type may be associated with a Haglund deformity or retrocalcaneal
bursitis. This is a typical overuse injury caused by accumulated impact
load (1), which occurs most often in runners
and repetitive jumpers. Insertional type occurs more in an older age
group than does noninsertional tendinopathy.
Treatment should be conservative
in 95% of cases. Rest, analgesics, cross training, physiotherapy,
orthotics with a heel lift, and, occasionally, casting should be used.
Steroid injections are very seldom indicated. (2,3).
indicated after 6 to 12 months of failed conservative treatment.
Surgery consists of the following: excise retrocalcaneal bursa, resect
superior prominence, and debride diseased or calcified portion of the
tendon. Reattach if necessary. The patient should be non–weight bearing
for 6 to 8 weeks. Rehabilitation is resumed but recovery might take up
to 1 year. Success rate is 70% to 86%. (4)
type is associated with typical hypovascular zone 2 to 6 cm proximal to
insertion. The etiologic profile includes repetitive microtrauma, more
common in males, older athletes, tight gastrosoleus and hamstrings,
functional overpronation. Extrinsic factors include improper training,
improper shoe wear, systemic or injected steroids, and fluoroquinolone
antibiotics (5). There are various
classification systems that could be simplified into peritendinitis
(sheath only), tendinosis (tendon only), or pantendinitis (sheath and
tendon) (6). Diagnosis is primarily by history
and clinical evaluation and is confirmed with ultrasound (operator
dependent) or magnetic resonance imaging (MRI). Typical signs and
symptoms are morning stiffness or pain, start-up pain, postexercise
pain, and tendon fullness or nodule.
Treatment in acute
situations includes pain relief, analgesics, ice, and restriction of
activities. A heel lift or boot brace can be used until symptoms
subside (2), followed by a rehabilitation program (7).
Other measures include stretching and strengthening of the Achilles and
gastrosoleus, eccentric muscle-tendon strengthening review, and
modification of training regimens (reduce frequency, duration, and
intensity and focus on low-impact activities), correction of structural
abnormalities (overpronation), and modifications in foot wear.
Treatment is 90% to 95% successful, but it usually takes 2 to 6 months
to recover from an Achilles tendinopathy.
Treatment of chronic
cases (>3 months) depends on severity. Peritendinitis is treated
with mechanical “brisement” or surgical debridement followed by an
early rehabilitation program (7). Chronic pantendinitis is treated with debridement, longitudinal tenotomy (8),
or tendon transfer depending on the clinical situation. It appears from
the literature that surgical treatment of chronic tendinitis might do
better than nonoperative treatment.
jumping place repetitive stress on the heel and create an overuse
syndrome with chronic inflammation.
To differentiate, a thorough history and examination is required. This
should include exact location and duration of pain and the relationship
athletic activity. Chronic pain at rest is unusual and might be due to
a tumor. The differential diagnosis includes the following:
Plantar fasciitis—by far the most common reason for plantar heel pain
Fat pad atrophy
Tendinopathy of flexor hallucis longus or flexor digitorum brevis
could be at insertion into medial calcaneal tuberosity or midfoot and
may be due to repetitive traction and microtears. Usually, plantar
fasciitis has an insidious onset as an overuse condition in long
distance runners. Midfoot plantar fasciitis is more common in sprinters
who run on their toes.
Symptoms and signs
include pain during the first minutes of walking, especially when first
getting out of bed. Pain may subside with low-intensity walking but
then recur with prolonged or more vigorous activities.
Always evaluate for leg length discrepancy.
Heel pain is more common in the shorter leg and may be treated with an
appropriate lift. Also inquire about a functional short leg syndrome
from running on the same tilt of the road. Plantar fasciitis is
frequently caused by a shortened Achilles tendon because limited ankle
dorsiflexion increases the stress on the plantar fascia. Fasciitis at
the insertion has localized deep tenderness. It is usually not
associated with increased pain or with passive dorsiflexion of the toes
(windlass mechanism). Midfoot fasciitis has tenderness in midfoot and
increased pain with passive dorsiflexion of the toes. Passive
dorsiflexion of the big toe aggravates both plantar fasciitis and
flexor hallucis longus tendinopathy. Resisted flexion of the big toe is
painful only with involvement of the tendon.
