Chapter 26

Pes Cavus
Fabian G. Krause, Gregory P. Guyton

CHAPTER CONTENTS overly simplistic. Bentzon2 and Hallgrimsson16 in 1939

proposed that extrinsic muscle imbalance underlay all
ETIOLOGY 1361 deformities. In 1959, Duchenne9 subsequently proposed
CHARCOT-MARIE-TOOTH DISEASE 1361 that the deformity results from an imbalance between the
POLIOMYELITIS 1363 extrinsics and the intrinsics. Neither approach is fully
Patterns of Foot Deformity in Polio 1363 satisfactory; a cavus foot is best thought of as an end result
Hindfoot Cavus 1363 that a variety of subtle neurologic lesions can produce.
Forefoot Cavus 1364 Brewerton et al5 specifically looked at the cause of pes
Other Deformities 1364 cavus in a series of 77 patients and found subtle neuro-
OTHER NEUROLOGIC LESIONS 1364 logic defects in 66% of them, leaving a large group of
POSTTRAUMATIC CAVOVARUS FOOT “idiopathic” cases. Of these, 11 of the 26 patients had a
DEFORMITIES 1364 family history of pes cavus, and 7 of the 26 had nonspe-
CONGENITAL PES CAVUS 1365 cific abnormalities upon electromyographic and nerve
Clubfoot Residuals 1365 conduction velocity examination. Most cases of idio-
The Idiopathic Cavus Foot 1365 pathic pes cavus likely represent a very subtle neurologic
EVOLUTION OF DEFORMITY 1365 lesion that is below clinical detection. Roughly half of the
BIOMECHANICAL CONSEQUENCES OF PES CAVUS 1366 detectable lesions are variants of Charcot-Marie-Tooth
Physical Examination 1368 disease, but a host of other less common conditions can
INVESTIGATIONS 1369 also be discovered (Table 26-1).19
Conservative Treatment 1370 Neurologic referral is mandatory in situations that
Surgical Treatment 1370 might point toward a correctable lesion of the spinal cord,
Decision Making 1370 such as a syrinx or spinal cord tumor. These include rapid
Soft Tissue Procedures (Video Clips 47, 49, and 51) 1370 progression, hyperreflexia, clonus, or significant asymme-
Bony Procedures (Video Clips 48, 50, 75, and 118) 1374 try between sides in motor pattern or deformity. A new
Outcome 1380 diagnosis of central neurologic disease is not uncommon
in foot and ankle practice.

Pes cavus describes a foot with a high arch that maintains

its shape and fails to flatten out with weight bearing. By
majority, the components of pes cavus are an increased
calcaneal pitch and varus of the hindfoot, plantar flexion
of the medial forefoot, and adduction of the entire fore-
foot. The predominant deformity in pes cavus may be in
the hindfoot, the forefoot, or a combination of both. A
precise radiographic definition of pes cavus is difficult
because the deformity is made up of various components
in the forefoot and hindfoot.
ETIOLOGY
Although the specific etiology of any cavus foot varies
with the disease process, all forms result from muscle
imbalance. Historical attempts to attribute all forms of
cavus foot to a single neurologic lesion have proven
CHARCOT-MARIE-TOOTH DISEASE
Charcot-Marie-Tooth disease (CMT) should at least be
considered in every patient who presents with pes cavus.
CMT is not, in fact, a single disease but rather a hetero-
geneous group of disorders caused by inheritable defects
in any of several constituent proteins of the myelin sheath
of peripheral nerve. The disorder was described in general
terms by the great French neurologist Jean Martin Charcot
and his pupil Marie in 1886 and independently by Tooth
in England later that year.6,44 Originally, Charcot attrib-
uted the disorder to a spinal defect, and it was Tooth’s
subsequent work that correctly classified it as a peripheral
nerve disorder. The disease is the most common inherit-
able defect of peripheral nerves, but approximately half
of the time it represents a new sporadic chromosomal
recombination error.

1361
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

Table 26-1 Etiology of Pes Cavus aberration is inheritable in an autosomal dominant

fashion, but many cases seem to represent sporadic chro-
Classification Specific Etiology
mosomal recombination events.
I. Neuromuscular CMT-1B accounts for 5% to 10% of CMT-1 patients
A. Muscle disease Muscular dystrophy and is associated with a point mutation in the myelin P0
B. Afflictions of Charcot-Marie-Tooth
gene. The phenotype is associated with a particularly
peripheral nerves and disease
lumbosacral spinal Spinal dysraphism
aggressive form of the disease.
nerve roots Polyneuritis CMT-1C represents the small remainder of CMT-1
Intraspinal tumor patients in whom the genetic defect is still unknown.
C. Anterior horn cell Poliomyelitis CMT-2 is the second most common general form of
disease of spinal cord Spinal dysraphism the disease and represents 20% of patients. It is autoso-
Diastematomyelia mal dominant like CMT-1 but has dramatically different
Syringomyelia
electrical findings: NCVs are near normal, and there is no
Spinal cord tumors
Spinal musculature atrophy evidence of demyelination. Four separate chromosomal
D. Long-tract and central Friedreich ataxia loci have been identified, but the product proteins
disease Roussy–Lévy syndrome involved remain unknown. In general, the course of
Primary cerebellar disease CMT-2 is more indolent than that of CMT-1.
Cerebral palsy CMT-X shows an X-linked inheritance pattern; male
II. Congenital Idiopathic cavus foot patients are affected and female patients are either unaf-
Residual of clubfoot
fected or mildly affected carriers. It is found in 10% to
Arthrogryposis
III. Traumatic Residuals of 20% of all CMT cases and is associated with defects in yet
compartment syndrome another myelin constituent protein, connexin 32.
Crush injury to lower CMT-4 is an autosomal recessive form of the disease
extremity and is quite rare. It in fact encompasses a large number
Severe burn of described genetic defects on different chromosomal
Malunion of fractured foot
loci; no product proteins have yet been described.
Modified from Ibrahim K: Pes cavus. In Evarts CM, editor: Surgery of The foot deformities in CMT do not result from abso-
the musculoskeletal system, New York, 1990, Churchill Livingstone, lute weakness of the motor units powering the foot but
pp 4015–4034.
of their relative imbalance. Initiation of the deformity
likely results from an imbalance of the failing foot intrin-
sics and the preserved extrinsics.3 Subsequently, a specific
The nomenclature associated with CMT is confusing pattern of extrinsic motor weakness is common in CMT
because of the historical lack of understanding of its in which the anterior and lateral compartment muscu-
cause. The archaic term peroneal muscular atrophy (PMA) lature is selectively affected, with certain curious excep-
was supplanted by Dyck and Lambert, who developed tions. The disease almost always affects the peroneus
an extensive classification of inheritable motor neuropa- brevis but spares the peroneus longus. This was first
thies based upon their electrodiagnostic patterns in the observed clinically by Mann and Hsu33 and subsequently
1960s and 1970s.12 Their scheme refers to a series of seven confirmed by Tynan et al,45 who demonstrated that the
hereditary motor sensory neuropathies (HMSN-I through cross-sectional area of the peroneus longus was preserved
HMSN-VII). on magnetic resonance imaging (MRI) of patients with
Since 1990 there has been an explosion of understand- the disease. An additional oddity can be observed in the
ing of the specific genetic defects underlying the CMT anterior compartment musculature; the extensor hallucis
disorders,4 leading to a new and still evolving reclassifica- muscle can be spared while the anterior tibialis is
tion of the disease. affected. This occurs despite the more distal location of
CMT-1 is the most common form and accounts for the extensor hallucis longus (EHL) and their shared pero-
more than 50% of all cases. It is autosomal dominant and neal innervation.
demonstrates slow nerve conduction velocities (NCVs) in The reasons for the unusual patterns of motor weak-
the range of 10 to 30 m/sec as a result of demyelination. ness in CMT remain poorly understood. The selective
CMT-1 can be further subdivided. denervation affects certain muscles in the anterior and
CMT-1A accounts for 80% of CMT-1 cases and is the lateral compartments, and only very late posterior com-
single most common form of the disease in general. Curi- partment involvement is seen. Denervation in CMT
ously, it is usually caused by a segmental trisomy along progresses very differently from a classic symmetric
chromosome 17. The area contains the gene for periph- polyneuropathy, such as that encountered in diabetes. At
eral myelin protein-22 (PMP-22), whose function remains least some speculation has been centered upon the
unknown. Although some cases have been linked to alter- possibility that some element of nerve compression can
native point mutations in PMP-22, the segmental trisomy play a role.14
responsible for most cases indicates CMT can be pro- Regardless of the cause of the patterns of weakness,
duced from a gene dosage effect. This chromosomal each of the deformities of the disease can be explained in

