The Adult Ankle and Foot

A large proportion of clinical complaints of the foot
center on the first metatarsophalangeal (MTP) joint. This articulation
alone bears one-third of the weight of the forefoot and helps stabilize
the longitudinal arch through the attachment of the plantar aponeurosis
into its base. Immediately after the foot hits the ground during
ambulation, weight is rapidly transferred from the heel to the
metatarsal head region. As a step is taken, the toes are pushed into
dorsiflexion. The plantar aponeurosis, which arises from the medial
tubercle of the calcaneus and inserts into the base of the proximal
phalanx, is pulled over the metatarsal head. In turn, this passively
depresses the metatarsal heads and raises the arch (Figure 21-1).
This construct is commonly called the “windlass mechanism” after the
nautical term for a device for raising a sail by pulling on a rope.

Any disorder of the first metatarsophalangeal joint has
the potential to disrupt this critical mechanical function. Weight is
then transferred to the lesser metatarsals, and secondary pathology in
the remainder of the forefoot can develop. Because of their significant
implications for the function of the foot, disorders of the hallux
deserve special consideration.

Primary degenerative arthrosis of the first metatarsophalangeal joint, frequently called hallux rigidus,
is a common problem. These patients develop a large dorsal osteophytic
ridge on the metatarsal head, which results in an impingement of the
proximal phalanx to dorsiflexion, limitation of motion, and pain. As
the arthritic process advances, the entire joint becomes involved.
During normal gait, dorsiflexion occurs at the metatarsophalangeal
joint, and if there is an obstruction to the dorsiflexion, then a
significant impairment in gait may occur. This is particularly
bothersome in patients who engage in athletics. The proliferative bone
around the metatarsal head can also result in significant increased
bulk of the joint, which makes wearing shoes difficult.

The patient’s main complaint with early stage hallux
rigidus is that of pain with dorsiflexion of the metatarsophalangeal
joint. This pain is aggravated by increased activities, particularly
running and other athletic endeavors. The patient may also complain
that, owing to the increased bulk of the joint, wearing shoes is
difficult. With advanced hallux rigidus, an arthritic pain pattern of
the first metatarsophalangeal joint predominates.

The physical examination frequently demonstrates an
abrasion or ulceration over the osteophyte on the dorsal or dorsomedial
aspect of the

metatarsal
head. The joint itself is enlarged, there is synovial thickening, and
there is significant tenderness around the joint, particularly along
the lateral aspect of the metatarsophalangeal joint and over the dorsal
ridge (Figure 21-9).
There is usually significant restriction of dorsiflexion, and
occasionally the proximal phalanx is held in a position of slight
plantar flexion if the deformity is severe. Forced dorsiflexion of the
joint causes pain. In advanced presentation, motion may be severely
limited. Pain and crepitus is elicited throughout the remaining arc of
motion.

The radiographs of the patient with hallux rigidus are
characteristic, demonstrating degenerative arthritis of the
metatarsophalangeal joint on the anteroposterior (AP) view. Besides the
narrowing of the joint, significant osteophyte formation is often
present along the lateral aspect of the joint. Medially, there rarely
is significant osteophyte formation. On the lateral view, there is a
dorsal osteophyte of varying degrees. Occasionally, there is an
osteophyte on the dorsal aspect of the proximal phalanx as well. In
advanced stages, the entire joint space may be compromised. This
continuum of disease has been staged as follows:

Grade 1 (mild): joint space is maintained; minimal bony proliferation or spurring on the dorsal aspect of the joint present

Grade 2 (moderate): advanced proliferation of dorsal
spurring and more significant joint space narrowing; proximal phalanx
may show dorsal spurring; reactive changes about the joint; plantar
joint space is preserved

Grade 3 (severe): advanced arthritis stage with
significant joint space narrowing and extensive proliferative bone
formation; loss of plantar joint space

Management of patients with hallux rigidus involves
activity modification, shoe adjustments ensuring adequate room for the
metatarsophalangeal joint, and stiffening the shoe by inserting either
an orthotic device or a piece of spring steel in the sole to decrease
dorsiflexion at the metatarsophalangeal

joint. Occasionally, nonsteroidal anti-inflammatory medications can be beneficial.

If conservative management fails, then surgical
intervention may be indicated if the neurovascular status of the foot
is satisfactory. The appropriate operative procedure depends on the
amount of arthrosis the patient demonstrates. For early stages of
hallux rigidus (grades 1 and 2), a cheilectomy procedure can be
effective. Cheilectomy involves resection of the dorsal 20 to 30% of
the metatarsal head along with the osteophytes along the lateral side
of the metatarsal head. The principle is to relieve the dorsal
impingement of the proximal phalanx as dorsiflexion occurs, which
usually relieves most of the pain. The procedure only reestablishes
about half of normal dorsiflexion but this is usually sufficient to
permit the patient to ambulate comfortably and resume most activities.

Arthrodesis of the metatarsophalangeal joint is an
excellent procedure for patients who have severe deformity or
significant arthroses (grade 3 hallux rigidus). Arthrodesis is also
useful for patients who have failed a previous cheilectomy and as a
salvage procedure for a failed bunion operation. The optimal
positioning of the arthrodesis is 15° of valgus and 10 to 15° of
dorsiflexion in relation to the plantar aspect of the foot (or 25 to
30° of dorsiflexion in relation to the first metatarsal shaft, which is
inclined in a plantar direction about 20°) (Figure 21-10).
After arthrodesis, the patient can be ambulated in a postoperative
wooden shoe until the arthrodesis site is solid, which is usually about
10 to 12 weeks after surgery. The main complications of arthrodesis are
malalignment of the arthrodesis site and nonunion, although uncommon.
If sufficient valgus and dorsiflexion is not placed into the
arthrodesis at the time of surgery, excessive wear on the
interphalangeal joint occurs—a potential problem.

