Download Musculoskeletal problems of the foot and ankle :: Baggett

Travis Baggett
30 June 2006
Musculoskeletal problems of the foot and ankle:
An overview of soft tissue and joint topics
I. Tendon, ligament, and fascia: Soft tissue syndromes of the foot
Plantar fasciitis
The plantar fascia of the foot forms a thick aponeurosis which attaches to the medial
tuberosity of the inferior calcaneus and fans out to insert upon each of the proximal
phalanges. It forms the longitudinal arch of the foot and functions as a shock absorber as
well as being integral in intrinsic foot dynamics while walking and weightbearing. Strain
of the plantar fascia typically occurs in the setting of repetitive microtrauma associated
with running or jumping, prolonged standing, obesity, and pes planus or other mechanical
foot issues predisposing to prolonged or excessive pronation. Rarely, plantar fasciitis can
be associated with systemic inflammatory diseases such as rheumatoid arthritis, gout, or
ankylosing spondylitis. While the term fasciitis seems to imply inflammation, biopsy
specimens in patients with the plantar fasciitis clinical syndrome have demonstrated
degeneration of fibrous tissue with or without inflammatory change. Heel spurs may be a
predisposing factor to, or a sequel of, plantar fasciitis, with new bone formation at the
insertion point on the anterior inferior calcaneus.
The classic clinical presentation is that of a runner, or alternatively an obese patient, who
reports anterior plantar surface heel pain that is characteristically worse with the “first
step” out of bed or with initiating walking after rest. Pain initially improves with
ambulation then worsens again with continued activity. Patients may have pes planus or
heel spurs as predisposing factors.
On exam, there is pain on palpation of the anteromedial aspect of the plantar surface of
the heel, which is heightened by holding the toes in dorsiflexion with the other hand.
Laboratory tests are not typically helpful in making the diagnosis, and imaging is not
usually needed unless there is clinical concern for ruling out calcaneal fracture or other
bony abnormalities. If conservative therapy fails, then plain radiography with lateral and
axial views is recommended to rule out an alternative process. Other available imaging
modalities include MRI, ultrasound, and stress scintigraphy.
Conservative therapy results in improvement in the vast majority of cases, despite the fact
that most noninvasive modalities have only limited data supporting their effectiveness.
Rest and icing is helpful for pain relief, and NSAIDs are recommended although their
efficacy has not been well-studied. Interventions to address obesity and symptomatic flat
feet help target predisposing factors. Cases associated with systemic inflammatory
diseases of course benefit from therapy targeting the disease of concern. Exercises and
various physical therapy modalities are other options. Silicone heel pads may add further
benefit. Use of athletic or supportive shoes and avoidance of any repetitive motions
which may have triggered the process are also recommended.
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If these conservative measures fail despite several weeks of concerted effort, then other
modalities may be explored. Corticosteroid injections into the plantar fascia have
demonstrated improvement in symptoms at one month, but not at six months. Plain films
are recommended prior to injection to rule out underlying tumor. Side effects include
increased risk of plantar fascia rupture and fat pad atrophy. Extracorporal shock wave
therapy is another option, although the data is mixed and perhaps suggestive of limited
efficacy at best. Surgical interventions are typically reserved for recalcitrant cases.
Techniques include heel spur resection, calcaneal drilling, stripping of the plantar fascia,
partial plantar fasciectomy, and neurolysis.
Achilles tendonitis and Achilles tendon rupture
The Achilles tendon is formed from the convergence of muscle fibers constituting the
gastrocnemius and soleus muscles of the calf and inserts into the superior aspect of the
calcaneus. As such, it serves an integral role in plantar flexion of the foot. Inflammation
or injury results in a clinical syndrome termed Achilles tendonitis. Rupture of the
Achilles tendon may also occur. Achilles tendonitis is typically due to overuse in
association with suboptimal footwear, a change in playing surface quality, or highly
intense activity. Fluroquinolone use has been shown to carry an increased risk of
Achilles tendonitis. Enthesopathies or calcific tendonitis, typically in association with
more systemic imflammatory disease states, may also affect the Achilles tendon and are
discussed elsewhere. Achilles tendon rupture occurs in association with chronic Achilles
tendonitis, history of steroid injection in or around the Achilles tendon, and extreme
stress of the tendon during intense physical activity with abrupt contraction of the calf
muscle.