1362

Table 26-2 Foot Deformities in Charcot-Marie-Tooth Disease
Deformity Weak Agonist Muscle(s) Intact Antagonist Muscle(s)
Equinus Tibialis anterior Gastrocnemius–soleus
complex (triceps-surae)
Adduction and Peroneus brevis Tibialis posterior
hindfoot varus
Plantar flexion of Tibialis anterior Peroneus longus
the first ray
Toe deformities Foot intrinsics Long toe flexors
Hallux claw toe Foot intrinsics EHL and FHL
From Guyton GP, Mann RA: The pathogenesis and surgical management of foot deformity in Charcot-Marie-Tooth disease, Foot Ankle Clin
5:317–326, 2000.
EHL, extensor hallucis longus; FHL, flexor hallucis longus.
the form of a weak agonist muscle and a more normally
functioning antagonist (Table 26-2). There is no evidence
of spasticity in the motor units that remain innervated.
The functional peroneus longus serves to plantar flex
the first ray while the denervated anterior tibialis fails
to provide any counterbalancing dorsiflexion. The first
metatarsal head is depressed and a forefoot cavus results.
Next to a relative talus dorsiflexion, an equinus contrac-
ture develops as the Achilles tendon (triceps surae) is
unopposed by the anterior tibialis. In addition, the toe
extrinsics force the toes into a clawed position that is not
counterbalanced by the denervated foot intrinsics. This
also serves secondarily to depress the metatarsal heads
and raise the arch. The supination and adduction of the
foot is worsened because the posterior tibialis is unop-
posed by the weakened peroneus brevis. In cases with
sparing of the EHL, the claw toe deformity of the hallux
is worsened even more dramatically because the patient
uses the EHL to dorsiflex the foot and compensate for the
weak anterior tibialis.
It is rare in clinical practice to encounter a patient at
such an early stage of disease that the foot is entirely
supple with no hindfoot or forefoot contractures.
However, rebalancing the foot through tendon transfers
can help prevent the development of further deformity if
it is done early enough.38 For instance, the overpull of the
peroneus longus that forces the forefoot into cavus can
be eliminated by transferring the tendon to the peroneus
brevis. This also serves to help oppose the tibialis poste-
rior and prevent adduction. The emphasis in early-stage
surgery on CMT should be on tendon transfers rather
than lengthening motor units. Because the long-term
outcome of CMT is one of progressive, inexorable weak-
ness, strength should be preserved whenever possible.
POLIOMYELITIS
The last great epidemic of polio in the United States
occurred in New England in 1955. Although the residual
Pes Cavus ■ Chapter 26
Action
Plantar flexion
Adducts the foot, inverts the subtalar joint
Plantar flexes the first ray, creates a secondary
forefoot cavus
Clawing occurs as the extrinsic forces are
unmodified by the intrinsics; also depresses
the metatarsal heads and accentuates cavus
Severe hallucal clawing occurs when a spared
EHL is used to assist a weak tibialis anterior
dorsiflex the foot
effects of the disease are now encountered with increasing
rarity, it still serves as a useful model of a process that can
produce either a forefoot cavus or a hindfoot cavus.8
Paralytic polio is the result of a ribonucleic acid (RNA)
virus that primarily affects the thalamus, hypothalamus,
motor centers of the brain stem and cerebellum, and the
anterior tracts of the spinal cord. There is a wide variety
of clinical presentations depending upon what portions
of the central nervous system (CNS) are affected, but as
a practical matter the lower extremity weakness patterns
of polio come from a strikingly selective destruction of
the anterior motor neurons in the spinal cord itself, pre-
serving function both proximal and distal to the lesion.
After an initial incubation period of 6 to 20 days, the
acute phase of the disease is associated with the most
dramatic paralysis and lasts approximately 7 to 10 days.
Clinically detectable weakness usually occurs when more
than 60% of the motor neurons to a muscle group are
affected. Muscle function can recover gradually thereafter;
the most substantial gains occur in the first 4 months, and
some return of function is usually seen up to 2 years after
the illness.
Patterns of Foot Deformity in Polio
Hindfoot Cavus
The gastrocnemius–soleus complex is the critical variable
in determining what variety of foot deformity will
develop. The classic cavus foot deformity resulting from
polio is that of a hindfoot cavus associated with a dra-
matically high calcaneal pitch angle. This is the result of
the paralysis of the gastrocnemius–soleus complex with
preservation of the remainder of the posterior compart-
ment, the intrinsic foot musculature, and the anterior
tibialis. When appropriate tension is missing from the
Achilles tendon, the long toe flexors still function to
depress the metatarsal heads, raising the arch. The intrin-
sics foreshorten the distance between the metatarsals and
the calcaneus, functioning much like a bowstring to raise
1363
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders
the calcaneal pitch. The result is a vertical posture of the
calcaneus.
Forefoot Cavus
A lesion slightly higher in the spinal cord can spare the
gastrocnemius–soleus complex but affect the tibialis ante-
rior selectively. This situation results in two particular
imbalances that drive depression of the first ray and a
forefoot cavus. First, just as in CMT, the peroneus longus
is unopposed and directly plantar flexes the first ray.
Second, the extensor hallucis longus is still functional and
serves as an accessory dorsiflexor of the foot. This creates
a claw toe as the foot is pulled up through the toe rather
than the usual midfoot insertion of the tibialis anterior.
The claw toe deformity itself also serves to depress the
metatarsal head.
Other Deformities
Because the motor neuron destruction in poliomyelitis is
often patchy and recovery is sometimes incomplete, the
patterns of motor weakness cannot always be so neatly
categorized. When the tibialis posterior is affected, either
alone or in combination with the tibialis anterior, the
result is a progressive planovalgus foot rather than a cavus
foot. Rarer still is isolated involvement of the peroneals,
which usually results in a very mild cavus foot dominated
more by varus of the hindfoot with attendant instability
of the ankle. The critical lesson is that, like all peripheral
neural lesions, the motor weakness patterns in polio all
must be evaluated and treated individually.
OTHER NEUROLOGIC LESIONS
Although CMT and polio represent the most historically
prominent etiologies of the cavus foot, a wide variety of
other lesions can lead to the deformity.
Friedreich ataxia is a familial progressive ataxia in
which posterior column function is steadily lost.36 It
occurs in an autosomal recessive form with an earlier age
of onset (11.75 years) and in a dominant form with a later
age of onset (20.4 years). No cases of onset after the age
of 25 have been reported. The disease is usually associated
with pronounced and progressive symmetric cavus foot
deformities with severe claw toe formation. In numerous
instances, the foot deformities have been the presenting
complaint.
A heterogeneous group of hereditary cerebellar ataxias
are also associated with cavus foot, but they are less easy
to categorize than Friedreich ataxia, which primarily
shows spinal cord involvement.
Roussy-Lévy syndrome is a rare syndrome of cavus foot,
sensory ataxia without obvious long-tract signs, periph-
eral motor atrophy, and kyphoscoliosis. Because it shares
characteristics of both diseases, it was poorly differenti-
ated from Friedreich ataxia and CMT for many years.37
The onset occurs very early in childhood and runs a rela-
tively benign course.
1364
Spinal muscular atrophy is a heterogeneous group of
disorders that are usually present from birth but have
some late-onset forms.41 They are characterized by an
inexorably progressive loss of anterior motor neuron
cells. The disorders are characterized by hypotonia and
can be associated with the cavus foot deformity, although
it is rarely the presenting feature.
Structural spinal cord disease often manifests with
cavus foot deformity and requires a high degree of suspi-
cion to detect. In particular, the unexplained onset of a
progressive bilateral cavus deformity, or essentially any
unilateral deformity, should warrant an imaging workup.
Spinal cord tumors are notorious for their early absence of
symptoms, and foot deformity might be the initial com-
plaint. Syringomyelia is a cavitation in the center of the
spinal cord that usually occurs in the cervical cord but can
also interrupt the neural pathways to the lower extremi-
ties and result in spasticity or deformity. Diastematomyelia
is a rare disorder in which a spicule of bone or fibrous
band sagittally divides the spinal canal in the thoracic or
high lumbar regions and separates the spinal cord into
two pieces, each surrounded by dura. Because the cord
and axial skeleton grow at different rates, a traction
myelopathy very slowly develops as the child matures.
The findings can be subtle, but making the diagnosis is
critical.
Spinal dysraphism in all its forms (spina bifida, myelo-
cele, myelomeningocele) is certainly more common and
can manifest with a variety of postural foot disorders
depending upon the particular patterns of involvement.
Fortunately, the diagnosis is almost always well estab-
lished early in life.
Cerebral palsy is, by definition, a static encephalopathy
and can result in a variety of foot deformities, including
pes cavus. Although the neurologic lesion is not progres-
sive, the flexibility of the postural disorders deteriorates
with time.
POSTTRAUMATIC CAVOVARUS FOOT
DEFORMITIES
Any traumatic condition that leads to an imbalance of the
intrinsic and extrinsic foot musculature can lead to a
cavus deformity. The deep posterior compartment of the
leg is most commonly involved in traumatic compart-
ment syndromes, and a Volkmann contracture in that
location will lead to a cavus foot with a prominent claw
toe component. Crush injuries of the leg and severe burns
or soft tissue loss can also have the same result, both from
direct injuries to the musculature and indirectly through
tibial nerve injury. Compartment syndromes confined to
the foot most commonly occur with calcaneus fractures
or with crush injuries to the forefoot; they have been
associated with the late development of claw toes but not
with cavus deformity.
Several forms of fracture malunion can also result in a
fixed cavovarus deformity. Most commonly, a talar neck
fracture with substantial medial comminution can fall