Occasionally, in an older person whose ambulatory
capacity is limited, a Keller procedure can be used for advanced hallux
rigidus. In this procedure, the proximal one-third of the proximal
phalanx is excised along with the dorsal osteophyte. The problem with
this procedure is that it detaches the intrinsic muscles from the base
of the phalanx, and as a result, the toe may drift into dorsiflexion or
possibly varus or valgus. It is, however, useful in the older patient
with marginal circulation.

The use of a Silastic prosthesis to replace the first
metatarsophalangeal joint is rarely indicated because stability of the
joint is compromised, which may result in a transfer lesion to the
adjacent metatarsal head. The active movement of the
metatarsophalangeal joint is usually significantly impaired because of
the inability to reinsert the intrinsic muscles once the prosthesis has
been placed. At times, there is a reaction to the prosthetic materials
and a silicon synovitis results. The life expectancy of a prosthesis is
rarely more than 5 years. Therefore, it should not be used in any
patient who is young and expects to place a great deal of stress on the
metatarsophalangeal joint.

Lesser toe deformities are afflictions of the toes other
than the great toe. They include mallet toe, hammertoe, and claw toe
deformities. Hard and soft corns also occur on the lesser toes. The
underlying cause is generally idiopathic or a combination of improper
shoe wear. Subtle or overt neuropathy may be contributory. The general
patterns of lesser toe deformities are described below:

Mallet toe: characterized by a fixed flexion deformity
of the distal interphalangeal joint, usually involving the second toe
but possibly involving the third or fourth toes.

Hammertoe: characterized by a flexion deformity of the
proximal interphalangeal joint, which may be either fixed or flexible.
The fixed deformity is one in which the proximal interphalangeal joint
cannot be straightened, and a flexible deformity is one in which the
proximal interphalangeal joint can be brought back into anatomic
alignment.

Claw toe: characterized by a deformity consisting of the
aforementioned mallet toe or hammertoe deformities along with
dorsiflexion at the metatarsophalangeal joint. This deformity may
involve a single metatarsophalangeal joint or multiple
metatarsophalangeal joints. The deformities can be either fixed or
flexible.

Symptoms generally arise secondary to irritation from
abnormal positioning. Mallet toes usually result in pain on the tip of
the toe secondary to pressure from the ground or pain over the distal
interphalangeal joint region secondary to pressure against the shoe.
With hammertoes, pain occurs over the tip of the toe and over the
proximal interphalangeal joint. The patient may develop callus
formation beneath the tip of the toe or over the proximal
interphalangeal joint region. Claw toes cause pain over the proximal
interphalangeal joint

region
where the toes strike the top of the shoe. If the hyperextension
deformity is severe at the metatarsophalangeal joint, progressive
dorsiflexion of the proximal phalanx with depression of the metatarsal
heads occurs causing plantar metatarsal head prominence. Increased load
over the prominence leads to callus formation and pain.

The conservative management of lesser toe deformities
consists of adequate padding, offloading with orthotic management, and
shoe wear modifications with an adequate shoe box to provide sufficient
space for the toes. Orthotic management may be accomplished by simple
(i.e., metatarsal pads) or complex (i.e., custom orthotics with
offloading bars) means with good results.

The operative treatment of lesser toe deformities can be
undertaken when conservative measures fail to provide relief. The goal
is to realign the toes at all involved levels to a more anatomic
alignment, eliminating prominent sources of irritation. The operative
treatment of a mallet toe consists of removing the distal portion of
the middle phalanx, which decompresses the distal interphalangeal joint
(Figure 21-11). If the deformity is extremely
fixed, then a release of the flexor digitorum longus tendon may also be
carried out. The operative treatment of a hammertoe consists of
excising the distal portion of the proximal phalanx and then holding
the toe in correct alignment for about 6 weeks, until a satisfactory
fibrous union has occurred (Figure 21-12).
Arthrodesis of the proximal interphalangeal joint can be attempted,
although the fusion rate is low (about 50%). For this reason, usually a
fibrous union is the procedure of choice. Claw toes require correction
of the hammer toe or mallet toe deformity as described above as well as
addressing the metatarsophalangeal joint

deformity (Figure 21-13).
If the patient has a fixed deformity, then release of the contracted
structures on the dorsal aspect of the metatarsophalangeal joint, which
consists of both extensor tendons, the joint capsule, and the
collateral ligaments, is undertaken to straighten the contracture at
the metatarsophalangeal joint. A Girdlestone flexor tendon transfer, in
which the flexor digitorum longus tendon is transposed to the dorsal
aspect of the proximal phalanx, is carried out to provide increased
plantar flexion pull at the metatarsophalangeal joint region. In these
cases, pin fixation is often used to maintain satisfactory alignment of
the corrected hammertoe and metatarsophalangeal joint until the soft
tissues have had a chance to heal. If the deformity is a dynamic one
and does not involve any fixed deformity, then a Girdlestone flexor
tendon transfer alone may produce a satisfactory clinical result.