The cornerstone of treatment is modification in training, for example,
reducing mileage, shortening workouts, and alternating activities such
as low resistance cycling and swimming pool running (9). There is not a single entity that works for everyone, but conservative measures usually include the following:
A shock-absorbing heel cup for heel pain
or a full length orthotic or UCBL (University of California Berkeley
Laboratory) orthotic for midsubstance pain.
Though not proven uniquely effective, analgesics, as they do decrease pain.
Physical therapy to include Achilles and plantar fascia stretching, hindfoot taping, contrast baths, and ultrasound treatment.
A night dorsiflexion splint might help to keep the fascia under tension to reduce early morning weight-bearing pain.
Injections may be used in refractory
cases. This has historically been done with steroids, although steroids
pose a risk of plantar fascia rupture. Consistent with the fact that
this has been noted to be a degenerative rather than an inflammatory
process, there is no data demonstrating that the anti-inflammatory
component of the steroid is necessary. For these reasons, many
physicians are moving away from injections, or injecting but without
the steroid component.
Shockwave therapy, which tries to spur on inflammatory response, might prove to be helpful in the future.The heel spur seen on roentgenograms is seldom, if ever, the cause of heel pain.
Plantar fascia release should be avoided in competitive athletes
because it may increase the compressive forces to the dorsal aspect of
the midfoot and decrease flexion forces on the metatarsophalangeal
joint complex (10). When indicated, the plantar
fascia is released from the calcaneus through a medial incision. The
patient is allowed to bear weight as tolerated with crutches, and
rehabilitation is started after 2 weeks.
Calcaneal fat pad trauma.
The patient complains of diffuse plantar heel pain that is exacerbated
with weight bearing and with activities on hard surfaces.
reveals diffuse tenderness localized to the fat pad. There is no
radiation of the pain. The heel pad feels soft and thin, and the
underlying calcaneus is palpable.
nonsurgical. A cushioned heel cup and shock-absorbing shoes might help.
The patient should reduce activities and avoid hard running surfaces.
Nerve entrapment syndromes
Entrapment of the first branch of the lateral plantar nerve is a common cause of chronic heel pain in athletes (11).
The site of compression is between the deep fascia of the abductor
hallucis muscle and the medial margin of the quadratus plantae muscle.
This injury is more common in athletes who spend a significant amount
of time on their toes such as ballet dancers, figure skaters, and
made on clinical grounds. Exclude the more common reasons for heel
pain. Early morning pain is less problematic; the pain increases as the
day goes on. Tenderness is specific over the area of compression and
may radiate down toward the toes (the Tinel sign).
similar to that for other causes of heel pain. If conservative
treatment fails, a release of the nerve may be done through a medial
Tarsal tunnel syndrome
could also be a source of heel pain. Compression of the posterior
tibial nerve within the tarsal tunnel results in tenderness over the
area that may shoot down toward the toes on the plantar aspect of the
foot. Excessive pronation in long-distance runners may place repeated
stress on the medial structures of the hindfoot.
there might be burning, pain, or tingling on the plantar aspect of the
foot. Pain is more diffuse than with the other causes of heel pain.
Electromyography and nerve conduction studies can be helpful but are
not always sensitive enough.
medial heel wedge or an arch support may decrease the tension on the
medial side of the ankle and therefore the nerve. Physical therapy can
also improve the biomechanics. Steroid injection into the tarsal tunnel
might give short-term pain relief. Tarsal tunnel release is helpful in
Metatarsalgia or pain over the metatarsal
heads is the most common forefoot problem. It typically occurs on the
second metatarsal head and can have numerous etiologies.
A tight or shortened Achilles tendon
limits ankle dorsiflexion, which, in turn, increases the forces on the
forefoot. A person compensates by using the long toe extensors to
augment dorsiflexion power, but this pulls the plantar fat pad away
from the weight-bearing surface under the metatarsal heads, further
aggravating forefoot pain.
Similarly, idiopathic claw toe deformities could displace the fat pad and cause metatarsalgia.
Metatarsophalangeal joint capsulitis
might cause pain over the plantar aspect of the joint. This is more
common at the second metatarsophalangeal joint and is associated with a
long second metatarsal or instability of the first ray.
A Morton (or common digital nerve) neuroma causes pain in the web space and is most common in the third web space (between the third and fourth metatarsals).