into a varus malunion. This substantially limits subtalar
joint eversion and leads secondarily to the calcaneus
assuming a varus malalignment. Alternatively, a varus
hindfoot can result from residual deformity from an
intraarticular calcaneus fracture or even medial impaction
of the tibial plafond.
CONGENITAL PES CAVUS
Clubfoot Residuals
The cavus foot deformity is one of four components of
the congenital clubfoot, easily remembered by the mne-
monic CAVE (cavus, adductus, varus, equinus). Adult
clubfoot residuals encountered after childhood casting
usually result from a failure of early casting to adequately
elevate the first ray before abducting the foot about the
fulcrum of the talar head as described by Morcuende
et al.35 The most severe deformities that result from
improper casting technique are usually not those of resid-
ual cavus but of a rocker-bottom foot that results when
the equinus is inappropriately corrected while the calca-
neus remains locked under the talus; the foot then dorsi-
flexes through the midfoot rather than through the ankle.
A wave of enthusiasm for surgical clubfoot correction
in the 1970s and 1980s is also now yielding residual
effects in the adult foot and ankle population. The results
of clubfoot correction surgery have proved to be substan-
tially less reliable than once thought.30,42 A patient pre-
senting with problems with a postsurgical clubfoot is just
as likely to have overcorrection into planovalgus as resid-
ual undercorrection in cavovarus. The one constant in the
surgically corrected clubfoot is a remarkable amount of
stiffness in adults. In a dynamic gait analysis study, Huber
and Dutoit18 specifically identified late subtalar stiffness
as the primary feature associated with a poor result after
childhood clubfoot surgery. It is rare that anything short
of triple arthrodesis can be entertained to address the
residual complaints.
The Idiopathic Cavus Foot
Despite the litany of potential known causes of the cavus
deformity, the largest single group of cases encountered
is symmetric and has no known cause. They can manifest
because of stiffness in the hindfoot, stress fractures along
the lateral column, recurrent ankle instability, or, com-
monly, for symptoms totally unrelated to the conforma-
tion of the arch.
EVOLUTION OF DEFORMITY
Pes cavus must be viewed as a spectrum of deformities in
which the underlying abnormality is that of an elevated
longitudinal arch, but after that a variety of bony and soft
tissue deformities can be present. The spectrum can range
from a mild cavus foot, with flexible claw toes as the only
significant clinical problem, to a severe fixed deformity,
Pes Cavus ■ Chapter 26
Figure 26-1 Pes cavus with a predominant hindfoot
deformity. Note the dramatically high pitch angle of the
calcaneus.
with altered weight bearing, callosities, lateral ankle laxity,
stress reactions, and pain. The shape of the foot varies
with the cause and duration of the motor imbalance that
created the deformity. When muscular imbalance in pes
cavus begins before maturation of the skeleton, there can
be substantial change of healthy osseous morphology.
After skeletal maturity, there is usually little or no change
in the morphology.1 The cavus foot is best understood by
systematically analyzing the bone deformities, the soft
tissue deformities, and the specific muscle functions that
are imbalanced.
The bony deformity may be predominantly in the
hindfoot, the forefoot, or a combination of both. A hind-
foot cavus describes an elevated pitch of the long axis of
the calcaneus, which is usually greater than 30 degrees in
a cavus foot (Fig. 26-1). Hindfoot cavus was a very
common deformity in the era of widespread poliomyeli-
tis; the focal nature of the disease in the anterior horn
cells of the spinal cord often led to gastrocnemius weak-
ness but sparing of the tibialis anterior and often the foot
intrinsics. The resultant imbalance of forces then often
led to dramatic calcaneal pitch angles and subsequent
soft tissue contractures. Pure hindfoot cavus is now less
common, while hindfoot varus is a predominant finding
in pes cavus with underlying neurologic disease. Elevated
calcaneal pitch is still encountered as a component of a
combined deformity in the idiopathic cavus foot with no
clear neurologic cause.
Most neurologic cavus deformities are thought to
occur from a forefoot-driven hindfoot varus resulting
from a muscle imbalance as in CMT. The peroneus longus
tendon is a direct antagonist to the tibialis anterior
tendon. Often spared by the neuropathy, the strong pero-
neus longus muscle overpowers the affected tibialis ante-
rior and initializes the deformity by plantar flexion of the
medial forefoot (Fig. 26-2). The tibialis posterior muscle
induces the hindfoot varus, and the Achilles tendon
further enhances the varus stress secondary to the plantar-
flexed first ray and varus heel alignment, which alters the
1365
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

A1 A2

B C
Figure 26-2 Left pes cavus of Charcot-Marie-Tooth patient with a predominant forefoot deformity. A, The driving force is the
plantar-flexed and adducted forefoot, clinically seen as depression of the first metatarsal head. The radiograph demonstrates
plantar flexion and adduction of the first metatarsal relative to the axis of the talus (talo–first metatarsal angle). B, Bilateral
plantar flexion of the first metatarsal accompanied by a varus heel deformity. C, Some cases demonstrate a more generalized
forefoot deformity with generalized forefoot equinus.

transmission of axial forces through the ankle joint. With
inversion of the hindfoot, the lateral foot supinates and
the peroneus longus muscle further plantar flexes the first
ray to restore the tripod position and a plantigrade foot.1
Soft tissue contracture converts a flexible to a fixed cavus
deformity over time.
Toe deformities are thought to occur from early degen-
eration of the intrinsic muscles of the foot. Because the
lumbricals are not acting to stabilize the metatarsalpha-
langeal (MTP) joint (intrinsics effect: MTP flexion, proxi-
mal interphalangeal [PIP] and distal interphalangeal
[DIP] extension), the unopposed extensor digitorum
longus hyperextends the unstable lesser toes at the MTP
level while the flexor digitorum longus and brevis flex the
phalanges.1 The plantar-flexed metatarsal heads and
plantar fascia shortening amplify forefoot plantar flexion.
The deformities might be as mild as flexible clawing of
the MTP joints in association with mild flexion of the
interphalangeal joints, or they can manifest as fixed claw
toe deformities. Once severe fixed claw toe deformities are
present, the forces from the extrinsic toe extensors serve
to hold the metatarsal heads in a plantar-flexed position
(Fig. 26-3). Of importance, the plantar fat pad is dis-
placed distally in severe cases as the toes pull up into
extension. Not only are the metatarsal heads driven plan-
tarward by the deformity, but they are also deprived of
their normal cushioning layer of fat.
The plantar fascia commonly develops a contracture
with time in all forms of cavus foot. It is anatomically
much thicker on the medial aspect of the foot, and as the
contracture develops, it not only holds the longitudinal
arch in an elevated position but also holds the forefoot
adducted and keeps the calcaneus inverted (Fig. 26-4).
Although some bony procedures can secondarily relax the
plantar fascia by altering the shape of the arch, they are
not always adequate by themselves.
Early in the development of many cases of forefoot
cavus the deformities remain relatively flexible. The arch
might not flatten while standing, but muscle forces are
holding it in position rather than bone and joint contrac-
tures. This is typical, for instance, of a very young patient
with Charcot-Marie-Tooth disease. The subtalar joint
compensates for the forefoot deformity by falling into a
varus alignment (Fig. 26-5). As the disease progresses, the
capsule and interosseous ligament of the subtalar joint
become contracted, and the once-flexible hindfoot defor-
mity becomes fixed.
BIOMECHANICAL CONSEQUENCES
OF PES CAVUS
The mechanics of all variants of the foot are similar. The
axes of the talus and the calcaneus are more collinear.
The talar head remains over the anterior process of the

1366
 Pes Cavus ■ Chapter 26

A B1

B2 B3
Figure 26-3 Metatarsophalangeal (MTP) joint deformities. A, Mild claw toes of the right foot with a near-normal left foot.
B, Examples of severe clawing of the MTP joints, including clawing of the hallux from the use of the extensor hallucis longus as
an accessory dorsiflexor.

A B
Figure 26-4 Contracture of the plantar fascia contributes to and fixes the deformity. The tight medial band of the plantar
fascia holds the forefoot in adduction and the hindfoot in varus. A, Cavus foot demonstrates adduction of the forefoot, an
elevated longitudinal arch, and varus of the calcaneus. B, Radiograph demonstrating severe adduction of the forefoot.

calcaneus, and the navicular moves to a superior instead
of a medial position to the cuboid; the subtalar joint axis
is more vertical; and the Chopart joint function is
impaired.1 When the hindfoot is locked in inversion,
there is less subtalar and transversal tarsal motion during
gait than in the normal foot. The ability of the foot to
absorb the impact of walking by pronation during the
early part of stance phase is diminished, and the first
metatarsal head and the lateral border of the foot are
overloaded.1 A cavus foot is always stiffer than one of
normal conformation.
The relative dorsiflexion of the talus within the ankle
mortise is caused by plantar flexion of the medial fore-
foot, limits ankle dorsiflexion, and is accompanied by

1367
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

A B

C1 C2
Figure 26-5 Varus heel deformity. A, In cases of forefoot-driven cavus, the varus heel is initially present as the natural
standing posture of the heel when the first ray is plantar flexed and adducted. With time, the hindfoot deformity can become
fixed. The presence of the deformity can be best assessed from behind. B, An axial view of the calcaneus demonstrates marked
varus deformity. C, The Coleman block test can be used to demonstrate persistent flexibility of the hindfoot. If the heel can be
forced into valgus by weight bearing on a block supporting only the lateral column of the foot, the subtalar joint remains
flexible. In this case, the cavus can be corrected by addressing the forefoot deformity alone.

anterior ankle impingement. Together with the hindfoot
varus position, relative talus dorsiflexion is thought to
contribute to an increased anteromedial contact stress in
the ankle joint. The association between lateral ankle
instability, cavovarus deformity, and ankle arthritis has
been discussed in the literature.13,46 A significant pressure
increase and reduction of the area loaded in the ankle
joint was also demonstrated in simulated pes cavus and
is considered to lead to ankle arthritis in long-standing
deformities with, but also without, lateral ligament
instability.24
In the forefoot, the weight-bearing area beneath the
metatarsal heads and heel pad is decreased, leading to
substantially higher plantar pressures in both locations.
In addition, because of the clawing and hyperextension
of the MTP joints, the toes do not participate in weight
bearing during toe-off, and power is diminished. The
plantar fascia normally functions as a passive windlass
mechanism to elevate the longitudinal arch, plantar flex
the metatarsals, and invert the calcaneus. In the cavus
foot, all three of these conditions are present perma-
nently, and the plantar fascia becomes contracted.
The muscle weakness patterns seen around the foot
vary with the cause of the condition, but adduction of the
forefoot is commonly seen when the posterior tibialis is
active in the presence of a weak peroneus brevis. Metatar-
sus adductus exacerbates the already considerable ten-
dency for excessive pressure in the lateral column of the
foot, and stress reactions of the fifth metatarsal can result.
Physical Examination
The patient encounter begins with a careful history of the
condition and a detailed family history. Generalized
lateral column pain seems to be the most common pre-
senting symptom associated with the cavus foot. Fre-
quently, patients report ongoing lateral hindfoot
instability despite one or more previous lateral hindfoot