Metatarsalgia is a
generalized term for pain beneath the metatarsal head region. During
normal walking, maximal pressure is applied to the metatarsal region
for 50 to 60% of the stance time. As a result, any type of abnormality
in this area may cause the patient significant disability. Most
commonly, metatarsalgia is secondary to a problem at the
metatarsophalangeal joint level. This may be a primary bony problem,
joint problem, or less commonly other causative dysfunction may exist.
Dysfunction of the metatarsophalangeal joint may be secondary to
synovitis associated with inflammatory arthropathy, nonspecific
synovitis, plantar plate degeneration, Freiberg infarction, or
dysfunction secondary to subluxation or dislocation of the
metatarsophalangeal joint. In

many
patients, metatarsalgia can be treated conservatively by obtaining a
shoe of adequate size and then adequately padding the metatarsal area
to relieve the areas of maximal pain. At times, however, this
conservative management fails, and operative intervention is indicated.

Nonspecific synovitis is a condition in which the
patient develops synovial proliferation around the second
metatarsophalangeal joint. This usually starts spontaneously, and
patients often feel as if they are walking on a painful lump on the
bottom of the foot. The physical examination demonstrates generalized
synovial thickening around the metatarsophalangeal joint. This is
sometimes associated with a hammertoe. This condition often responds to
conservative management consisting of adequate shoes and padding and
nonsteroidal anti-inflammatory medications. Occasionally, injection of
corticosteroid into the joint relieves the condition. If the condition
persists, synovectomy of the metatarsophalangeal joint should be
considered. At times, this condition results in a patient developing a
subluxation of the metatarsophalangeal joint frequently associated with
a fixed hammertoe deformity. If symptomatic, this deformity
additionally requires correction as discussed previously.

Degeneration of the plantar plate occurs occasionally
and is due to cystic changes in the dense plantar plate, which helps to
stabilize the metatarsophalangeal joint. It is associated with pain
beneath the metatarsal head and often a progressive cockingup of the
metatarsophalangeal joint may develop. Usually, patients do not develop
the generalized synovial reaction noted in patients with nonspecific
synovitis. The problem can usually be handled conservatively, although
occasionally arthroplasty of the metatarsophalangeal joint is indicated.

Subluxations and dislocations of the metatarsophalangeal
joint are due to multiple causes, including degeneration of the plantar
plate, which permits the extensor tendons to pull the proximal phalanx
up into dorsiflexion; chronic pressure of the great toe against the
second toe, which may result in a dislocated second metatarsophalangeal
joint; nonspecific synovitis; or an undetermined cause. When a severe
subluxation or dislocation occurs, the proximal phalanx pushes the
metatarsal head into a plantar position (Figure 21-14).
As a result, pain and often a large callus develop beneath the
metatarsal head. The patient often complains of pain over the dorsal
aspect of the toe as well because this strikes the top of the shoe.
Under these circumstances, conservative management consists of a shoe
with an adequate toe box to alleviate the pressure on the toe and
metatarsal head along with adequate padding to relieve the pressure
beneath the metatarsal head. If conservative measures fail, then an
operative procedure to reduce the metatarsophalangeal joint may be
indicated. These procedures are often successful in alleviating this
condition.

Freiberg infarction is an avascular necrosis of unknown
origin that occurs in the metatarsal head. This infarction results in
collapse of the metatarsophalangeal joint (Figure 21-15).
This process is often associated with generalized discomfort around the
joint, and the joint may develop a significant synovial reaction or
enlargement due to collapse of the bony structures. This condition can
often be managed conservatively with adequate shoes and padding,
although nonsteroidal anti-inflammatory medications are useful during
the acute phases. If the problem significantly limits the patient,
arthroplasty may be indicated to remove some of the proliferative bone
about the joint.

In inflammatory arthropathy, such as rheumatoid
arthritis, psoriatic arthritis, or gout, proliferative synovial tissue
develops around the metatarsophalangeal

joint,
which results in an enlargement of the joint as well as a significant
inflammatory response by the body. Under these circumstances, placing
pressure on the metatarsal head region causes the patient significant
discomfort and may make walking extremely difficult. Gout is usually
localized to the first metatarsophalangeal joint, whereas rheumatoid
and psoriatic arthritis involve multiple metatarsophalangeal joints.

Conservative management of this problem involves placing
the patient into an adequate shoe, often extra-depth shoe that has a
large toe box with enough room for the patient’s forefoot deformities
and for an orthotic device to help relieve the stress on the metatarsal
heads (Figure 21-16). Gout can often be handled
therapeutically, although in some cases with large tophaceous deposits,
alteration in shoe wear is necessary.

If the conservative management fails, then a forefoot
reconstructive procedure should be considered. The early joint changes
begin with a synovitis-type picture, and over time, the deformities may
progress to subluxations and dislocations. This process, particularly
in the rheumatoid forefoot, can be helped if synovectomies of the
metatarsophalangeal joints are performed before significant capsular
destruction has occurred. For advanced rheumatoid forefoot deformity,
arthrodesis of the first metatarsophalangeal joint to deformity and
lesser metatarsophalangeal joints’ decompression by surgical resection
of the metatarsal heads is the procedure of choice (Figure 21-17).
This procedure allows the fat pad to be drawn back down onto the
plantar aspect of the foot and creates a soft cushion for the foot that
relieves the metatarsalgia. The lesser toe deformities are corrected by
manual osteoclasis and pinning, which corrects the fixed deformities.
After this procedure, patients often have increased ambulatory capacity
and can wear store-bought shoes.