The differential diagnosis of midfoot to forefoot pain always includes stress fractures (see IV below)
The goal is to unload the metatarsal area. Orthotics, metatarsal bars,
cushioned shoes, analgesics, and Achilles stretching are the
cornerstones of initial management. If conservative management does not
help, surgical correction of claw toes or excision of neuroma might be
of a painful, acquired flatfoot deformity in adults. It is more common
in women 40 years of age and older (12,13,14).
Numerous reports describing the condition have been published over the
past 20 years, but it still remains a condition that is not commonly
recognized. This could be due to the insidious nature of the condition,
usually without a history of acute trauma (12).
virtue of its lever arm length and muscle strength, the TP tendon is
the main dynamic stabilizer of the hindfoot against valgus deformity.
It also plays a major role in maintaining the medial longitudinal arch.
Insufficiency of the TP results in excessive strain on the static
ligament–bone hind- and midfoot constraints. The soft tissue gradually
elongates, the arch flattens, and the peroneus longus and brevis
tendons have an unopposed abduction force on the forefoot.
Etiology of TP tendon rupture.
To understand the etiology of TP tendon tears, it is important to
remember its function. It resists considerable forces in maintaining
the medial longitudinal arch. It also helps lock the mid- and hindfoot
to allow a solid lever arm during the push-off part of the gait cycle.
Approximately 20% of TP ruptures are associated with rheumatic
conditions (12). An estimated 80% of TP tendon ruptures develop spontaneously. There are several theories to explain this phenomenon.
The acute angle around the medial malleolus could lead to excessive
friction that leads to slow deterioration over many years. This also
explains the age predilection of this condition.
Laboratory studies have identified an area of poor blood supply to the
tendon behind the medial malleolus. This could lead to a decrease in
healing potential after minor trauma.
Achilles tendon contracture.
Either due to gastrocnemius alone or in combination with soleus, a
contracture or shortness of the Achilles tendon increases the workload
and force on the TP during the gait cycle.
Contrary to popular belief, TP tendon rupture or insufficiency is
common in American society. A proper history and thorough physical
examination is usually all that is needed to make this a
Onset is insidious, with discomfort reported on the medial side of the
foot without any preceding acute trauma. Women are affected more often
then men, and persons in their 40s are most often affected. There is
not necessarily a relation to activity level.
Initially, patients complain of only mild to moderate pain and of
swelling and discomfort on the medial side of the foot and ankle. It is
usually not incapacitating; rather, there is a chronic medial
weight-bearing ache that limits physical activities. Without treatment,
the symptoms might increase over a variable length of time. In a late
stage, the patient might complain of additional weight-bearing pain on
the lateral aspect of the ankle, a progressive deformity, and an
In an early stage, one can see and
palpate the swelling behind the medial malleolus and over the course of
the TP tendon to its insertion in the navicular. The tenderness is
usually over the same area.
In a more advanced stage, the hallmark
deformity becomes apparent. This is a combination of hindfoot valgus,
forefoot abduction, and flattening of the medial longitudinal arch.
Much information can be gathered by
observing the patient. When viewed from posterior, the amount of heel
valgus above the normal neutral to 5 degrees in the weight-bearing
position can be noted. The “too many toes” sign is indicative of
forefoot abduction. The patient is also asked to raise on the toes. A
normal TP locks the hindfoot in varus to give a solid lever for
push-off. With an insufficient TP, the heel does not move into varus,
and it is impossible to raise oneself on the toes.
Frontal and side views confirm the
forefoot abduction and loss of medial arch. An apropulsive, antalgic
gait is usually noticed if the patient is asked to walk at a rapid pace.
Physical examination further confirms the
clinical suspicion. Tendon and muscle power around the ankle is tested.
The TP is evaluated with the foot in plantar flexion, and the patient
is asked to invert the foot against resistance. Look for recruitment of
the tibialis anterior to augment this action.
The flexibility of the Achilles tendon is
tested with the knee first extended to determine the role of the
gastrocnemius in possible tightness, and then with the knee flexed to
isolate the soleus by eliminating the influence of the gastrocs.
Range of movement of the ankle,
especially the subtalar joint, is evaluated, and any pain is noted. In
advanced cases, there might be tenderness on the lateral aspect of the
ankle as a result of impingement of the fibula on the calcaneus.
Diagnostic workup. Thorough history and clinical examination is usually all that is needed to make the diagnosis.
