31.
Achilles Tendinitis
The Achilles tendon is the strongest tendon in the body. It is surrounded
by a peritenon without a definite tendon sheath. The blood supply of the
tendon arises distally from calcaneal arterioles and proximally from
intramuscular branches, and there is a hypovascular area 2 to 6 cm proximal to
the calcaneal
insertion32.
Achilles tendon disorders can be classified as non-insertional or insertional.
The most common chronic disorder of the Achilles tendon is tendinitis.
Non-insertional Achilles tendinitis usually occurs in the hypovascular
region33.
Overtraining or overuse is considered to be the most important factor
contributing to the development of Achilles
tendinitis34.
Repetitive trauma may lead to microtears within the
tendon34, and
rupture occurs with a prodromal phase in about 15% of individuals. Puddu et
al. described three
stages35: Stage I,
which is an inflammation of the peritenon (peritendinitis); Stage II, which is
peritendinitis with tendinosis; and Stage III, which is tendon degeneration
without inflammation of the peritenon or tendinosis.
The focus of nonoperative treatment has been on decreasing inflammation as
well as on diminishing the forces and movement of the tendon. These treatments
include physical therapy, nonsteroidal anti-inflammatory drugs, heel lifts,
night splints, and immobilization. Brisement (injection of saline solution and
a local anesthetic into the tendon sheath) has been proposed for the treatment
of acute Stage-I tendinitis. In one study, forty-one patients who had had
symptoms for an average of eighteen weeks were treated nonoperatively, and 51%
had resolution of the symptoms after eighteen weeks of
therapy36. Younger
patients (average age, thirty-three years) had better recovery than did older
patients (average age, forty-eight years).
Surgical management of non-insertional Achilles tendon disorders involves
treatment of the peritenon and the tendon as necessary. Treatment of
peritendinitis involves excision of the inflamed peritenon, and treatment of
peritendinitis with tendinitis or tendinosis involves excision of the inflamed
peritenon and tendon. Any nodules are débrided, and any tears are
repaired37. Puddu
et al. advocated longitudinal incisions into the tendon to promote
vascularization35.
Insertional Achilles tendon disorders are commonly associated with a
Haglund deformity, which is a prominence of the posterosuperior part of the
calcaneus. This prominence may lead to enlargement of the retrocalcaneal
bursa, and this complex then impinges on the inserting fibers of the Achilles
tendon, producing Achilles tendinitis and retrocalcaneal bursitis. Calcific
deposits may develop in the chronically inflamed tendon.
The Haglund deformity is seen on a lateral radiograph of the calcaneus
(Fig. 5), and two different
techniques have been proposed to evaluate it. Pavlov et al. described the
parallel pitch
lines38. With this
method, a lower line is drawn from the anterior tuberosity to the medial
tuberosity. A perpendicular line is then drawn to the posterior lip of the
talar articular facet. Another line, parallel to the lower line, is then drawn
from the perpendicular line. Any projection above the upper line is considered
to be abnormal (Fig. 6). Fowler
and Philip described the posterior calcaneal
angle39. With this
technique, a line is drawn from the anterior tuberosity to the medial
tuberosity, and another line is then drawn from the posterior bursal
projection to the posterior tuberosity. The angle of intersection of these two
lines is then measured. An angle of <69° is considered to be normal
(Fig. 7).
Nonoperative treatments of insertional Achilles tendon disorders are the
same as those for non-insertional tendinitis. However, the results of
nonoperative treatment of insertional disorders have not been as encouraging,
with thirty-nine of sixty-five heels in one study having failure of
nonoperative treatment after an average of sixty-two
weeks40. Surgical
treatment should address both the soft-tissue and the osseous abnormalities.
Excision of the superior calcaneal prominence and the retrocalcaneal bursa and
débridement and repair of the Achilles tendon are recommended. Calcific
deposits and areas of degeneration in the Achilles tendon are excised. In a
biomechanical study, it was found that 50% of the Achilles tendon could be
resected without risking rupture of the remaining
tendon41. If
>50% of the Achilles tendon is removed, transfer of the flexor hallucis
longus tendon is recommended to reinforce
it42.