Pain over the plantar metatarsal head may be due to a prominent fibular condyle, a long metatarsal (Figure 21-18),
a so-called Morton foot in which the first metatarsal is short, a
hypermobile first ray in which the first metatarsocuneiform joint is of
insufficient stability to provide adequate weight bearing, or after
trauma in which a metatarsal may be pushed into a plantar or dorsal
angulation. Occasionally, after metatarsal surgery to alleviate
pressure on one metatarsal, a condition known as a transfer lesion
may occur. This results in pressure beneath the adjacent metatarsal
head due to lack of weight bearing on the previously operated
metatarsal. In most of these

cases,
a callus develops beneath the prominent metatarsal head, which is
usually the source of the patient’s pain. Conservative treatment
involves modifications to provide adequate padding around the area to
alleviate the pressure on the involved metatarsal head. If this fails,
then a surgical procedure may be indicated either to relieve the
prominence or to elevate or shorten the metatarsal and correct any
associated joint deformity. One such procedure is the Weil osteotomy,
which involves an extra-articular osteotomy of the distal metatarsal
allowing decompression and shortening, relieving plantar prominence and
joint subluxation.

Forefoot pain due to dermatologic problems can often be
a significant cause of discomfort for the patient. The most frequently
encountered problems include hard or soft corns, plantar warts, seed
corns, or hyperkeratotic skin. A wart is a vascular lesion secondary to
a virus and can be differentiated from keratotic skin by carefully
trimming the area and observing small punctate bleeders secondary to
the fine end arteries, which are present in a wart and not in a
keratotic lesion. Treatment includes

dermal
burning with liquid nitrogen; by using Cantharone, which after multiple
applications usually relieves the wart; or occasionally by curettage.
Burning the bottom of the foot with electrocautery or surgically
excising the wart are not recommended unless other options fail,
because they result in a scar on the plantar aspect of the foot, which
may become symptomatic.

A seed corn is a small invagination of skin that results
in a small keratotic lesion, which at times can be painful. These
usually can be managed by trimming the lesion; or if this fails,
curettage may alleviate it. Hyperkeratotic skin is observed in some
patients and is probably due to a biochemical abnormality that is
poorly understood. In these patients, surgical intervention is not
indicated; rather, frequent trimming of the hyperkeratotic skin usually
is adequate treatment and often can be taught to the patient.

A corn is a keratotic lesion that develops on the skin
in response to pressure against the skin by an external force (a shoe).
As a general rule, a small bony prominence, termed an exostosis,
lies beneath the skin, and the shoe covering the foot chafes against
this area. Corns are divided into hard and soft corns, depending on
their location. A hard corn occurs between the skin and the shoe,
whereas a soft corn occurs between one toe and an adjacent toe. In both
cases, however, the cause is due to an underlying exostosis. The
patient’s main complaint is that of buildup of hypertrophic skin over
the exostosis. In time, this may become rather large and painful. The
conservative management is to trim the lesion and place a soft support
around it to alleviate the pressure on the involved area. Usually, a
broader, softer shoe helps to accommodate this problem. If conservative
management fails, then a surgical procedure may be undertaken that
removes the offending prominence.

Other soft tissue problems resulting in forefoot pain
include atrophy of the plantar fat pad, synovial cyst arising from the
metatarsophalangeal joint, soft tissue tumors such as a lipoma,
permanent changes secondary to a crush injury, or a plantar scar
secondary to trauma. Atrophy of the plantar fat pad occurs most
frequently in older people and can present a significant problem for
the patient. Because of loss of adequate padding beneath the metatarsal
heads, some callus formation often results, and the metatarsal heads
are sensitive to weight bearing. Unfortunately, there is no way to
remedy this situation other than to place the patient in a soft-soled
shoe with adequate support in the metatarsal area to alleviate the
discomfort.

A soft tissue tumor such as a lipoma can also produce
metatarsalgia due to its physical prominence. If this fails to respond
to conservative management, such as adequate padding and shoe wear,
surgical excision may be carried out.

Flatfoot is a global term with multiple potential
origins. The presence of pes planus itself is not necessarily
pathologic. Rather, it is a sign that the underlying cause of the foot
deformity should be explored in order to guide treatment. An attempt
should be made to differentiate between a congenital versus acquired
condition, after which specific diagnoses within each category may be
considered. Asymptomatic flexible flatfoot is extremely prevalent,
generally requires no treatment, and can be considered a normal variant
of foot architecture.

Physical examination demonstrates a diminished
longitudinal arch and assessment of alignment reveals excessive
hindfoot valgus and forefoot abduction. From behind, the excessive
forefoot abduction is demonstrated as the “too many toes” sign, in
which an excess of the toes are visualized because of the marked
abduction of the forefoot (Figure 21-19).
Patients should be thoroughly accessed for motion limitations,
particularly of the subtalar joint, which may suggest an underlying
coalition. Posterior tibial tendon strength and function should be
accessed. When testing the posterior tibial tendon, the foot should
begin in a plantarflexed and everted position. The patient should then
be asked to invert the foot against the examiner’s resistance from this
position, eliminating the inversion power of the anterior tibial
tendon, which may mask posterior tibial tendon weakness. The ability to
perform multiple single heel-rises with initiation of heel inversion
confirms intact posterior tibial tendon function (Figure 21-20).