In most cases beyond stage 1, weight-bearing radiographs show specific
changes. The most obvious is the change in the talo-first metatarsal
alignment on the anteroposterior and lateral views. In a normal foot,
the talo-first metatarsal alignment is in a straight line. In TP tendon
ruptures, the alignment is altered to varying degrees because of the
a tear or degeneration in the TP tendon and shows the abnormal
alignment of the bony elements, but it is costly and usually
unnecessary. It is helpful in early, subtle injuries of the tendon and
to rule out other causes of medial midfoot pain such as navicular
(CT) is not necessary as a primary diagnostic tool, but it can be
helpful to determine the integrity of the peritalar joints and,
therefore, in planning the surgical
procedure. It is of great value in the continuing study of the changes
in the foot secondary to TP tendon ruptures.
Stage 1a: mild, occult (13%).
Symptoms last less than 1 year, there is mild swelling and tenderness
over the TP tendon and slight weakness in inversion power, and there is
minimal hindfoot valgus on weight bearing.
Stage 1b: moderate (44%).
Symptoms last up to 18 months, and there is definite tenderness,
swelling, and weakness of the TP tendon. Moderate pes planus and heel
valgus occur as a result of dorsolateral peritalar subluxation.
Stage 2: advanced (17%).
Symptoms last for 1.5 to 2.5 years. There is more pronounced flatfoot
deformity caused by peritalar subluxation, and there is considerable
heel valgus and moderate prominence of the talar head medially. The
subtalar joint is usually still mobile and the deformities passively
Stage 3a: complete (15%).
Stage 3b: peritalar dislocation (11%).
Progressive dorsolateral peritalar subluxation reaches the point of
dislocation in the neglected case. Symptoms last between 4 and 20
years. Pain occurs also on the lateral side as a result of impingement
of the calcaneus on the distal fibula. The fibula takes an increasing
amount of load on weight bearing. It becomes hypertrophic, and stress
fractures are not uncommon. The talocalcaneal relation is completely
distorted, with minimal actual articular contact. The majority of these
deformities are fixed and not passively correctable.
Nonsurgical. Other than certain grade 1a
tears, nonsurgical management of TP tendon tears is essentially
palliative. In most cases, it will neither result in healing of the
tendon nor correction of the deformity. Noninvasive means are therefore
only useful if there are factors present that contraindicate surgical
intervention. This includes advanced age, significant medical problems,
low activity level, and minimal discomfort. It is still advisable to
start most patients on conservative treatment before electing to do
should be directed to control pain, inflammation, and development of
deformity. Options include the use of crutches, minimal weight bearing,
or casting in a recent onset case. Nonsteroidal anti-inflammatory drugs
(NSAIDs) might help relieve pain and swelling. In more advanced cases,
orthotics come into play. These include heel or sole lifts, inserts,
UCBL type heel cups, and modified, accommodative shoes. In severe
deformities, shoe modifications that incorporate calipers could be used.
Surgical treatment options include tendon repair, tendon augmentation,
and bony stabilization of both nonessential and essential joints.
Stage 1. A tendon repair is still
feasible. The TP tendon is usually augmented with a second tendon. A
multitude of augmenting techniques have been described (12,14).
This includes the use of the flexor digitorum longus, flexor hallucis
longus, or peroneus longus that serve as dynamic stabilizers. Free
tendon grafts are also used to repair the TP tendon, although the
results are variable. It is of utmost importance to evaluate for
tightness of the Achilles tendon and to lengthen it if necessary.
Stage 2. In more advanced cases, tendon
repair and augmentation is usually not sufficient to relieve pain and
prevent deformity. The surgical option is dependent upon the degree and
mobility of the deformity. If the peritalar subluxation is still
correctable, the bony stabilization is done in nonessential joints.
This includes the lateral column distraction fusion that reduces the
peritalar subluxation and heel valgus without compromising the
important subtalar and talonavicular movement. Other options include a
medial column or a subtalar fusion, with or without an Achilles
Stage 3. The surgical treatment of
subtotal peritalar dislocation with a fixed hindfoot deformity (grade
3b) usually requires a triple arthrodesis.
The foot and ankle are the most common areas for stress fractures. A
stress fracture is defined as a partial or complete fracture resulting
from its inability to withstand repetitive stress applied in a
repeated, subthreshold manner. It is, therefore, a series of events
causing stress fractures. Ninety-five percent of stress fractures are
in the lower extremities, +/- are of the foot and ankle. All the bones
of the foot and ankle can sustain stress fractures. The metatarsals,
though, are involved in 55% of cases, whereas the sesamoids and talus
are involved in less than 1%. Stress fractures occur in all sports but
especially in running and running-based sports (15).