Patients with Achilles tendonitis are usually physically active and typically present with
pain over the posterior aspect of the heel along the course of the Achilles tendon 2-5cm
from the calcaneus. Pain is exacerbated by dorsiflexion of the foot, and a friction rub of
“wet leather” may be palpated over the tendon during passive dorsiflexion and plantar
flexion. Resisted plantar flexion of the foot will exacerbate the pain. Bilateral tendonitis
is suggestive of a systemic rheumatic disease or fluoroquinolone use.
Achilles tendon rupture characteristically produces a sharp, memorable, intense pain in
the posterior heel or distal posterior leg, with the patient feeling as though they have been
“shot,” “kicked,” or “cut.” On exam, active plantar flexion is weak or absent. A
Thompson test is performed by squeezing the posterior calf with the patient laying prone
and the knee passively flexed, or with the patient kneeling on a chair. Failure of plantar
flexion of the foot with this maneuver is considered a positive test for Achilles tendon
rupture.
Labs are generally unnecessary unless there is clinical suspicion for a systemic
rheumatologic disease. Imaging is also typically unnecessary, unless for the purpose of
ruling out alternate pathology of the lower leg, heel, or foot. Plain films are best utilized
in discerning any underlying bone or joint process. MRI may be most useful in teasing
out Achilles tendinitis versus a partial rupture of the tendon. Ultrasound is helpful in
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determining the presence of a DVT or a Baker’s cyst, although in experienced hands may
also provide a diagnosis of Achilles tendon rupture if present or distinguish between full
and partial thickness tears.
Treatment of Achilles tendonitis involves gentle stretching exercises, massage
techniques, alteration in exercise habits which may have predisposed to the injury, and
use of heel inserts or orthotic foot devices. NSAIDs can be used for pain management.
Topical glyceryl trinitrate ointment also showed improvement in pain symptoms in a
placebo-controlled trial. Corticosteroid injection is controversial and should be done only
under fluoroscopy in patients with ongoing symptoms despite close adherence with
conservative measures. Risks include increased risk of future tendon rupture.
Percutaneous longitudinal tendonotomy may be helpful in select rare cases.
Treatment of Achilles tendon rupture includes initial crutch ambulation with no weightbearing. Subsequent management options include serial casting versus surgical end-toend repair. Overall the rates of healing are similar, although nonoperative management
with serial casting appears to be associated with higher rates of repeat rupture.
Posterior tibial tendonitis
The tibialis posterior tendon arises from the large muscle units of the posterior tibia,
fibula, and interosseous membrane, and courses down posterior to the medial malleolus
which acts as a lever point, and inserts into various bony structures on the base of the
foot. Its primary function is to stabilize the hindfoot and midfoot against eversion forces,
maintaining the arch and preventing chronic pronation. Posterior tendonitis is
characterized by inflammation and dysfunction of the tibialis posterior, resulting in pain
along the medial ankle and subsequent flattening of the arch on the affected side if
unchecked. The inflammation is typically due to repetitive trauma, as in other forms of
tendonitis, although can be associated with systemic inflammatory diseases such as
rheumatoid arthritis as well.
A characteristic presentation is that of either an obese middle-aged female or a
competitive athlete with pain around the medial malleolus that is worse with prolonged or
strenuous activity. Exam reveals swelling over the medial ankle with tenderness to
palpation along the course of the tibialis posterior tendon, typically most prominent just
behind the medial malleolus. Patients with later stages of disease may demonstrate pes
planus. Pain will be heightened by having the patient stand upon their tip toes. Failure of
inversion of the heel when doing so indicates tibialis posterior insufficiency or rupture.