Surgical treatment offers more favorable results than does nonoperative
treatment, with reports of excellent results in 50% of patients and good
results in 47%40.
In one series, almost 70% of the patients had complete pain relief; however,
14% had worsening of the
symptoms43.
Therefore, although surgical results are quite good, a number of patients
continue to have discomfort.
Os Trigonum Syndrome
The os trigonum is a secondary center of ossification of the talus lateral
to the groove for the flexor hallucis
longus44,45.
It may or may not be attached to the talus by a cartilaginous articulation. It
is present in 1.7% to 7% of normal
feet46. Os trigonum
syndrome usually affects athletes and ballerinas. Forced plantar flexion
causes impingement of the os trigonum against the posterior part of the tibial
plafond. Flexor hallucis longus tendinitis may develop.
Patients with os trigonum syndrome usually have the gradual onset of pain
in the anterior aspect of the retrocalcaneal space. Pressure over the
posterior lip of the talus can exacerbate the pain, and forced ankle plantar
flexion may reproduce the
pain47.
An os trigonum may be seen on plain radiographs of the hindfoot.
Computerized tomography scanning provides better visualization of the lesion.
Lateral radiographs made with the ankle in forced plantar flexion may
demonstrate posterior impingement. Magnetic resonance imaging may show bone
marrow edema within the os trigonum and fluid surrounding
it48,49
(Fig. 8). In a study of 100
soldiers, bone scintigraphy demonstrated increased uptake in the area of the
os trigonum in twenty-seven (14%) of the
feet50. However,
only ten of those twenty-seven feet had a symptomatic os trigonum. Therefore,
the diagnosis of os trigonum syndrome is made on the basis of a combination of
the history and physical and radiographic findings. Nonoperative treatment of
this condition includes restriction of activity, immobilization, and
nonsteroidal anti-inflammatory drugs. When these steps fail, surgical excision
of the os trigonum has had a generally favorable
outcome51.
Ankle Sprain
The most common injury of the lateral aspect of the ankle is a tear of the
anterior talofibular ligament. There are more than 27,000 ankle sprains daily
in the United States, and most are asymptomatic by eight weeks after the
injury. Approximately 20% of individuals who sustain an ankle sprain have
residual symptoms. Persistent symptoms may be manifestations of late effects
of the ligament injury itself or they may represent other pathological
entities.
Incomplete rehabilitation is a common reason for persistent pain following
an ankle sprain. Many patients benefit from participation in a structured
rehabilitation program. When the patient's condition fails to improve, other
sources of continuing symptoms must be sought. Residual pain may be caused by
chronic ligamentous instability, or an unrecognized injury of the subtalar
joint may be responsible for persistent symptoms after what was initially
diagnosed as an ankle sprain. Other entities that must be considered in the
presence of chronic anterolateral ankle pain following a sprain include
syndesmotic ligament sprain, sinus tarsi syndrome, chronic tendon dysfunction
or rupture, tendon subluxation, nerve injury, tumor, chronic regional pain
syndrome, and missed
fracture52,53.
As is the case with any diagnosis, the most important information derived
from an evaluation of what appears to be a simple sprain is the history of
injury and subsequent rehabilitation and treatment. One should also elicit
information regarding recurrent injury. In addition to evaluating the lateral
ligaments, the examiner should pay particular attention to the lateral process
of the talus, the anterior process of the calcaneus, the fibula, the talar
neck, the sinus tarsi, the Achilles tendon, the peroneal tendons, muscle
weakness, and heel varus. A bone scan may help to demonstrate an occult
fracture, and magnetic resonance imaging may be useful for demonstrating
soft-tissue lesions such as tendon abnormalities. If warranted by a positive
bone scan, a computerized tomography scan can be useful for locating and
defining subtle bone lesions such as loose bodies or fractures of the lateral
process of the talus or the anterior process of the
calcaneus52-54.