The weight-bearing radiographic findings in the
evaluation of a patient with pes planus are present irrespective of the
underlying cause. On the lateral radiograph, a line drawn through the
long axis of the talus should nearly bisect the navicular and first
metatarsal shaft (Figure 21-21). Mild flatfoot is indicated by a sag in this line of up to 15°; a sag from 15 to 40° indicates moderate flatfoot; and a sag greater than 40° indicates severe flatfoot.
In the AP radiograph, a line drawn through the long axis of the talus
and calcaneus should measure about 15°. An increase in this angle
indicates varying degrees of

flatfoot. Observation of the talonavicular joint demonstrates lateral subluxation of the navicular off the head of the talus (Figure 21-21).
Associated radiographic findings may suggest the specific underlying
cause of the deformity (i.e., midfoot arthrosis, tarsal coalition).

The most common causes of congenital pes planus include
asymptomatic flexible pes planus, tarsal coalition (peroneal spastic
flatfoot), and residual congenital deformity (i.e., residual clubfoot).
Asymptomatic flexible pes planus is a variation of normal foot
architecture. This diagnosis generally requires no treatment beyond
simple reassurance. Conservative treatment for symptomatic patients
involves fitting the foot with a firm shoe that has an extended medial
counter to help support the talonavicular joint, a medial heel wedge to
help tilt the heel into a neutral position, or a well-molded,
semiflexible arch support to further support the longitudinal arch.
These treatment modalities suffice in most patients with symptomatic
hypermobile flatfoot of congenital origin. If surgery becomes
necessary, it is usually in the form of extra-articular osteotomies
meant to improve hindfoot alignment (i.e., lateral column lengthening
procedures). Rarely, stabilization of the foot with arthrodesis of the
joints of the hindfoot may be necessary. The surgeon must always be
cautious, however, when carrying out a stabilization procedure of the
hindfoot because an excessively flexible foot is being replaced with a
rigid foot, and this does not always ensure that the patient will
become asymptomatic. In contrast to hypermobile congenital flatfoot,
patients with tarsal coalition as a cause of congenital pes planus
demonstrate a limitation of tibiotalar, subtalar, or transverse tarsal
joint range of motion. This is a condition created by a failure of
segmentation of

the tarsal bones in early development (Figure 21-22).
Most often, the talocalcaneal and calcaneonavicular joints are
affected. Incidence is reported to be less then 1%, and bilateral
coalitions may be present in approximately 50% of those affected.
Afflicted individuals notice the condition in adolescence, as the
coalition may mature from a cartilaginous to a bony interface and cause
symptomatic mechanical irritation. Pain along the peroneal muscles may
be present and this is thought to be due to the patient’s attempt to
compensate and correct the overall hindfoot alignment. It is this
latter symptom that lends an alternative name to tarsal coalition:
peroneal spastic flatfoot. The acute treatment of a symptomatic
coalition is based on relieving the stress at the site of the
coalition, generally best performed with immobilization. Patients who
have recurrent symptoms despite conservative care may require surgical
resection or fusion of the involved areas of the coalition.

The most common causes of acquired pes planus include
posterior tibial tendon dysfunction (PTTD) and midfoot arthrosis. These
patients can be differentiated from those with congenital flatfoot by
history. Patients with acquired flatfoot had at one time a normal
architecture of the foot and have since suffered progressive collapse
to flatfoot deformity. PTTD is the most common cause of adult acquired
flatfoot deformity. The process is initiated by tenosynovitis with
progressive inflammation that subsequently causes enlargement and
fraying of the tendon, which may progress to frank rupture. As the
tendon weakens, the hindfoot demonstrates valgus malalignment secondary
to medial column structural laxity. In addition, forefoot abduction
occurs.

Four stages of PTTD exist: Stage 1 PTTD demonstrates
mild pain along the tendon. The patient retains strength as
demonstrated by a preserved ability to perform a single heel-rise. This
is the tenosynovitis or tendonitis stage and the patient

can
generally be managed nonoperatively with a period of immobilization. In
no instance should the tendon be injected with corticosteroid, for a
number of studies suggest an increased risk of tendon rupture (as high
as 25%) with steroid administration. If symptoms persist, a
tenosynovectomy of the posterior tibial tendon sheath should be
performed to prevent progression of disease. Stage 2 PTTD is
characterized by pain along the tendon, inability to perform a single
heel-rise or initiate inversion of the heel on heel rise, and postural
foot changes (excessive hindfoot valgus or forefoot abduction). The
foot does, however, remain supple and motion is retained. This is the
“flexible” stage, and the tendon is generally no longer functional.
Nonoperative treatment can produce acceptable results with aggressive
orthotic management and potentially the long-term use of a solid
plastic ankle-foot orthosis, particularly in elderly patients. Many
patients, however, improve only with surgical intervention. The most
common surgical procedures include posterior tibial tendon debridement,
tendon transfer (i.e., flexor digitorum longus [FDL] transfer), and
extra-articular osteotomy procedures to correct bony malalignment
(i.e., medial calcaneal slide, lateral column lengthening procedures).
Stage 3 PTTD is defined by fixed postural abnormalities secondary to
severe chronic malalignment and joint involvement. This is the “rigid”
stage and cannot be managed effectively surgically with extra-articular
alignment correction or soft tissue procedures alone. If the patient
fails nonoperative management, hindfoot arthrodesis is required
(selective or triple arthrodesis procedures) to correct the foot to a
plantigrade position. Stage 4 PTTD includes the rigid hindfoot changes
and additionally involves the tibiotalar joint. If orthotic treatment
is ineffective, pantalar fusion (ankle arthrodesis and triple
arthrodesis) is required.