Sedentary people starting a fitness program are more prone to stress
fractures. This is a well-demonstrated phenomenon in new military
recruits. Stress fractures are more likely to develop in women. Leg
length discrepancy, malalignment, prior injury, cavus feet that lack
normal pronation, as well as poor physical condition, predispose to
The history is fairly typical, with pain
being intensified by ongoing training. There might be an association
with a recent increase in duration and intensity of training. It is
usually insidious with an increase of pain over a period of time.
There should always be a high index of
suspicion for stress fractures with insidious onset of pain. Physical
examination should localize the involved area.
should be the first-line imaging test for evaluation of possible stress
fractures. However, one must be aware of their lack of sensitivity.
Callous formation is the abnormality seen on plain films and represents
the active bone healing the injury. Plain films will thus be normal for
the first few weeks. Furthermore, a large percentage will always appear
normal on x-rays. Thus, if one’s clinical evaluation is suspicious for
stress fracture, further imaging is often necessary (16).
The gold standard for recognizing a stress reaction in bone used to be
a technetium bone scan. The bone scan becomes positive after a week of
ongoing stress reaction in the bone. A negative bone scan effectively
rules out a stress fracture (16).
MRI. It is
useful to list the indication, as special short time inversion recovery
(STIR) images may be helpful. It is the most sensitive and specific
method of diagnosing and grading stress fractures and is especially
helpful in the feet (17).
The combination of a negative
roentgenogram and positive bone scan represents an early fracture, and
treatment at this stage may prevent longstanding problems. CT scan has
a place in diagnosing talus and midfoot fractures because these bones
are cancellous in structure and stress fractures are difficult to
identify on plain radiographs.
The most critical or at-risk stress fractures of the foot are of the navicular, proximal second metatarsal (18) and intraarticular fractures, and the great toe sesamoids. The navicular is particularly difficult to diagnose (19). Workup should include plain films, MRI bone scan, and CT scan. Significant disability can result from delayed diagnosis.
Treatment greatly depends on the location
of the stress fracture. Treatment should include 6 weeks of casting
followed by verification of union by CT. Resumption of leg-based
athletics is at 12 to 18 weeks after initiation of treatment. Custom
orthotics should be used when the patient returns to athletics (16).
Noncritical fractures include distal metatarsals 2, 3, and 4, the lateral malleolus, and the calcaneus (20).
Treatment should be aimed at keeping the level of activity below that
which causes pain. This implies decreasing the level of activity or
substituting swimming, biking, circuit training, or other low impact
activities. Orthotics within shoes can limit stress in the involved
area (19). Activities can progress as long as
they are not painful. There are reasons to try to limit NSAIDs as their
anti-inflammatory properties can inhibit bone healing and their pain
relief properties may give the patients a false level of reassurance (21).
Turf toe is
defined by some as a sprain of the plantar capsuloligamentous complex.
Others use the term to be more encompassing for a variety of injuries
around the first metatarsophalangeal joint. Differential diagnosis
includes injury to the medial or lateral ligamentous structures, the
phalangeal sesamoid ligament, a fractured sesamoid, osteochondral or
chondral injury, chondral contusion caused by direct linear impact, and
dislocations and injury to the interphalangeal joint (22).
This injury is common in football players but is also seen in
basketball and track athletes. Careful history and clinical evaluation
is necessary to localize injury. Anteroposterior, lateral, oblique, and
sesamoid views should be obtained.
Initial conservative treatment
consists of the general approach: rest, ice, compression, and
elevation. A postoperative shoe with firm sole to limit movement helps
in ligamentous injuries. The patient’s foot is immobilized for 3 weeks
and rehabilitation is started as tolerated. Sesamoid fractures are
treated with a cast shoe with the great toe in 10 degrees of flexion
for 8 to 10 weeks.
consists of debridement and drilling of articular surface if pain
persists in a case of chondral fracture. Partial excision or internal
fixation of sesamoid fracture is undertaken when the fracture does not
Hallux rigidus is degenerative arthritis of the first metatarsophalangeal joint. In most cases, there is no specific predisposing factor.