Chronic ankle instability may be mechanical and/or functional. Mechanical
instability implies mobility beyond the normal, physiologic range. This can be
observed on physical examination. Functional instability is the patient's
subjective sensation of the ankle giving way. When an ankle is mechanically
unstable, an anterior drawer test shows >10 mm of anterior translation or
an increase in translation of 3 mm in comparison with that on the
contralateral side. On inversion stress radiographs made with the ankle in
plantar flexion, the talus is seen to tilt >9° in the mortise or 3°
more than the talus is tilted on the other side. A functionally unstable ankle
may be symptomatic despite a normal, physiologic range of motion. The patient
reports a history of the ankle frequently giving way. This may be due to
muscle weakness, proprioceptive dysfunction, or an internal derangement of the
ankle such as an intra-articular loose body.
Surgery is indicated for chronic mechanical ankle instability if a
conservative program of treatment has
failed55-57.
Nonoperative treatment can emphasize functional treatment,
including58
peroneal muscle strengthening, ankle braces that prevent inversion of the
subtalar joint, or a small lateral heel wedge. Surgical repair has a poor rate
of success when the instability has been present for more than ten years or
the patient has an associated arthropathy, generalized hypermobility, or
uncorrected hindfoot varus.
There are two major types of surgical repair for chronic lateral ankle
instability: anatomic and nonanatomic. The anatomic repair that is used most
often is the Gould modification of the Brostrom
repair59. This
procedure shortens the anterior talofibular ligament and, if necessary, the
calcaneofibular ligament. It also reinforces these ligaments with the extensor
retinaculum. For nonanatomic repairs, part or all of a peroneal tendon, the
plantaris tendon, or a free tendon graft is used to reconstruct the lateral
collateral ligaments.
Subtalar Sprains and Instability
Subtalar sprains present with symptoms similar to those of ankle sprains.
They are often associated with injury of the calcaneofibular ligament, as this
is one of several ligaments stabilizing this joint. Clinical evaluation can be
difficult and may be unreliable. A patient with a subtalar sprain often
describes an inversion mechanism and may have difficulty or pain with walking
on uneven surfaces. The patient has tenderness on palpation of the sinus
tarsi, and there may be increased inversion or internal rotation of the
subtalar joint when compared with that on the contralateral, uninjured side.
This abnormal motion may be demonstrated with a Broden stress radiograph of
the ankle.
Conservative treatment of these injuries is similar to that of lateral
ankle sprains. In general, if conservative therapy is ineffective, repair of
the calcaneofibular ligament is recommended. Direct repair of the
talocalcaneal ligaments has been described. Tendon reconstruction of the
calcaneofibular ligament may be undertaken, and occasionally joint arthrodesis
is required60.
Sinus Tarsi Syndrome
Sinus tarsi syndrome may be a source of residual lateral ankle pain. The
syndrome is diagnosed when a patient has pain or tenderness in the sinus tarsi
region accompanied by the sensation of instability. The pain is thought to be
a manifestation of a residual synovitis from an injury to the interosseous
talocalcaneal ligament. Magnetic resonance imaging may be helpful for
clarifying this diagnosis.
Treatment is aimed at the symptoms, and injection of a local anesthetic and
corticosteroids is successful in two-thirds of
patients61. If
injections are not effective and no other diagnosis is evident after a
thorough investigation, surgery may be considered. Excision of the contents of
the sinus often relieves
pain61.
Anterior and Anterolateral Impingement
Both osseous and soft-tissue lesions may be responsible for anterior ankle
pain associated with dorsiflexion. The osseous phenomenon
(Fig. 9) was well described in
the middle of the last century and has been referred to as footballer's
ankle. It is manifested by anterior tibial and/or talar osteophytes. In
addition to causing pain with ankle dorsiflexion, these osseous lesions can be
painful on direct palpation.