1368

ligament repairs or reconstructions that failed later
because the predisposing hindfoot statics were not
corrected.
The patient’s gait is carefully observed for the nature
of ground contact, the position of the heel, and the posi-
tion of the toes during stance. Any fall of the heel toward
further varus as weight transfers onto the limb should be
noted by observing the patient walk from behind. During
swing phase, the examiner should check for the possibil-
ity of a footdrop and the use of the extensor hallucis
longus as an accessory dorsiflexor, leading to a cock-up
deformity of the first MTP joint.
The heel pad could be seen easily from the front (“peek
a boo”) with the patient standing and feet aligned straight
ahead. In a normal foot, the heel pad is not visible on the
medial side of the foot when viewed from the front
because of the slight amount of valgus positioning of the
average heel, which places the heel pad behind the normal
hindfoot.
The relative position of the hindfoot to the forefoot
must be noted along with the rigidity of that relationship.
The normal hindfoot will be positioned in slight valgus
when standing flat and deviate into varus when rising
onto the toes. The patient is asked if he or she experiences
a subjective instability in the tiptoe position.
The Coleman block test can be used to determine the
ability of the hindfoot to fall back into an appropriate
valgus posture. The heel alone or heel and lateral column
of the foot are supported on a small flat wooden block
while the forefoot or the medial column, respectively,
remain unsupported. If the hindfoot is not fixed and the
deformity is being driven by a first ray fixed in plantar
flexion, the calcaneus will noticeably tilt into valgus when
viewed from behind. In theory, a foot that exhibits flexi-
bility on the Coleman block test can be corrected by
working on the forefoot deformity alone.
With the patient seated, the examiner observes active
and passive range of motion of the ankle, subtalar, trans-
verse tarsal, and MTP joints. The forefoot should also be
examined after manual correction of the hindfoot varus
deformity to assess the amount of fixed forefoot prona-
tion and to determine the need for medial metatarsals
dorsiflexion osteotomies. Limited and painful ankle dor-
siflexion may demonstrate anterior or anteromedial ankle
impingement because of the relative talar dorsiflexion
within the ankle mortise. The hindfoot is assessed for any
chronic ligamentous incompetence. Clinical signs of the
lateral border overload range from calluses to proximal
diaphyseal or metaphyseal fractures of the lateral meta-
tarsals. Peroneal tendon pathology, including tears and
subluxation, are commonly present, as is tightness of the
gastrocnemius–soleus complex.
Muscle function is very carefully assessed and docu-
mented for evaluation disease progression. Special atten-
tion should be paid to the ability of the peroneus longus
to selectively plantar flex the first ray because this can
point to the potential for a tendon transfer to effectively
assist in treatment. A patient who does not carry a known
Pes Cavus ■ Chapter 26
neurologic diagnosis should also undergo a neurologic
screening, including testing for long-tract signs, reflexes,
hamstring tightness, and any asymmetry. Intrinsic wasting
is usually easier to pick up in the upper extremity, and in
suspected cases of CMT or other systemic peripheral neu-
ropathies, an examination of the intrinsic musculature of
the hands is in order. Subtle disease can usually be dis-
cerned in the loss of muscle mass and strength of the first
dorsal interosseous along the radial border of the second
metacarpal. The patient exhibits weakness in abducting
the index digit away from the midline with the rest of the
hand held in a neutral position to isolate the intrinsics.
Because of the very subtle findings associated with
structural disease of the spinal cord, substantial unex-
plained asymmetry or rapid progression of the deformity
warrants a neurologic referral and corresponding imaging.
INVESTIGATIONS
Standing anteroposterior (AP) and lateral radiographs of
the foot and ankle are essential. A line drawn down the
axis of the talus should pass through the axis of the first
metatarsal on both AP and lateral weight-bearing images
of the foot in the normal situation. The axes should ordi-
narily be collinear, 0 degrees ± 5. The lateral talo–first
metatarsal angle (the Meary angle) can be used to assess
the severity of a forefoot plantar flexion, whereas, as
opposed to other measured angles, the extent appears to
correlate with the development of anteromedial ankle
arthritis.24 The AP talo–first metatarsal angle defines the
amount of forefoot adductus. The calcaneal pitch angle is
elevated in cases of hindfoot cavus.
Further findings on the lateral radiographs are an
increased navicular height, an increased Hibbs angle
(measured by a line through the axis of the calcaneus and
the first metatarsal—in normal feet the angle is 45 degrees,
and in cavus feet, it is near 90 degrees), and a posterior
fibula with a “flat-topped” talus. The latter appearance is
an artifact because in pes cavus a standard lateral view is
in fact an oblique view.
On the AP radiograph of the foot, the talocalcaneal
angle is almost parallel in moderate and severe hindfoot
varus. The presence of any associated metatarsus adductus
should be noted by drawing of the AP talo–first metatar-
sal angle because this can require some degree of addi-
tional surgical attention or limit the degree of correction
that can be achieved.
The extent and progression of any ankle arthritis and
talar tilt is recorded on extra AP and lateral standing ankle
radiographs. The Saltzman view can be added to assess
the angles of the tibiotalar and the subtalar joint.
Computed tomography (CT) examination with the
foot supported in the typical 90-degree position, with
sagittal and coronal reformats, and three-dimensional
modeling rules out occult degenerative joint disease and
tarsal coalitions. MRI or ultrasound can occasionally be
helpful to reveal any inflammation, splitting, or tears
of the tendons. MRI can also detect early cartilage
1369
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders
degeneration and osteochondral lesions when arthritis is
not yet visible on plain radiographs or CT.
A digital dynamic pedobarography can be helpful to
determine a pathologic plantar pressure distribution.
Associated changes are the lateralization of the line of
center of pressure and increased zone of pressure under
the first metatarsophalangeal joint in case of a plantar-
flexed first metatarsal.
Conservative Treatment
Many cases of cavus deformity represent stable or slowly
progressive deformities that are appropriately managed,
at least initially, by nonoperative means. In the case of an
adolescent with progressive deformity and a still-supple
foot, however, there may be much to be lost by delay. Soft
tissue surgery alone might manage the deformity early in
the course of the disease, avoid ankle arthritis, and prevent
the necessity of osteotomies or fusions.
A stretching program to maintain motion is an impor-
tant component of conservative management, particu-
larly in cases of neurologic origin. Eversion and
dorsiflexion should be emphasized. Metatarsalgia might
be an early presenting complaint from uncovering of the
metatarsal heads as claw toes develop. Accommodative
manufactured shoes with extra-depth toe boxes can be of
substantial benefit.
Orthoses are a valuable adjunct to the conservative
treatment of cavus feet. The reduced weight-bearing area
in cavovarus feet is enlarged with orthotic devices. Typical
custom foot orthotics for cavus may include an elevated
heel to accommodate a tight gastrocnemius muscle and
a recess under the first metatarsal head to accommodate
the plantar-flexed first ray and allow some degree of hind-
foot eversion.34 A forefoot wedge, beginning just lateral
to the first metatarsal recess, extends to the lateral border
of the device to mirror the forefoot pronation.
Basically, the more fixed the cavus deformity is, the less
likely is much benefit from orthoses, and discomfort and
calluses may develop in supported areas. Once the defor-
mity becomes fixed, patients tolerate corrective orthoses
poorly. For lateral ankle instability, a high-top boot or an
off-the-shelf ankle brace offer hindfoot stabilization.
Lace-up braces are easier to fit inside a shoe or boot and
stabilize the ankle comparably to plastic upright braces.
Preexisting ankle instability usually worsens by high-
arched orthoses amplifying hindfoot varus.
Severe muscle weakness is usually treated with full-
length custom ankle–foot orthoses (AFOs) to prevent
foot drop. The integration of orthotic modifications into
the AFO improves proprioception and ankle stability
more than the brace alone. Many patients can be managed
by hinged AFOs with dorsiflexion assistance to allow a
much more normal gait pattern. In some cases of equinus
deformity, full clamshell braces or casts are needed
because the strong or unopposed plantar flexors will over-
come the correction obtained with a posterior brace or
anterior strap.
1370
Surgical Treatment
Decision Making
The goal of surgical management is to produce a planti-
grade, stable foot, to alleviate discomfort, and to improve
function. Surgical realignment should be recommended
when signs of tendon or hindfoot joint degeneration
arise, resulting from recurrent hindfoot instability or ele-
vated hindfoot joint contact stresses by varus alignment.
Earlier surgery may be appropriate due to lateral column
pain or progressive deformity.
Basics of dynamic and static realignment are that
tendons contributing to the deformity should be trans-
ferred to a more functional location (i.e., peroneus longus
to brevis), contracted structures should be released to
allow restoration of normal foot shape (i.e., plantar
fascia), and osteotomies are preferred over arthrodesis of
nonarthritic joints to help realign the foot to a more
functional position (calcaneal osteotomy instead of cor-
rective subtalar fusion). If the deformity is fixed, however,
an arthrodesis might be necessary to produce a planti-
grade foot.
There is no simple boilerplate approach applicable to
all cavus feet. A suggested algorithm is provided in Figure
26-6. The key to surgical decision making is to adopt
procedures that are necessary to match each specific
deformity. It is not uncommon to have a foot with a
combination of fixed and supple deformities; a particular
case might require a combination of bone and soft tissue
procedures.
Soft Tissue Procedures
PLANTAR FASCIA RELEASE (STEINDLER STRIPPING)
The contracted plantar fascia plays a major role in main-
taining height of the longitudinal arch and varus posi-
tioning of the calcaneus in the patient with pes cavus.
Release and stripping of the plantar fascia often help to
reduce the height of the longitudinal arch in patients who
retain some degree of flexibility (Video Clip 47).43 At
times, the procedure may be carried out in conjunction
with a lateralizing calcaneal osteotomy, a triple arthrod-
esis, or a first metatarsal osteotomy.
Surgical Technique
1. The patient is placed in a supine position. The normal
external rotation of the lower extremity provides ade-
quate visualization of the foot. A tourniquet is used
around the thigh.
2. An oblique skin incision is made, starting distal to the
weight-bearing area of the calcaneal fat pad and
passing over the contracted plantar fascia. This incision
does not put the medial calcaneal branches to the heel
pad at risk of being cut.
3. The incision is deepened through the fat, exposing the
plantar fascia on the plantar aspect of the foot as well
as medially over the fascia of the abductor hallucis
muscle.
 Pes Cavus ■ Chapter 26

Pes cavovarus

Flexible?

Yes No
(Coleman block positive) (Coleman block negative)

Plantar flexed medial forefoot? Standard OR-steps Advanced or severe hindfoot arthritis?
=> Step 1: MT I (II, III) dorsiflexion => Lateralizing calcaneal- => Instead of or in addition to
osteotomy osteotomy lateralizing calcaneal-
=> Step 2: PL to PB transfer => PL to PB transfer osteotomy:
=> Step 3 (rarely): release of planter => MT I (II, III) dorsiflexion realigning subtalar, double, or
fascia osteotomy triple arthrodesis

Persistent hindfoot varus? Ankle arthritis?