Imaging studies include plain radiographs of the foot and ankle to rule out bony
pathology. MRI, ultrasound, and scintigraphy are other modalities, although their role
has yet to be well-defined. MRI may be useful in determining the presence of fractures
not seen on plain radiograph, or if operative repair is planned, to assess the extent of
tendon degeneration.
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Conservative therapy with immobilization in a short leg cast or plastic boot for 2-3 weeks
will result in pain relief in most cases. NSAIDs are helpful in mediating pain symptoms,
and passive stretching may improve mobility. Steroid injections, as in the treatment of
Achilles tendonitis, are controversial due to the increased risk of subsequent tendon
rupture and recommendations on this are mixed. Operative measures are reserved for
recalcitrant cases. Methods of intervention include tendon sheath release, excision of
scar tissue, partial synovectomy, and tendon sheath endoscopic techniques. In the case of
posterior tendon rupture, surgical options include end-to-end re-anastamosis, primary
reattachment to its insertion site, tendon reconstruction, tendon transfer, or arthrodesis.
Enthesitis / enthesopathy
Enthesopathy, often used interchangeably with the term enthesitis, refers to inflammation
of the entheses, or sites of insertion of ligaments, tendons, fascia, or other soft tissue
structures into bones. While it can occur at any site in the body, it not uncommonly
occurs in the foot and ankle, with typical sites of presentation including the achilles
tendon insertion point on the posterior superior calcaneus or the plantar fascia insertion
point at the medial inferior tubercle of the calcaneus, producing marked tenderness and
pain at these locations. Alternatively, involvement of the phalanges of the foot can
produce diffuse toe swelling leading to a "sausage digit" effect with little pain. Unlike
the previously discussed soft tissue syndromes of the foot, this entity is relatively specific
for systemic rheumatic disease, namely spodyloarthropathy, with a strong association
with the presence of the HLA-B27 haplotype. Sausage digits can also be seen in psoriatic
arthritis. An iatrogenic cause of enthesitis should be considered in patients taking
fluoroquinolones.
Patients present with the above complaints or physical features. The clinical appearance
will be similar to that of achilles tendonitis or plantar fasciitis, although the presence of
bilateral symptoms or other arthropathies, including back pain, knee, hip, shoulder, or
hand involvement, should clue the physician in to a more systemic process. Laboratory
work-up should be directed at assessment for possible spondyloarthropathy, including
sacroiliac imaging and possibly testing for HLA-B27 as well as non-specific markers of
inflammation such as ESR and CRP. Plain radiographs of the foot may reveal spurring or
calcification at the affected entheses from new bone formation at the site inflammation.
Treatment of enthesopathy should ultimately be directed at the underlying
cause. Local pain relief measures, including use of NSAIDs, will be similar to
those in Achilles tendonitis and plantar fasciitis.
Ankle sprain
Ankle sprain refers to injury of the ligamentous structures anchoring together the multiple
bones of the foot. They are classified anatomically as lateral, medial, or high
(syndesmotic). Lateral ankle sprain is the most common sprain pattern, and typically
results from inversion of the foot resulting in strain of the lateral ligament complex. The
lateral ligament complex consists of three ligaments which insert on the anterior and
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posterior talus and the calcaneus. The anterior talofibular ligament is the most commonly
injured. Medial ankle sprains affect the medial deltoid ligament complex, and typically
occur with a lateral insult resulting in forced eversion of the ankle. Because the medial
deltoid ligament is mechnically quite strong, medial sprains rarely occur. When a
sufficient enough force is sustained to overcome the strength of the ligament, then
fracture of the medial malleolus typically accompanies. A high, or syndesmotic, ankle
sprain refers to injury to the anterior, transverse, and posterior tibiofibular ligaments or
the interosseous membrane, typically occurring in the setting of forced eversion and/or
dorsiflexion of the ankle. All structures are vital to ankle stability. Ankle sprains are
graded in severity on a scale of I to III. Grade I injuries are characterized by mild
stretching with microscopic tears. Grade II involves an incomplete tear of the ligament,
and grade III denotes complete tear.