Posttraumatic deformity of the hindfoot or midfoot can
cause a symptomatic acquired flatfoot deformity. Individuals sustaining
a calcaneus or talus fracture may develop hindfoot valgus and collapse
of the transverse tarsal joints leading to a flatfoot posture. Primary
or posttraumatic midfoot arthrosis may lead to a collapse of the arch
and pain (Figure 21-23). These deformities may
be the direct result of the fracture and residual deformity, or it may
be secondary to collapse following the development of arthrosis. The
treatment for this complication must be individualized given the
flexibility and severity of the deformity. Simple arch supports,
University of California Berkeley Laboratories (UCBL) inserts, or an
ankle-foot orthosis may be sufficient. Surgical stabilization generally
involves arthrodesis with interposition of bone graft to lengthen
collapsed joints and restore overall foot alignment.

A cavus, or high-arched, foot is the opposite of a
flatfoot deformity. The foot is often stiff, and the elevated arch does
not normalize with weight bearing. The deformity itself may have
primarily a hindfoot basis, a forefoot basis, or a combination of both.
There should be high index of suspicion for an underlying neuromuscular
disorder, although the most common cause is idiopathic. Any new onset
presentation should be considered evidence of a possible spinal cord
lesion until proven otherwise. The neuromuscular origins associated
with a cavus foot include Charcot-Marie-Tooth and polio. Congenital
causes (i.e., clubfoot residual) and posttraumatic causes (i.e.,
compartment syndrome sequelae) may also cause the deformity.

Patients present with pain due to the abnormal
distribution of weight and decreased surface area present for weight
bearing. The rigid deformity compounds the problem as the foot is
unable to absorb the weight-bearing impact. As progressive deformity
develops, patients may experience pain on the lateral aspect of the
foot, over the fifth metatarsal head, and with severe hindfoot varus
secondary ankle instability complaints.

On physical examination, the patient with a cavus
deformity demonstrates a high arch while standing, which is associated
with a varus deformity of the heel, adduction of the forefoot, and
often clawing of the toes. The foot frequently is rigid with restricted
motion in all the joints, fixed dorsiflexion contracture of the
metatarsophalangeal joints, and fixed hammering of the proximal
interphalangeal joints. Muscle testing is essential to determine the
cause of the deformity, as most cases are due to hindfoot or forefoot
muscle imbalances. This testing allows for localization of deformity
and for accurate surgical planning if tendon transfer procedures are
being considered. The degree of rigidity of the hindfoot varus can be
assessed with the Coleman block test. The heel is placed on a block of
wood and the forefoot is allowed to contact the ground, leaving the
hindfoot unrestricted. If the hindfoot varus corrects to neutral, the
deformity is considered flexible. In a rigid deformity, the hindfoot
varus will not correct.

Weight-bearing radiographs of the foot should be
obtained to determine the source of the deformity. Primary hindfoot
cavus will demonstrate an elevated calcaneal pitch angle with an
increased pitch of the calcaneus in relation to the floor of greater
than 30°, a normal talometatarsal angle, an elevated longitudinal arch,
and forefoot supination (Figure 21-24).
Forefoot cavus will demonstrate a normal calcaneal pitch angle, an
elevated arch, loss of alignment of the talometatarsal angle, and
increased forefoot plantar flexion.

The nonoperative treatment of the cavus foot is usually
to provide an accommodative shoe with adequate support and cushioning
to help absorb some of the impact of ground contact. If a neurologic
disorder

exists,
a polypropylene ankle-foot orthosis (AFO) may be necessary to provide
stability. Surgical treatment of the cavus foot depends on the precise
cause of the problem. The main goals of surgery are to produce a
plantigrade foot and, if possible, to lower the longitudinal arch. The
type of surgical procedure indicated depends on the specific bony
abnormality present and the location of the maximal deformity.
Correction should be performed with extra-articular osteotomies with or
without tendon transfers at the sites of involvement (i.e., Dwyer
calcaneal osteotomy, first metatarsal osteotomy, and plantar fascia
release) (Figure 21-25).
For patients with severe deformity or with progressive neurologic
disease, arthrodesis procedures may be optimal. The goal of all of the
surgical procedures is a plantigrade foot, which is stable for
weight-bearing.

Arthrosis of the foot and ankle may be primary or
secondary. Although primary arthrosis of the ankle and subtalar joint
is uncommon, it does occur in the talonavicular, tarsometatarsal, and
first metatarsophalangeal joints. Why some joints are affected by
primary arthroses and others are usually affected after trauma remains
an enigma. Because the foot and ankle are weight-bearing structures,
joint afflictions may severely limit a person’s ability to remain
functional. As a general rule, the diagnosis of arthrosis is not
difficult to make, and in most cases conservative management can
benefit the patient. If conservative management fails, then
stabilization of the involved joint may be considered.

Recurrent ankle sprains are a major complaint in young
athletic populations. Although the majority of patients who suffer an
ankle sprain go on to heal without instability, a small percentage
develop chronic laxity of the lateral ankle ligaments. The broad and
strong deltoid ligament on the medial side of the ankle is rarely
affected. Essentially all cases of lateral ankle ligament laxity
involve the anterior talofibular ligament, a thickening of the ankle
capsule from the anterior margin of the fibula to the neck of the talus
that prevents anterior translation of the talus in the ankle mortise.
More severe cases also demonstrate involvement of the stronger
calcaneofibular ligament that runs from the tip of the fibula and
courses deep to the peroneal tendons to cross the subtalar joint and
inserts on the calcaneus. It serves to prevent direct inversion
instability both of the ankle and subtalar joint (Figure 21-30).