=> Lateralizing calcaneal osteotomy => Anterior ankle arthrotomy,
cheilectomy

Equinus deformity? Persistent plantar flexion

=> Achilles-lengthening or of medial forefoot?
gastrocnemius recession => Plantar fascia release

Further options: Persistent forefoot

=> Repair/reconstruction of lateral hindfoot deformity?
ligaments => Forefoot reconstruction
=> PL to PB transfer, TA-lateralization or TP 1st toe clawing?
to PB transfer with neurologic etiology => Jones procedure

Equinus deformity?
=> Achilles-lengthening or
gastrocnemius recession

Further options:
=> Repair/reconstruction of lateral hindfoot
ligaments
=> TA-lateralization or TP to PB transfer
with neurologic etiology

Figure 26-6 Pes cavovarus treatment algorithm. PB, Peroneus brevis tendon; PL, peroneus longus tendon; TA, tibialis anterior
tendon; TP, tibialis posterior tendon.

4. The origin of the plantar fascia is transected while
tension is being applied to it by dorsiflexing the MTP
joints. In this way, the plantar fascia will separate as it
is cut. Often, some deeper septa must be carefully
transected. The lateral plantar nerve passes just distal
to the cut, so the surgeon must be cautious when tran-
secting the septa.
5. After releasing the plantar fascia, the surgeon palpates
along the medial aspect of the foot, particularly in a
severely deformed case, to release the superficial and
deep fascia surrounding the abductor hallucis muscle.
This is a very important part of the release, particularly
in cases involving significant adduction of the
forefoot.
6. Once the cuts have been made by blunt dissection and
stretching the fascia, the wound is carefully inspected
to ensure that no tight bands of fascia remain, either
on the plantar aspect of the foot or along the abductor
muscle.
Postoperative Care
The patient is placed into a short-leg compression dress-
ing incorporating plaster splints. The sutures are removed
in 12 to 14 days, after which the patient is placed in a

1371
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders
A B
Figure 26-7 Cock-up deformity of the first metatarsophalangeal joint from the use of the extensor hallucis longus as an
accessory dorsiflexor with a weak anterior tibialis. A, Resting. B, With active attempted dorsiflexion of the ankle.
short-leg cast. Weight bearing is begun as tolerated,
whereas 4 weeks of immobilization is usually adequate if
plantar fascia release is carried out as an isolated
procedure.
FIRST-TOE JONES PROCEDURE
The procedure is used to correct a hyperextension defor-
mity of the first MTP joint caused by weakness of the tibi-
alis anterior. Although the EHL is also located in the
anterior compartment and is innervated more distally
than the tibialis anterior, its function can be spared in a
surprising number of conditions. In modern practice, this
is usually seen in CMT or variants of cerebral palsy, but
it was historically common in polio.22 In these cases, the
EHL is functioning as an accessory dorsiflexor of the ankle
joint, which results in hyperextension of the MTP joint
and secondary flexion of the interphalangeal joint (Fig.
26-7). Moving the insertion of the EHL tendon into the
base of the first metatarsal facilitates dorsiflexion of the
ankle and also relieves the cock-up deformity of the MTP.
To prevent a floppy first toe, a fusion of the interphalan-
geal joint is usually performed.
Surgical Technique
1. The procedure is carried out with the patient supine.
A tourniquet is used around the thigh (Fig. 26-8 and
Video Clip 51).
Interphalangeal Joint Arthrodesis
2. An elliptic skin incision is centered over the dorsal
aspect of the interphalangeal joint of the hallux. The
collateral ligaments are cut to expose the articular
surfaces.
3. The extensor hallucis longus tendon is freed from its
retinacular attachments along its mediolateral aspect.
4. The surfaces of the interphalangeal joint are removed
with a power saw to create two flat surfaces. The inter-
phalangeal joint is placed in a few degrees of plantar
flexion and neutral varus/valgus alignment.
5. A 2.5-mm hole is drilled in an antegrade manner from
proximal to distal through the midportion of the
1372
Skin Screw
incision
Figure 26-8 The first-toe Jones procedure moves the pull of
the extensor hallucis longus (EHL) tendon from the great toe
to the neck of the first metatarsal. Interphalangeal joint
arthrodesis of the hallux is then performed to prevent a
floppy toe. The procedure aids the ability of the EHL to serve
as an accessory dorsiflexor and helps eliminate depression of
the first metatarsal head. (From Mann RA, Coughlin MJ: The
video textbook of foot and ankle surgery, St Louis, 1991,
Medical Video Productions.)
distal phalanx. Where the drill bit begins to pressure
the skin on the tip of the toe, a generous transverse
incision is made to prevent maceration of the tissue.
6. The drill bit is removed and brought back through the
hole from distal to proximal. Holding the interpha-
langeal joint in a reduced position, the surgeon
extends the drill hole into the proximal phalanx.
7. The hole is measured. A 4.0-mm solid-shaft cancel-
lous lag screw or headless screw is inserted, providing
compression to the arthrodesis site.
8. A Kirschner wire (K-wire) may be placed obliquely
across the interphalangeal joint to control any rota-
tional forces. This is removed after approximately
4 weeks.
Extensor Hallucis Longus Tendon Transfer
9. A longitudinal incision is made over the dorsal aspect
of the first metatarsal.

10. The extensor tendon, which was previously freed dis-
tally, is now freed proximally and delivered into the
wound.
11. A transverse drill hole is made and cleaned in the
distal portion of the first metatarsal. The size is
selected to snugly fit the tendon.
12. The extensor hallucis longus tendon is passed through
the drill hole and sutured onto itself, holding the
ankle in 10 degrees of dorsiflexion and placing a mod-
erate amount of tension on the tendon transfer.
Postoperative Care
The patient is placed into a short-leg compression dress-
ing incorporating plaster splints. A popliteal block can be
useful to control postoperative pain. The sutures are
removed at 10 to 12 days, and the patient is placed in a
short-leg walking cast for 4 weeks. At 6 weeks postopera-
tively, ambulation as tolerated is allowed. If the interpha-
langeal joint fusion is not complete at that time, an
additional period of ambulation in a postoperative shoe
may be necessary.
PERONEUS LONGUS TO BREVIS TRANSFER
Many cases of cavus foot, particularly in CMT, are associ-
ated with preserved function of the peroneus longus
muscle in the presence of a failing tibialis anterior.15 This
pulls the first ray plantarward and leads to a forefoot
cavus deformity as well as a secondary hindfoot varus. A
transfer of the peroneus longus to the peroneus brevis can
dramatically improve the situation by both weakening
the plantar pull on the first metatarsal and augmenting
the function of the usually failing peroneus brevis.
Surgical Technique
1. The surgery is carried out with the patient supine. A
small bump under the ipsilateral hip can facilitate
access to the lateral aspect of the foot. A thigh tourni-
quet is used (Video Clip 49).
2. A 4-cm incision is made over the anterior margin of
the peroneus longus on the lateral aspect of the foot
as it courses toward the cuboid to turn underneath the
foot. This incision is then deepened through the sub-
cutaneous fat to access the peroneus brevis. Care
should be taken to avoid injury to the sural nerve,
which usually passes through the proximal aspect of
the incision.
3. The peroneus longus and peroneus brevis each lie in
separate sheaths in this area, and they must be released
to access the tendons. The peroneus longus crosses
underneath the brevis and is not always easy to find.
4. The peroneus longus is then cut as far distally as pos-
sible as it makes the turn around the cuboid to pass
underneath the midfoot. If an os peroneum is present
in the tendon, it is excised and the cut is made through
this area.
5. The foot is held in maximum eversion, and the pero-
neus longus is woven two or three times in Pulvertaft
fashion through the distal aspect of the peroneus
Pes Cavus ■ Chapter 26
brevis. A 2-0 coated polyester suture (Ethibond;
Ethicon360, Menlo Park, Calif.) is used to join the
tendons. If other procedures are to be carried out on
the foot, the final tensioning and suture of the tendon
is saved until the end of the case.
Postoperative Care
The foot is placed in a short-leg compression dressing
reinforced with plaster splints. After 10 to 12 days, the
sutures are removed and a short-leg weight-bearing cast
is applied. If no other procedures are being performed, a
transition to regular footwear is usually made after a total
of 4 to 6 weeks of immobilization.
TIBIALIS ANTERIOR LATERALIZATION
The transfer of the insertion of the anterior tibial tendon
to the lateral cuneiform is a very powerful step of the
dynamic realignment when sufficient strength remains in
the tendon. It provides both hindfoot stability and lateral
shift of the ankle center of force by changing the strong
inversion moment into a light eversion moment while
still maintaining dorsiflexion power. Minimal risk of
overcorrection is present with transfer of the tendon to
the lateral cuneiform, and the procedure is technically
simpler than the split anterior tibialis transfer previously
advocated.17 A long history of the procedure exists in the
treatment of mild clubfoot residuals after cast correction
by the Ponseti method.35 However, because transferred
muscles generally lose one fifth of their strength, tibialis
anterior muscle strength of at least 4 of 5 preoperatively
is required for a reasonable effect, and the procedure may
not be appropriate in cases of CMT.47
Surgical Technique
1. The procedure is carried out with the patient supine.
A tourniquet is used around the thigh.
2. A medial longitudinal 3- to 4-cm incision is made
from the tuberosity of the navicular to the base of the
first metatarsal, and the tendon is released at its inser-
tion to bone.
3. A second 3- to 4-cm longitudinal anterior incision is
made slightly above the superior extensor retinaculum.
The retinaculum is incised as needed to pull out the
tendon.
4. The tendon end is grasped with a thick nonabsorbable
suture. It is then rerouted subcutaneously to the level
of the lateral cuneiform and pulled out through a third
3-cm longitudinal incision centered over the lateral
cuneiform.
5. There the fibers of the extensor digitorum brevis
muscle are bluntly separated, and the correct entry
point of the bone tunnel (dorsolateral edge of the
center of the lateral cuneiform) is verified
fluoroscopically.
6. A 6-mm hole is drilled from there through all the
cuneiforms to the medial cuneiform, and the tendon
is drawn into this tunnel until appropriate tension is
obtained. It is fixed by transosseous suture at the
1373
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders
medial cuneiform and into the surrounding soft tissues
at the lateral entry. Alternatively, a dorsal to plantar
tunnel can be created through the lateral cuneiform
and fixation achieved with an interference screw.
Postoperative Care
A short-leg compression dressing reinforced with plaster
splints is applied. The sutures are removed after 12 to 14
days, and a short-leg weight-bearing cast is applied. If
this is the only procedure, a transition to regular footwear
is usually made after a total of 4 to 6 weeks of
immobilization.
Results and Complications
Patients who undergo tibialis anterior transfer were seen
to have a lower mean talo–first metatarsal angle than
those who had not, suggesting that, in its native position,
the tibialis anterior may contribute to cavus.47 In general,
tendon tranfers result in a decrease in their overall
strength. The tibialis anterior also typically loses strength
with progression of the Charcot-Marie-Tooth disease, and
over time, the transfer may become less effective.
CLAW TOE CORRECTIONS
Associated claw toe deformities are common in pes
cavus. Often, dynamic claw toes resolve with realignment
of the hindfoot and midfoot deformity. Treatment of
the claw toe deformity depends upon whether a fixed or
flexible deformity is present. With fixed deformity at the
MTP joints, release of the extensor tendons and joint
capsules is required. To hold the toes in the neutral posi-
tion, usually a flexor tendon transfer needs to be done.
With fixed deformity of the proximal interphalangeal
joint (hammer toe), a proximal interphalangeal joint
arthrodesis or a DuVries phalangeal arthroplasty with
removal of the distal portion of the proximal phalanx is
indicated. Some authors prefer one of the latter two pro-
cedures as the standard procedure because they have a
similar effect on the long flexor tendons, require less
dissection, and are more reliable, particularly in neuro-
logic diseases.29 However, if the claw toe deformity is
passively correctible, a flexor tendon transfer alone usually
suffices.
The surgical techniques for flexor tendon transfer (Girdle-
stone procedure), DuVries phalangeal arthroplasty to correct
a hammer toe, and release of the MTP joints in a fixed con-
tracture are described in Chapter 7 (Video Clip 75).
LATERAL LIGAMENT REPAIR/RECONSTRUCTION
Regardless of the repair or reconstruction technique to
restore lateral hindfoot stability, the operation will likely
fail when hindfoot varus static is not realigned at the
same time. The association of lateral ligamentous hind-
foot instability, cavus deformity and ankle arthritis has
been made by various authors who all advise not only
correction of the deformity with osteotomies and tendon
transfers but also lateral hindfoot ligament reconstruction
to prevent recurrence.13,40,46
1374
The surgical techniques for lateral hindfoot ligament
repair and reconstruction are described in Chapter 30.
Bony Procedures
OSTEOTOMIES
At times, a specific bony deformity is present in pes cavus
that significantly impairs the patient’s ability to maintain
a plantigrade foot, but the remainder of the foot remains
relatively supple. This usually takes the form of a fixed
varus deformity of the hindfoot or a fixed plantar flexion
of the first ray. If the fixed deformity can be corrected, a
plantigrade foot can be achieved without an arthrodesis.
In general, an osteotomy that includes the first metatarsal
or calcaneus or both is carried out in conjunction with a
plantar fascia release and peroneus longus to brevis
tendon transfer.
DORSIFLEXION OSTEOTOMY OF THE FIRST RAY
Particularly in cases of CMT, plantar flexion of the first
metatarsal can become fixed, with a resultant fixed fore-
foot valgus deformity. This forefoot equinus deformity
can also involve the second and, rarely, the third metatar-
sal. As a result of this deformity, as the head of the first
metatarsal contacts the ground, the forefoot is twisted
into an inverted position. If this is associated with a varus
deformity of the calcaneus, a weak peroneus brevis
muscle, or a contracted plantar fascia, dramatic increases
in stress on the lateral ankle ligaments can result. This
stress can lead to chronic lateral ankle ligament instability
over time.
Dorsiflexion of the first ray is achieved either by a
dorsally closing osteotomy of the medial cuneiform
(reversed Cotton osteotomy), by a corrective first meta-
tarsocuneiform arthrodesis when the joint is arthritic, or
by a dorsally closing osteotomy of the first metatarsal.
DORSIFLEXION OSTEOTOMY OF
THE FIRST METATARSAL
In general, a first metatarsal osteotomy is carried out not
as an isolated procedure but as part of a more compre-
hensive cavus foot correction. In the patient with mild
and flexible deformity, sometimes only a plantar fascia
release and a dorsiflexion osteotomy of the first metatar-
sal are required. More often, however, a calcaneal oste-
otomy, plantar fascia release, and first metatarsal
osteotomy are done together. The first-toe Jones proce-
dure can also be added without complication. In a similar
but more powerful technique, a dorsiflexion of the first
ray can also be achieved by removal of a dorsally based
wedge of the medial cuneiform (reversed Cotton osteot-
omy), whereas the osteotomy is sometimes difficult to
close because of the Lisfranc ligament.
Surgical Technique
1. The patient is placed in a supine position. If this is an
isolated procedure, the first metatarsal osteotomy can
be carried out under an ankle block only. If it is part
 Pes Cavus ■ Chapter 26