Patients will present with a characteristic history of pain that is sudden in onset and
triggered by a precipitating event. The mechanism of injury will help in identifying the
ligament complex most likely injured. Exam may be notable for swelling and
ecchymoses of the ankle. The thrust of the physical exam is not only to help identify the
injured area, but to determine the need for imaging to rule-out fracture. The entire foot,
as well as the fibula, distal tibia, and Achilles tendon should be palpated. Active and
passive range of motion as well as weight-bearing status should all be assessed. The
“squeeze test” involves squeezing the fibula against the tibia at the mid-calf level. A
positive test will produce pain at the anterior tibiofibular ligament when a syndesmotic
sprain is present. Similarly, pain at the site of the anterior tibiofibular ligament with
forced external rotation of the foot with the leg held in a neutral position is indicative of a
syndesmotic sprain. Anterior drawer test of the ankle is performed to determine
compromise of the anterior talofibular ligament as seen in lateral ankle sprain. The test is
performed by stabilizing the lower leg with one hand while providing gentle forward
thrust with the other hand cupping the heel. In anterior talofibular injury, there will be
greater anterior movement, although this test may not be reliable acutely due to severe
pain, swelling, and spasm of surrounding musculature. Also of limited utility acutely is
the talar tilt test, which assesses the degree of permissive inversion of the foot while
stabilizing the lower leg. An exaggerated degree of inversion when compared to the
uninjured side suggests compromise of the calcaneofibular ligament in the setting of
lateral ankle sprain.
The Ottawa ankle rules are frequently used in determining the need for radiographic
imaging in the setting of traumatic ankle or foot injury. According to these rules, plain
films of the ankle are indicated only if a patient has malleolar pain with tenderness to
palpation over the distal tip or posterior edge of either mallelous, or malleolar pain with
inability to bear weight immediately after the injury and for four steps in the ED. Plain
radiographs of the foot are indicated only if the patient has midfoot pain with tenderness
to palpation over the base of the 5th metatarsal or the navicular bone, or midfoot pain with
inability to bear weight immediately after the injury and for four steps in the ED. Plain
films are obtained primarily to rule-out underlying fracture. MRI should be obtained
only in the event of ankle pain refractory to 6 to 8 weeks of conservative management.
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Management strategies for lateral (and far less commonly medial) ankle sprains without
fracture or neurovascular compromise include rest, ice, elevation, compression, and early
mobilization. NSAIDs are useful for controlling pain. Some evidence suggests that
“Aircasts” may be superior to standard elastic bandage wraps in providing therapeutic
compression and ankle support. Range of motion and strengthening exercises are crucial
to recovery and prevention of long-term ankle instability and should be initiated early,
even in grade III sprains. Immobilization is rarely required and should not be routinely
recommended. Ultrasound, laser therapy, and hyperbaric oxygen all appear to be
ineffective. The benefits of and role for surgery in lateral ankle sprain is disputed, but
surgical repair of ligamentous injury is very rarely undertaken. Candidates for operative
intervention may include competitive athletes with severe sprains and a high likelihood of
recurrent injury. Referral to an orthopedist should be made for any patient with a
syndesmotic ankle sprain.
II. Joint and bursa: Arthritis and bursitis syndromes of the foot
Inflammatory arthritides
Inflammatory arthritides capable of affecting the foot and ankle are many, and include
rheumatoid arthritis, the spondyloarthropathies (ankylosing spondylitis, psoriatic arthritis,
Reiter’s syndrome, and IBD-associated arthritis), and inflammatory arthritides associated
with connective tissue diseases (SLE, scleroderma, MCTD, Sjogren’s, and
polymyositis/dermatomyositis). While the pathophysiology and corresponding work-up
is unique in each disease state, the pattern of symptoms will be generally similar in that
joint manifestations will be most prominent in the morning with significant stiffness that
characteristically improves with activity through the day. Since these are all systemic
inflammatory disease states, other locales of arthritis and/or other evidence of end-organ
involvement will generally be apparent.