Bony deformities can predispose patients to develop
lateral ankle ligament laxity. When weight bearing, the axis of the
calcaneus ordinarily rests in approximately 5 to 7° of valgus compared
with the axis of the tibia. This places the line of force lateral to
the center of the ankle and does not stress the lateral ankle
ligaments. When a varus alignment to the hindfoot is present, however,
the lateral ankle ligaments are subject to repetitive loading. The
clinical examination of a patient with chronic ankle sprains should
include a standing examination from the rear to check hindfoot
alignment. Hindfoot varus is most often seen in conjunction with a
cavus foot.

In addition to the static ligamentous structures,
dynamic support from the peroneal tendons is also important in
maintaining ankle stability. The peroneal muscles contract reflexively
in response to sudden inversion moments about the subtalar joint and
ankle. Because of the peroneal muscle action, many patients with lax
ankles on clinical examination do not have a clinical problem with
major ankle sprains. In those that do, physical therapy

aimed
at peroneal strengthening and proprioceptive training can be effective
in reducing the risk for further major episodes. The mechanism of
action is unclear. It takes approximately 50 ms for electrical activity
to appear in the peroneal musculature following a sudden unexpected
inversion force. Another 70 ms is required for the muscle to develop
any significant tension. There is little data to suggest that training
can reduce this reaction time. More likely, patients develop more
strength in the peroneal tendons and develop motor patterns in which
the muscles begin to fire before the foot hits the

ground.
While this can be effective, some degree of ligament integrity is
required to prevent ankle sprains when the foot is going to be subject
to sudden unexpected loads as is common in cutting and jumping sports.

The diagnosis of lateral ankle ligament laxity requires
both a history of major recurrent ankle sprains and evidence of
mechanical laxity on the clinical examination. The ankle should be
tested both in direct anterior subluxation (the anterior drawer test)
and in inversion (Figure 21-31). Stress
radiographs, in which an ankle mortise view is taken while an inversion
force is applied, are unreliable. No standards exist to define a
threshold of ankle laxity and a large number of false-negative results
can be expected because a patient will guard the joint with the
peroneal muscles during this awkward test.

The repetitive subluxation events in lateral ankle
ligament laxity yield a high rate of associated injuries in other
structures about the hindfoot. A high index of suspicion should be
maintained in particular for tears of the peroneal tendons and
osteochondral lesions of the talus.

Direct repair of the lateral ankle ligaments, usually by
imbrication into a small bone trough around the front of the fibula, is
known as the Broström procedure. Because it uses the native ligaments
and restores the normal anatomy, no limitation of ankle or subtalar
motion occurs after the procedure and it is highly effective in
restoring stability to the joint. It is the preferred technique for the
majority of patients.

Instability may recur after a Broström repair in
approximately 15% of cases. One important risk factor for failure is
benign joint hypermobility syndrome, a subtle disorder of collagen
leading to global ligamentous laxity. It is now regarded by most
authorities as synonymous with the mild type III variant of
Ehlers-Danlos syndrome. Patients being considered for ligament repair
should be evaluated clinically for signs of global ligamentous laxity
and for a history of instability problems in other joints.

In the case where a previous direct ligament repair has
failed or global ligamentous laxity is present, an augmented
reconstruction of the lateral ankle ligaments is appropriate. Over 30
procedures have been described to accomplish this using a variety of
materials including split or whole peroneus brevis, fascia lata,
hamstring tendon, and tendon allograft. All of these augmentation
procedures have some potential for causing a pathologic limitation of
subtalar motion if the grafts are not placed at the origin and
insertion of the anterior talofibular ligament and the calcaneofibular
ligament. Whatever graft material is used, the repair should attempt to
mimic the normal anatomy as possible.

Pain in the heel pad area may vary from an annoyance to
a significantly disabling problem. Heel pain has multiple origins, and
it is imperative that a careful history and physical examination be
carried out to pinpoint, as precisely as possible, the cause of the
pain. In this way, specific treatment can be formulated to relieve the
condition. Heel pain can result from disorders of the Achilles tendon,
soft tissue disorders near the heel, hindfoot bony injury (i.e. stress
fracture), bony prominence irritation, or neurologic disorders about
the hindfoot.

Heel pain associated with Achilles tendon disorders is a
common problem, particularly with the athlete. Multiple descriptive
terms (i.e., tendinitis, tendonitis, tendinosis, tendinopathy,
peritendinitis, partial rupture, and so on) have been ascribed to the
specific Achilles tendon disorders based on the location of disease and
affect on the tendon. These terms are often confusing, occasionally
misleading, and many of these disorders often coexist. Perhaps a more
simplistic approach is to consider these disorders as a spectrum of
disease of the Achilles. The origin, pathogenesis, and natural course
of many of these disorders are unknown. Patients generally present with
complaints of pain with activities, particularly those sports related.
In acute conditions, pain may occur with all activities. In chronic
conditions, pain may initially occur only with exertional activities
and over time may progress to constant pain, occurring even at rest.
Clinical examination may reveal a diffuse selling, crepitation, and
tenderness along the tendon in acute disorders. Chronic disorders may
present with more subtle and variable findings; often, nodular swelling
of the tendon may present suggestive of tendinosis (Figure 21-32).
Pain may occur directly over the Achilles tendon proximally, however,
it may also occur distally at the heel. If the pain is located at the
insertion of the Achilles tendon into the calcaneus, it may be due to
some degeneration of the Achilles tendon. In this case, there is
thickening of the tendon