Possible etiologies include congenital
flattening of the metatarsal head, metatarsus primus elevatus,
osteochondritis of the head, a long hallux, pes planus, and
osteochondral injuries (turf toe).
Hallux rigidus presents a significant
problem for an athlete. Dorsiflexion of the big toe plays an important
role in activities such as accelerating and jumping. Compensation by
rolling onto the lateral aspect of the foot might cause stress and
strain on the ankle, knee, and hip.
Enlargement around the metatarsophalangeal joint is usually obvious.
This is due to a combination of bony prominences and synovitis.
Dorsiflexion is limited and reproduces the patient’s pain. Radiographic
findings might be minimal in early stages. With time, obvious
degenerative changes and osteophytes within the joint become apparent.
Sesamoids are generally not involved.
Differential diagnosis includes gout or other inflammatory arthritis.
Pressure against the toe is alleviated by modifying foot wear,
incorporating a higher and wider toe box, a stiffer shoe, a rigid
insert, or a rocker bottom sole. NSAIDs or injected steroids might give
Fusion is a good option in older people but would significantly impair
athletic performance. In athletes, a cheilectomy with or without a
dorsiflexion osteotomy of the proximal phalanges (Moberg procedure) is
preferred (23,24). The
patient is permitted to ambulate weight bearing as tolerated in a
postoperative shoe. Rehabilitation starts 7 to 10 days after surgery
with active and passive range-of-motion exercises. The patient should
wear a soft shoe to allow motion at the metatarsophalangeal joint with
walking. Athletes could resume cycling, swimming, and any activity that
avoids significant impact against the metatarsophalangeal joint, but
should avoid running, jumping, and similar activities for 10 to 12
weeks. Metatarsophalangeal joint arthroplasties (excision or prosthetic
replacement) have very limited application in the young, active
there appears to be a significant hereditary component. Shoe wear has
been suggested as an etiological factor, as a tight toe box and a high
heel will place an increased laterally and distally directed force on
the great toe. Joint laxity is associated with an increased rate of
hallux valgus. Not all hallux valgus deformities are symptomatic.
Typically, patients will describe pain over the medial bunion that
corresponds to bursal inflammation. In more severe deformities the main
complaint is that of second and third ray metatarsalgia.
What causes pain?
Shoe wear: type and any recent changes?
What activities does it affect?
Compare shoe size to foot size. Any change in shoes due to bunions?
Evaluate callus pattern: lesser metatarsal overload, great toe pronation
Evaluate gait: excessive pronating, →
more force on the medial rays, → increased valgus angulation of first
Metatarsophalangeal (MTP) joint. Evaluate kinetic chain of gait from
the pelvis down.
Angle of long axis of first and second metatarsals
Shoe modification is the most important. The shoes should be big enough, have a low heel, and a wide and high toe box.
Orthotics to support the medial arch and unload the lesser metatarsal heads might be of benefit.
Bunion pads might help for medial eminence pain.
Silastic spacers could be used between the toes.
Physical therapy if biomechanical factors seem to be resulting in excessive foot pronation
Should never be for cosmetic reasons
Refer to an orthopaedic surgeon or
podiatrist if there is not adequate pain relief after 6 months of
appropriate conservative care.
the MTP joint and a flexion deformity of the proximal interphalangeal
(PIP) joint. This frequently involves multiple toes and is usually an
indication of a muscle imbalance between the intrinsic or extrinsic
muscles of the toes. The most common complaint is pain and friction
over the dorsum of the PIP joint. With time, the plantar fat pad
dislocates distally and exposes the metatarsal heads. This results in
of the PIP joint; often with this the MTP joint and the distal
interphalangeal (DIP) joint are spared. The most common cause of a
hammer toe deformity is a result of the toe hitting against the tip of
the shoe resulting in a flexion deformity. These patients typically
will have symptoms as a result of a painful corn at the tip of the toe
or a callus along the dorsum of the toe as indicated in this patient.
Muscle imbalance, specifically gastrosoleus contracture
Intrinsic muscle imbalance
Flexible (correctible) deformity: usually does well with conservative treatment
Rigid (impossible to passively correct the PIP or DIP deformity)
Shoe modifications: should be big enough,
low heel, wide and high toe box. This is especially important for the
Orthotics with a metatarsal bar might help to reduce the plantar fat pad and reduce the metatarsal pain.
Silatic spaces and claw toe splints might be helpful.
Surgical treatment. Only indicated if conservative measures fail
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