Rheumatoid arthritis bears some dedicated discussion since it represents the most
common and most severe inflammatory arthritis capable of affecting the foot. Diffuse
involvement of the metatarsophalangeal joints is characteristic, as well as the toes and
hindfoot to a lesser extent. Exam may be notable for soft tissue swelling of the
surrounding area, with tenderness to palpation as well as fullness or overt effusion. In
more advanced stages of disease, dorsal subluxation with upward displacement of the
toes – the so-called “cock-up deformity” – may occur. Hallux valgus deformity and
lateral drift of other toes, as well as flexion deformities at the interphalangeal joints, may
also result. Involvement of the ankle will produce swelling around the tibiotalar joint.
Diffuse erythema and edema over the dorsum of the foot may herald tarsal involvement.
Laboratory testing should be guided by clinical suspicion based on the history and
physical examination. Radiographic findings will vary depending upon the underlying
disease process. In RA, bony erosions may be apparent, in addition to the later-stage
joint changes discussed above in more advanced disease. The arthritis associated with
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connective tissue disease states, however, is typically nondestructive, and plain films may
appear normal.
The management of inflammatory arthritis pain of the foot is guided by the underlying
disease process. In general, anti-inflammatory medications such as NSAIDs and steroids
are effective in mitigating severe pain, but do not mediate the underlying diseaseprocesses themselves. Disease-specific therapy is ultimately necessary for modulating
progression.
Crystal arthropathies
The crystal arthropathies are a group of disorders in which mono- or oligo-articular
arthritis is induced by intra-articular deposition of crystals leading to acute joint
inflammation. The crystal-induced arthritides include gout, calcium pyrophosphate
deposition (CPPD), and less commonly hydroxyappatite deposition and calcium oxalate
deposition. While all can present with foot involvement, gout is the most commonly
occurring and clinically important crystal-induced arthritis involving the foot. Gouty
arthritis is precipitated by tissue deposition of monosodium urate crystals in the
synovium, leading to inflammatory and degenerative consequences. The classical
location is in the MTP of the great toe (known as “podagra”), but other joints in the foot
and ankle can also be involved. Precipitants of an acute gouty attack include purine loads
(as in some meats), alcohol, surgery, infection or other metabolic stress states,
dehydration, and diuretic use (especially thiazides). A chronic sequel of recurrent gout is
tophi formation with deposition of urate in soft tissues. Adjacent bony erosions may
occur in the setting of chronic tophi.
Patients will classically be middle-aged obese white males with acute-onset joint
monoarticular joint inflammation. One of the above precipitants may be elicited on
history. Exam reveals an exquisitely tender joint that patient is apprehensive to have
moved or manipulated. An effusion will be present, with erythema and warmth of the
overlying skin. Patients are not infrequently febrile and ill-appearing. Arthrocentesis
will reveal synovial fluid with negatively-birefringent needle-shaped crystals when
examined under polarized microscopy. Cell counts of the fluid can demonstrate 20,000 –
100,000 WBCs/hpf with greater than 50% PMNs. A gram stain and culture should
always be performed to rule-out septic arthritis, which can coexist with an acute gouty
flare. Blood laboratory tests may demonstrate leukocystosis, an elevated sedimentation
rate, and an elevated uric acid level, although this is not specific for the diagnosis of an
acute attack. Plain films of may demonstrate an effusion and/or rule-out an underlying
fracture as a potential alternative or coexistent cause for monoarticular inflammation.
Plain films in chronic tophaceous gout may reveal bony erosions with an overhanging
edge. These occur adjacent to tophi, which are radiographically lucent unless secondarily
calcified.