Soft-tissue impingement is often seen following multiple ankle sprains or a
single high-grade sprain and is characterized by pain at the anterolateral
aspect of the
ankle52,53,62.
The findings on plain radiographs are usually normal, but magnetic resonance
imaging may demonstrate thickening of the anterolateral capsule. The distal
fascicle of the anterior inferior tibiofibular ligament may impinge on the
anterolateral aspect of the talus. Well-organized scar tissue can develop
after an injury. This has an arthroscopic appearance similar to that of a
meniscus of the knee and is referred to as a meniscoid
lesion53
(Fig. 10). Anterior
impingement can be treated conservatively with physical therapy and shoe
modifications. A heel-lift decreases ankle dorsiflexion and reduces symptoms.
Surgical treatment of the lesion includes osseous or soft-tissue
débridement, either arthroscopically or with an open
procedure62.
Nerve Injury
Nerve injury is an uncommon source of anterior or lateral ankle pain, but
it does occur. The superficial peroneal, deep peroneal, or sural nerve may be
injured from direct trauma, traction, or
compression63.
Symptoms may include local tenderness accompanied by burning and a positive
Tinel sign. An injection of local anesthetic may be used as a diagnostic tool.
Desensitization and the use of amitriptyline or Neurontin (gabapentin) can
help to reduce symptoms. Surgical decompression or neurectomy and burial of
the nerve ending in soft tissue or bone may be effective, but neurectomy
leaves an area of decreased sensation distally.
Peroneal Tendon Lesions
Peroneal tendon ruptures are rare. Of the two peroneal tendons, the
peroneus longus ruptures more frequently. The patient reports having
experienced acute pain and hearing a pop after an
injury64. The event
may be confused with a ligament injury. Physical examination reveals swelling
and tenderness over the posterior aspect of the distal part of the fibula or
between the tip of the fibula and the base of the fifth metatarsal. Resisted
eversion produces pain, and eversion strength is diminished.
A plain radiograph may show a fracture of the os peroneum or a change in
the position of the os peroneum, both of which provide indirect evidence of a
peroneus longus rupture. Magnetic resonance imaging is the best imaging
technique for demonstrating this lesion and will usually demonstrate tendon
tears.
Peroneus longus tears are best treated surgically; however, custom braces
can be used for patients who are not surgical candidates. Direct repair of the
tendon may be possible, but resection of the torn or scarred segment or a
fractured os peroneum may be necessary. Following resection, tenodesis of the
proximal and distal segments to the peroneus brevis is indicated.
Peroneus brevis tears are usually chronic and longitudinal. These tears are
referred to as split tears and are generally located at the tip of
the fibula65
(Fig. 11). The injury may be
associated with chronic ankle instability. Retromalleolar swelling and
tenderness are found on physical examination. Chronic split tears of the
peroneus brevis tendon are seen on axial magnetic resonance imaging of the
ankle. Treatment may be nonoperative or operative. Nonoperative treatment does
not result in an anatomically healed tendon, but it may alleviate symptoms. It
consists of administration of nonsteroidal anti-inflammatory drugs,
immobilization, and use of shoe modifications such as a lateral heel-wedge or
outflare. Surgical treatment begins with débridement of small tendinous
strips and tenosynovium and may include repair of split tears and
tubularization of the tendon remnant.
The differential diagnosis should also include dislocation or subluxation
of the peroneal tendon. An acute dislocation may be confused with a routine
ankle sprain. In the presence of an acute dislocation, pain is located
posterior to the lateral malleolus and the patient may complain of a painful
sensation, sometimes with snapping. Some investigators think that a shallow
retromalleolar groove may predispose a patient to these problems. With the
initial injury, the superior peroneal retinaculum may be elevated off of the
lateral malleolus and a small avulsion fracture from the retinacular
attachment to the fibula may be observed. Chronic symptomatic dislocation
requires surgical repair, and numerous approaches have been described, with
the most common being direct repair of the superior peroneal retinaculum.
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