of a more comprehensive cavus foot correction,
general anesthesia is used (Video Clip 50).
2. An incision is made over the dorsal aspect of the first
metatarsal, starting over the medial cuneiform and
ending over the distal third of the metatarsal.
3. The incision is deepened to the extensor tendon,
which is immobilized and retracted medially or
laterally.
4. The metatarsocuneiform (MTC) joint is identified,
and the proposed osteotomy site is marked on the
bone starting about 1.5 cm distal to the joint (Fig.
26-9A and B).
5. A 2.7-mm or 3.5-mm screw is centered in the proxi-
mal portion of the metatarsal above the proposed
osteotomy.
6. A 0.062-inch K-wire is used to make a transverse drill
hole in the dorsal part of the metatarsal 1 cm distal
to the osteotomy.
7. The osteotomy is a dorsal closing wedge that usually
removes 4 to 6 mm of bone, depending upon the
degree of plantar flexion of the first metatarsal that
must be corrected.
8. The first cut is made parallel to the MTC joint. A
convergent cut is then made distally, aiming for
the plantar cortex. Care is taken to leave the plantar
cortex intact. A greenstick fracture is made as the oste-
otomy is closed, resulting in a more stable construct
than if the cuts were fully completed. It is better to
undercut the osteotomy than to remove too large a
segment.

Following
osteotomy

A Axis of first metatarsal

B C D

E F
Figure 26-9 Technique of the dorsiflexion osteotomy of the first metatarsal. A, A dorsally based wedge of bone is removed
approximately 1 cm distal to the first metatarsocuneiform joint. The plantar fascia is often released when carrying out this
procedure for a cavus foot. B, A 3.5-mm screw is placed in the proximal fragment to serve as a post. C, The osteotomy site is
closed down, and the plantar aspect of the foot carefully palpated. If the first metatarsal is still too plantar flexed, a larger
wedge is removed. D, The osteotomy site is fixed by placing a length of 22-gauge wire through a transverse drill hole in the
distal fragment and then fixing it to the screw. E and F, Preoperative and postoperative radiographs demonstrate dorsiflexion of
the first metatarsal after proximal osteotomy. (From Mann RA, Coughlin MJ: The video textbook of foot and ankle surgery,
St Louis, 1991, Medical Video Productions.)

1375
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders
9. After the osteotomy has been created, the plantar
cortex is loosened by rocking the bone back and forth
until the dorsal gap can be closed (Fig. 26-9C).
10. To determine whether enough bone has been removed,
the ankle is brought up into dorsiflexion and the
forefoot is carefully evaluated, comparing the level of
the first and fifth metatarsals in relation to the long
axis of the leg. The surgeon must imagine that the foot
is in a plantigrade position and that the first and fifth
metatarsals are on the same plane.
11. If the size of the osteotomy cut is correct, internal fixa-
tion is inserted.
12. A piece of 22-gauge wire is passed through the trans-
verse drill hole that was made distal to the osteotomy
site in step 6. The wire is then brought up around the
screw head in the proximal portion of the metatarsal
and tightened with a wire twister while the osteotomy
is held closed (Fig. 26-9D).
13. Once the osteotomy site has been completely closed,
the bottom of the forefoot is again carefully exam-
ined. If the degree of dorsiflexion is adequate, the
surgeon may proceed with closure of the wound. If it
is not adequate, the wire is removed and more bone
is removed from the osteotomy site (Fig. 26-9E).
Alternatively, a 3-hole 2.0 DCP is used to compress
the osteotomy site by eccentric drilling.
14. Occasionally, the second metatarsal needs to be dor-
siflexed, which is done using the same procedure.
15. The foot is placed in a compression dressing. If this is
the only procedure being carried out, splints are not
required.
Postoperative Care
A popliteal block can be useful to control postoperative
pain. If this is the only procedure being carried out, the
patient is permitted to ambulate as tolerated in a postop-
erative shoe. If it is done in conjunction with other
procedures, the patient is placed in a short-leg non–
weight-bearing cast. In general, the osteotomy heals in
approximately 6 weeks, after which ambulation is permit-
ted as tolerated.
CALCANEAL OSTEOTOMIES
Patients with a moderate-to-severe cavus deformity
usually have a varus deformity of the hindfoot. A fixed
varus deformity is treated with the lateralizing calcaneal
osteotomy, that is, as described by Dwyer,10,11 Malerba
and De Marchi,32 or Knupp.10,11,23,32 Whenever possible,
realigning osteotomies are preferred over arthrodesis. If
the patient lacks adequate dorsiflexion and has a high
calcaneal pitch angle (a hindfoot cavus), a Samilson39
osteotomy is carried out to allow the calcaneal tuberosity
and the attached Achilles tendon to slide vertically,
thereby effectively lengthening the gastrocnemius–soleus
complex and correcting the effective pitch angle of
the calcaneus. These procedures are usually carried out
with a plantar fascia release and a first metatarsal
osteotomy.
1376
In the presence of a horizontal ankle joint line and a
cavus foot, it appears more reasonable to redistribute the
ankle joint contact forces by realigning the foot deformity
rather than by creating a new deformity, that is, with a
supramalleolar osteotomy. Furthermore, this would create
additional problems in the forefoot by accentuating the
plantar flexion of the first ray.
Calcaneal osteotomies act by shifting the ground
contact point and, consequently, the weight-bearing axis
through the ankle joint. They are particularly useful in
patients with recurrent hindfoot sprains as a result of heel
varus and can be used with either a supple or a stiff sub-
talar joint.34 The lateralizing calcaneal osteotomies also
lateralize the lever arm of the Achilles tendon during toe-
off. The contribution of the Achilles tendon toward the
tibialis posterior is thus reduced in favor of the peroneus
brevis. From recent static biomechanical studies, there is
evidence that in simulated pes cavus common lateralizing
calcaneal osteotomies substantially contribute to normal-
ize the elevated contact stress in the anteromedial ankle
joint, which is thought to cause ankle arthritis in long-
standing pes cavus.24 Osteotomies that include lateraliza-
tion of the tuberosity, including a simple slide and the
Z-osteotomy with additional lateralization of the tuberos-
ity,23 reduced contact stresses more effectively than, for
instance, the Z-osteotomy without additional lateraliza-
tion of the tuberosity32 and are therefore recommended
for moderate-to-severe hindfoot varus realignment.
Both the Dwyer osteotomy and its modifications with
translation, as well as the Z-osteotomy, can accomplish
correction of hindfoot varus and are described below.
DWYER CALCANEAL OSTEOTOMY
WITH OPTIONAL LATERAL AND/OR
DORSAL TRANSLATION
Surgical Technique
1. The patient is placed in a lateral or in a supine position
with a bolster beneath the ipsilateral hip for adequate
exposure of the lateral aspect of the calcaneus. A tour-
niquet is used on the thigh.
2. The skin incision is perpendicular to the axis of the
calcaneus, begins about 2 cm posterior to the tip of the
fibula, and is carried obliquely past the tip of the fibula
toward the plantar aspect of the calcaneocuboid joint
(Fig. 26-10A and Video Clip 48).
3. The deep incision is carried just below the peroneal
tendon sheath, and the calcaneus is exposed as
required. Care is taken not to injure the sural nerve.
Dorsally and plantarly, the soft tissues are stripped off
to place Hohman retractors.
4. A transverse osteotomy is made in the calcaneus that
starts about 2 cm posterior to the posterior facet of the
subtalar joint and runs in line with the skin incision,
perpendicular to the calcaneus axis. If possible, the
medial cortex of the calcaneus is left intact.
5. A second cut is now created, removing a pie-shaped
wedge of bone from the lateral aspect of the calcaneus.
The size of the wedge depends upon the severity of the