Management of an acute attack involves use of NSAIDs, colchicine, or steroids (systemic
or intrarticular). Chronic management involves decreasing urate production by avoiding
foods high in purines, alcohol, dehydration, and drugs known to cause hyperuricemia.. If
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attacks are frequent, chronic medical prophylaxis with hypouricemic agents may be
necessary. Therapies include allopurinol, a xanthine oxidase inhibitor, and probenicid or
sulfinpyrazone, which are uricosuric agents for under-excretors of uric acid
(<600mg/day).
Osteoarthritis
Osteoarthritis is degenerative joint process characterized by articular cartilage failure
with osteophyte formation, subchondral sclerosis, and an array of biomechanical
alterations of the synovial membrane and joint capsule. Primary OA is idiopathic in
nature without an identifiable predisposing cause and characteristically affects the
fingers, hips, knees, and spine, but can also involve the feet and ankles. Foot
involvement in systemic OA is traditionally in the first metatarsophalangeal joint, and
may result in valgus or rigid deformities of the great toe. Less commonly OA may affect
the subtalar joint, which creates difficulties with weight-bearing and inversion or eversion
of the foot. Secondary osteoarthritis occurs in response to an identifiable trigger, such as
trauma, metabolic conditions, anatomic factors, or as a sequel of a prior inflammatory
insult to the joint(s). Secondary OA of the foot typically occurs in the aftermath of joint
damage due to trauma or prior inflammation. OA occurring in uncharacteristic portions
of the foot without a history of trauma should prompt investigation for other systemic
diseases, namely acromegaly, CPPD, hydroxyappatite deposition disease, ochronosis, or
epiphyseal dysplasia.
Patients with OA of the foot will present with pain that is characteristically worse with
activity. Morning pain and stiffness may be present but typically resolves within thirty
minutes to an hour and is less significant than the pain brought about later in the day with
activity. Labs are helpful only in so far as they may exclude an inflammatory arthritis or
one of the less common disease processes mentioned above. Plain radiographs will
demonstrate articular space narrowing, bony eburnation, osteophyte formation, and
subchondral cysts. Dorsal osteophytes are typically seen when hallux rigidis deformity is
present.
Management is largely conservative. Anti-inflammatory medications may be useful for
pain control. Weight reduction and use of supportive footwear help to address the
mechanical stress upon the foot. Surgical options include fusion of one or more joints,
and repair of hallux valgus or hallux rigidis deformities.
Retrocalcaneal bursitis and Haglund’s syndrome
The retrocalcaneal bursae both overlie and underlie the insertion point of the Achilles
tendon onto the posterior calcaneus, and are termed the subcutaneous and subtendinous
bursae respectively. Inflammation of these bursae with repetitive trauma or friction can
lead to painful posterior heel pain. This may be commonly associated with a prominent
superior calcaneal tubercle, which is termed Haglund’s syndrome.
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Patients present with posterior heel pain that is gradual in onset and aggravated by
activity or certain footwear. There is typically start-up pain after resting or upon getting
out of bed in the morning. Exam will reveal swelling and tenderness over the posterior
heel in the area of the Achilles insertion. Occasionally the inflamed fluid-filled bursa can
be balloted, which should be distinguished from the more diffuse swelling seen in
Achilles tendonitis. Dorsiflexion of the foot will typically aggravate the pain. In the case
of Haglund’s syndrome, a bony prominence is apparent on the posterior heel. The
diagnosis is clinical and requires no specific laboratory or radiographic work-up, unless
to exclude calcaneal fracture if suspected.
Management includes use of heel cups or heel padding to raise the heel, shoes with laces
or straps that provide a good fit with minimal heel counter-friction and sliding, backless
shoes, or a heel counter with a V-shaped or U-shaped cutout to minimize friction.
Corticosteroid injections into the bursa, being careful to avoid injecting through or into
the Achilles tendon may be considered, although should be performed by an experienced
provider. Immobilzation of the foot in a removable cast for 2 weeks following injection
is recommended due to the residual risk for tendon rupture even when the tendon is not
injected, due to the close location of the bursa to the Achilles tendon itself. Surgical
resection of the bony prominence in Haglund’s syndrome may be considered in refractory
cases.
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