near
its insertion, which at times may become large. This can be associated
with increased warmth over the area as well. Calcification at the
insertion of the Achilles tendon may indicate some degeneration and on
rare occasions is a source of pain. At times, pressure from a
prominence on the posterosuperior aspect of the calcaneus, known as a Haglund deformity,
can be the cause of the pain. In the patient with a Haglund deformity,
a lateral radiograph of the calcaneus reveals a large posterosuperior
prominence on the calcaneus that is responsible for the problem.
Initial conservative treatment should be directed toward activity
modification, inflammation control, and occasionally immobilization.
Corticosteroid use is generally not recommended. If patients fail
conservative treatments, surgical intervention may be considered. The
procedure of choice depends on the spectrum of disease present and
should address all pathology. This may include synovectomy, tendon
debridement, tendon repair, tendon augmentation (i.e., tendon transfer
[FHL] or Achilles turndown flap), or resection of any bony pathology
(i.e., Haglund deformity). The goal of treatment is to return the
patient to their desired level of activity without pain.

Soft tissue causes of heel pain include plantar
fasciitis and atrophy of the heel pad. Heel pad atrophy is most
frequently seen in older patients who develop thinning of the fat pad,
which decreases the cushion on the heel. The diagnosis is made by
palpation of the heel pad and the observation of lack of adequate fatty
tissue. Treatment is conservative with orthotic management for adequate
heel cushioning. Plantar fasciitis is the most common cause of inferior
heel pain and is very common. It commonly occurs with the first step
after a period of rest (e.g., first step in morning) and often improves
with activity. This disorder is an inflammatory process and it is
postulated that with repeated stress, microtears occur at the bony
attachment of the fascia to the calcaneus leading to a chronic
inflammatory process. Obesity, repetitive stress in athletics, middle
age, and the presence of abnormal foot mechanics (i.e., pes cavus or
pes planus) have been associated as risk factors. Although commonly
associated with “heel spurs,” only 50% of patients with plantar
fasciitis have “heel spurs” present radiographically and this finding
of itself is not the cause of the patient’s subcalcaneal discomfort.
Pain is usually located near the tubercle of the calcaneus or just
distal to it and palpation along this region reproduces the patient’s
discomfort. At times, the fasciitis involves the origin of the abductor
hallucis muscle, and in these cases, the pain is located along the
plantar medial aspect of the heel and is aggravated by palpation of the
origin of the muscle. The condition is usually self-limiting and if
treatment is begun soon after the onset of symptoms, most patients can
expect resolution within 6 weeks. A multitude of treatment options
exist and should be exhausted prior to considering surgical
intervention. Initial treatment most often consists of Achilles tendon
stretching exercises (particularly when limited dorsiflexion is
present), oral anti-inflammatory drugs, shoe inserts, and night splints
(preventing plantar flexion). For more recalcitrant cases, periodic
immobilization may be necessary. Corticosteroid injection at the site
of maximal tenderness may be beneficial, but should be used in
moderation, rarely exceeding 2 to 3 injections. Extracorporeal shock
wave therapy has recently shown benefit in the treatment of refractory
fasciitis and should be considered prior to surgical intervention. In
rare cases where 6 to 12 months of nonsurgical management has failed to
provide relief, surgical intervention, consisting of partial plantar
fascia release with or without decompression of the first branch of the
lateral plantar nerve and adductor hallucis fascia, should be
considered.

Bone-related problems may be the source of heel pain.
Occasionally, a stress fracture may involve a calcaneal spur on the
plantar aspect of the calcaneus as a cause of heel pain. This
occasionally can be demonstrated radiographically, however, often a
bone scan is necessary. A bony ridge along the medial or lateral aspect
of the insertion of the Achilles tendon may also be a source of heel
pain. This bony ridge results in a mechanical problem causing chafing
against the counter of the shoe.

The cause of heel pain can be multifactorial, but it is
imperative that the clinician accurately diagnoses the origin and
directs treatment accordingly. In general, treatment consists of
nonsteroidal anti-inflammatory medications, relief of stress over the
involved bony prominence, use of a soft orthotic device in the shoe to
relieve the heel, cast immobilization, or some combination of these. As
a general rule, surgery is not necessary for heel pain. There certainly
are exceptions, but the physician should be as conservative as possible
in the management of heel pain.

Pathology of the foot in diabetes represents a vast
public health problem. A typical newly diagnosed patient with diabetes
has a roughly 15% chance of developing a foot ulcer over the course of
his or her

disease.
At any given time, roughly 5% of neuropathic diabetics have an ulcer of
the foot. Given the increasing trends toward obesity and type II
diabetes in Western society, the problem is only likely to become more
acute.

Diabetic foot pathology essentially refers to two
distinct clinical problems: neuropathic ulceration and the Charcot
foot. Both are secondary phenomena to diabetic neuropathy. A recent
important prospective study, the Diabetes Control and Complications
Trial, demonstrated the arrested progression of diabetic neuropathy
with intensive glucose control and close monitoring of glycosylated
hemoglobin levels. As a rule, the risk of foot pathology is greatly
reduced by diabetics who are successful at long-term diabetic control
and can maintain their glycosylated hemoglobin levels under 8%.