varus deformity. Usually, 5 to 7 mm of calcaneus is
removed with the second cut (Fig. 26-10B).
6. Once the second cut is completed, a greenstick fracture
is made on the medial side of the calcaneus by manip-
ulating the fragments back and forth. The osteotomy
is then closed. Sometimes, temporary insertion of a
stout pin into the posterior tuberosity can serve as
a joystick to facilitate closing the osteotomy. The
Line of
osteotomy
A Skin incision
B C Pin fixation
Figure 26-10 The Dwyer calcaneal osteotomy. A, Skin
incision is made along the inferior margin of the peroneal
tendons, with caution taken to avoid injury to the sural
nerve. B, A lateral closing wedge of bone is taken of
sufficient size to correct the deformity. C, Fixation is achieved
with a longitudinal pin, a longitudinal screw, or a lateral
staple. (From Mann RA, Coughlin MJ: The video textbook of
foot and ankle surgery, St Louis, 1991, Medical Video
Productions.)
A B
Figure 26-11 Preoperative (A) and postoperative (B) radiographs demonstrate the results of the Dwyer calcaneal osteotomy.
The tarsal canal is visible on end preoperatively, indicating a varus deformity of the heel, whereas the position of the subtalar
joint changes once the heel is brought into valgus.
Pes Cavus ■ Chapter 26
position of the bone is carefully evaluated. If an inad-
equate degree of correction has been obtained, more
bone needs to be removed. This may result in substan-
tial hindfoot shortening.
Alternatively, the tuberosity is fully osteotomized.
This allows further correction in two planes, including
further lateralization of up to 7 mm for more severe
deformities and vertical translation to reduce the cal-
caneal pitch. Vertical translation accomplishes the
goals of the “Samilson” osteotomy, an operation
designed purely to address the excessive calcaneal
pitch in poliomyelitis.22
7. The osteotomy site is fixed with single or multiple
5.0- to 7.3-mm screws placed down the long axis of
the calcaneus through a separate stab incision (Fig.
26-10C). If a screw is used, it should be placed lateral
to the midline, and the patient should be warned that
it may require later removal if it irritates the back of
the foot against the heel counter of a shoe.
Postoperative Care
The patient is placed into a short-leg compression dress-
ing incorporating plaster splints. A popliteal block can be
useful in controlling postoperative pain. The sutures are
removed 10 to 12 days after the procedure, and a short-leg
non–weight-bearing cast is applied. Ambulation is per-
mitted in the cast 4 weeks after the procedure, and casting
is discontinued 8 weeks postoperatively if radiographs
demonstrate union.
Results and Complications
The postoperative results after a Dwyer calcaneal osteot-
omy are usually most satisfactory in mild-to-moderate
hindfoot varus (Fig. 26-11). Occasionally, the sural nerve
becomes entrapped in scar tissue or disrupted, which can
create a problem for the patient.
Sometimes it is difficult to judge whether adequate
bone has been removed. The surgeon must attempt to
line up the calcaneus with the long axis of the leg when
trying to decide if a sufficient degree of correction has
been achieved.
The only significant error that can be made when per-
forming this procedure is to fail to remove sufficient
1377
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

bone, leaving the hindfoot in varus. In cases that require
much correction, removal of large wedges may result in
substantial hindfoot shortening, whereas the moment
arm of the Achilles tendon is decreased, weakening toe-
off. Alternatively, the tuberosity may be fully osteoto-
mized and lateralized 6 to 8 mm.
Because translation of the calcaneal ground contact
point by lateral sliding is more effective than rotation by
lateral closing wedges, translating or combined translating-
rotating osteotomies are usually preferable for the realign-
ment of more severe hindfoot varus.28
Z-OSTEOTOMY23,32
Surgical Technique
1. The patient is placed in a supine position with a bolster
beneath the ipsilateral hip or in the lateral position for
adequate exposure of the lateral aspect of the calca-
neus. A tourniquet is used on the thigh.
2. The skin incision is perpendicular to the axis of the
calcaneus, begins about 3 cm posterior to the tip of the
fibula, and is carried obliquely past the tip of the fibula
toward the plantar aspect of the calcaneocuboid joint
(Figs. 26-12 to 26-14 and Video Clip 118).
3. The deep incision is carried just below the peroneal
tendon sheath, and the calcaneus is exposed as
required. Care is taken not to injure the sural nerve.
Dorsally and plantarly, the soft tissues are stripped off
to place Hohman retractors. The exposure of the cal-
caneus should extend from its dorsal aspect behind the
fibula to just proximal to the calcaneocuboid joint.
4. Hohman retractors are used to protect the soft tissues.
K-wires should be inserted and checked under fluoros-
copy to ensure that the osteotomy is appropriately
positioned and perpendicular to the calcaneal axis.
The horizontal part of the osteotomy is about 2 cm
long and parallel to the plantar fascia. The anterior
vertical cut is made 1 to 2 cm posterior and parallel to
the calcaneocuboid joint, and the posterior vertical cut
is placed in the posterior half of the cavity of the tuber-
osity. Sparing the Achilles insertion is important.
5. Four K-wires are then used to define the corners of the
wedge to be removed. The base of the wedge is 8 to
10 mm in width, depending on the desired amount of
correction. The wedge is mobilized with the oscillating
saw and osteotomes without harming the soft tissues.
A laminar spreader is used to mobilize the osteotomy.
The lateral gap is then carefully closed as described by
Malerba and De Marchi.32 An additional lateral dis-
placement of the tuberosity fragment (6-10 mm) is
done as described by Knupp et al.23 An option is that
the calcaneus can also be lengthened by displacing the
tuberosity posteriorly.

Translation

Rotation Rotation

A B
Figure 26-12 The Z-osteotomy with removal of a laterally based wedge of 8 to 10 mm (A), according to Malerba (rotation of
the ground point). A more powerful correction is achieved with additional lateralization of the tuberosity (B) according to
Knupp and Hintermann (rotation and translation of the ground point). (Modified from Krause FG, Sutter D, Waehnert D, et al:
Ankle joint pressure changes in a pes cavovarus model after lateralizing calcaneal osteotomies. Foot Ankle Int 31:741-746, 2010.
Used with permission.)

1378

Figure 26-13 Preoperative Saltzman hindfoot view of a
hindfoot varus. Intraoperative lateral and axial fluoroscopy,
and postoperative Saltzman hindfoot view after a
Z-osteotomy of the calcaneus with lateralization of the
tuberosity, according to Knupp and Hintermann. A peroneus
longus to brevis tendon transfer and a dorsiflexion osteotomy
of the first metatarsal were added. (Courtesy M. Knupp, MD,
Department of Orthopaedic Surgery, Kantosspital Liesthal,
Switzerland. Used with permission.)
6. The osteotomy is secured with one or two K-wires. The
desired correction is carefully evaluated clinically and
under fluoroscopy. The osteotomy site is fixed by one
or two 3.5-mm or larger screws placed down the
long axis of the calcaneus through a separate stab
incision.
Postoperative Care
The patient is placed into a short-leg compression dress-
ing incorporating plaster splints. A popliteal block can be
useful in controlling postoperative pain. The sutures are
removed 10 to 12 days after the procedure, and a short-leg
non–weight-bearing cast is applied. Partial weight bearing
is permitted in the cast 3 to 4 weeks after the procedure,
and casting is discontinued 6 to 8 weeks postoperatively
if radiographs demonstrate union.
Results and Complications
Transient and irreversible tibial nerve palsy after lat-
eralizing calcaneal osteotomies has been described.27
Particularly after large corrections in CMT cases and
posttraumatic cases, the rate is substantial. Although the
Pes Cavus ■ Chapter 26
nerves themselves do not appear noticeably enlarged by
the eye, CMT nerves may be slightly thicker and more sen-
sitive to compression compared with normal nerves.14 A
routine release of the nerve’s compartment (inferior flexor
retinaculum) when performing a lateralizing calcaneal
osteotomy for hindfoot varus in patients with Charcot-
Marie-Tooth disease is therefore recommended.27
Consolidation of the osteotomy is reported to be fast
and reliable, and most patients show consolidation on
the radiographs 6 weeks postoperatively.
MIDTARSAL OSTEOTOMIES
Various types of midfoot osteotomies have been pro-
posed for the patient with a forefoot equinus or anterior
cavus deformity with the apex located at the Chopart and
midtarsal joints. These include the Cole osteotomy, which
consists of removing a dorsal wedge of bone from the
navicular, cuneiforms, and cuboid.7 A similar, more distal
osteotomy has been proposed by Japas, in which a
V-shaped osteotomy is made within the tarsal bones.21
The distal portion is then depressed to allow the forefoot
to be brought out of its equinus position.
Although, in theory, midfoot osteotomies are preferred
because they correct a typical deformity closer to its apex
than a basilar osteotomy of the first metatarsal, in prac-
tice, this is not the case. Inevitably, all variations of the
midfoot osteotomies result in multiple intraarticular cuts
that can lead to early arthritis. The residual deformity
from the much safer extraarticular osteotomy through the
first metatarsal is well tolerated, and this approach should
be universally preferred. Midfoot procedures should be
reserved for patients who already have arthritis, and the
joints should then be arthrodesed in conjunction with the
cavus correction.
ARTHRODESIS PROCEDURES
The triple arthrodesis is the requisite operation for more
severe, fixed postural deformities of the hindfoot of any
kind. In the cavus foot, it is important to remember that
other procedures, such as a first metatarsal osteotomy or
Jones procedure, can be carried out in addition to a triple
arthrodesis if the conditions warrant. Routine joint prepa-
ration and cartilage removal often prove adequate for
milder degrees of deformity. Because the posterior facet
of the subtalar joint is approached from the lateral side,
there is a natural tendency to remove more bone laterally
and position the calcaneus toward valgus using standard
techniques, just as one would perform a triple arthrodesis
for hindfoot arthritis.
Long-term follow-up studies of standard triple arthrod-
esis for patients with Charcot-Marie-Tooth disease and
cavus deformity have shown a high incidence of osteoar-
thritis of the remaining foot joints after this procedure.
One study reported degenerative changes of the ankle and
midfoot in 77% and the need for subsequent ankle
arthrodesis for the treatment of degenerative joint disease
in 20% after an average follow-up of 20 years.48 Also, a
literature review reveals poor results in as many as 47%
1379
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders

A B C

157.9° (22.1°)

82.6° (97.4°) 171.9° (8.1°)

75.0° (105.0°)

25.0° (155.0°) 24.1° (155.9°)

D E
Figure 26-14 Preoperative anterior (A), oblique (B), and posterior (C) photographs and postoperative anteroposterior (D) and
lateral (E) weight-bearing radiographs of a 56-year-old male patient with idiopathic pes cavus and grade III anteromedial ankle
arthritis. Operative deformity correction included a lateralizing sliding osteotomy of the calcaneal tuberosity, dorsiflexion
osteotomy of the first metatarsal, peroneus longus to brevis transfer, and lateral malleolus shortening osteotomy to reduce
the varus tilt of the talus. No progression of the ankle arthritis was seen at latest follow-up 4 years postoperatively.

of patients, recurrence rates of 9% to 20%, nonunion in
6% to 33% of patients, and incomplete correction of the
deformity in as many as 70% of patients.
Because hindfoot joints usually are already stiff in
severe cavus deformities, there is little, if any, motion loss
after a triple arthrodesis.34 Therefore reducing the foot
into normal heel valgus with a triple arthrodesis may
result in further plantar flexing an already plantar-flexed
first ray in long-standing deformities. The ankle will tip
into varus postoperatively if this is not corrected with a
dorsiflexion osteotomy. A satisfactory plantigrade posi-
tion is essential for good results.34
Outcome
Few level III and IV studies have been published that
assess the outcome of operative treatment of mainly fixed
neurologic and idiopathic cavus deformities. Because of
various etiologies and the limited number of patients
treated, the reader is unable to draw definite conclusions.
Nevertheless, each study offers some information about
successful operative treatment and the pitfalls of certain
treatment choices. The natural course of the disease
without operative treatment has not yet been described.
The surgeon must therefore thoughtfully apply the lessons
learned from the available literature.
An overview is given in Table 26-3. The outcome of
various procedures reveals significant improvements of
function and relief of pain and about two thirds good and
excellent results, even in the long term. Worse outcome
after cavus realignment is reported when advanced ankle
arthritis stage II and above is present preoperatively, indi-
cating the importance of detecting ankle arthritis early
and preventing its progression.20,26 Another study revealed
an association of radiographic evidence of ankle arthritis
with a higher Foot Function Index (FFI) pain subscore,
which suggests that arthritis prevention may have a greater
impact on patient outcome than achievement of radio-
graphic alignment.47 The unfavorable combination of
recurrent lateral ankle sprains or chronic instability and
hindfoot varus as commonly seen in pes cavus likely
increases the risk for accelerated ankle arthritis, but it is
also common in patients without instability because of
elevated anteromedial ankle contact stresses in pes
cavus.24,46 To prevent arthritis progression, a more aggres-
sive dynamic and static realignment with slight overcor-
rection is recommended.
Worse outcomes after surgery have also been reported
for patients with neurologic as opposed to idiopathic pes
cavus. Despite appropriate pes cavus realignment, neuro-
logic patients appear to suffer more from pain and activity
impairments.31
After joint-preserving realignment surgery, cavus
patients were seen to have a slower gait velocity and lower
cadence, but the proportion of time spent in stance and
swing phase was near that of normal individuals.47
Although patients may have some deformity recurrence
postoperatively, most are able to wear normal shoes and
do not need orthoses.47

1380
 Table 26-3 Pes Cavus Outcome Studies of the Last Decade
Ankle Mean
Mean Age Arthritis at Follow-up Radiographic Findings
Author Number at Surgery Etiology Flexibility Surgery Procedure (months) Outcome (Mean) at Follow-up Evidence
Sammarco 21 ft 33 All neurologic Flexible None A, B, H 71 AOFAS: from 46 to 89 Lateral talo–MT I III
et al, 2001 15 pts Maryland Foot Score: angle decreased 6.5
from 72 to 90 degrees
Arch height decreased
6.8 mm
Fortin et al, 13 ft 51 All idiopathic Flexible and Stage 1-3 A, B, D, F 33 Karlsson score: from Not reported III
2002 10 pts rigid 33 to 82
Vienne et al, 9 ft 25 Idiopathic and Flexible Stage 0-2 A, C, D 37 AOFAS: from 57 to 87 Not reported III
2007 8 pts residual
clubfoot
Ward et al, 41 ft 16 All neurologic Flexible None B, C, G, H, 312 SF36 mental: 50 OA most often in TMT IV
2008 25 pts K (26 years) SF36 physical: 38 1 joints
FFI pain: 35
FFI disability: 41
FFI activity limit: 22
Kroon et al, 19 ft 40 Idiopathic 11 Flexible and None 2xA, B, C, 50 AOFAS: 83 Talo–first metatarsal IV
2009 15 pts Neurologic 4 rigid E, F, G, I FFI pain: 13 angle from 22 to 17
FFI activity limit: 13 degrees
Irwin et al, 22 ft 48 All idiopathic Rigid Group 1 A, B, C, D, 60 AOFAS group 1: 86, Arthritis progression IV
2010 22 pts stage 0-1 G, H group 2: 59 mainly in group 2
Group 2 VAS: 21 and 40 resp.
stage 2-3
Maskell et al, 29 ft 43 All idiopathic Rigid None A, B, C, D, 51 AOFAS: from 45 to 90 Talo–first metatarsal III
2010 23 pts E, J angle from 9.9 to
2.4 degrees
Krause et al, 13 ft 47 Idiopathic 7 Rigid Stage 1-3 84 AOFAS: from 45 to 71 III
2013 13 pts Neuropathic 6

AOFAS, American Orthopaedic Foot and Ankle Society; EHL, extensor hallucis longus; FFI, Foot Function Index; IP, interphalangeal; OA, osteoarthritis; pts, patients; SF36, 36-item short Form Health
Survey; TMT, tarsometatarsal; VAS, visual analog scale.
Operative procedures: A, lateralizing calcaneal osteotomy, B, first metatarsal dorsiflexion osteotomy; C, peroneus longus to brevis transfer; D, lateral ligament reconstruction; E, Achilles lengthening
tenotomy; F, anterior ankle debridement (cheilectomy) for osteotphytes; G, EHL transfer (Jones procedure) and IP fusion; H, plantar fascia release; I, tibialis posterior transfer to lateral cuneiform;
J, gastrocnemius recession; K, tibialis anterior transfer to lateral cuneiform; L, deltoid ligament release; M, fibula osteotomy.
Pes Cavus ■ Chapter 26

1381
 Part VI ■ Arthritis, Postural Disorders, and Tendon Disorders
REFERENCES
1. Aminian A, Sangeorzan BJ: The anatomy of cavus foot deformity,
Foot Ankle Clin 13:191–198, v, 2008.
2. Bentzon PGK: Pes cavus and the m. peroneus longus, Acta Orthop
Scand 4:50, 1933.
3. Berciano J, Gallardo E, Garcia A, et al: New insights into the
pathophysiology of pes cavus in Charcot-Marie-Tooth disease
type 1A duplication, J Neurol 258:1594–1602, 2011.
4. Bertorini T, Narayanaswami P, Rashed H: Charcot-Marie-Tooth
disease (hereditary motor sensory neuropathies) and hereditary
sensory and autonomic neuropathies, Neurologist 10:327–337,
2004.
5. Brewerton DA, Sandifer PH, Sweetnam DR: “Idiopathic” pes
cavus: an investigation into its aetiology, Br Med J 2:659–661,
1963.
6. Charcot JM, Marie P: Sur une forme particulaire d’atrophy mus-
culaire progressive souvent familiale débutant par les pieds et
les jambes et atteignmant plus tard les mains, Rev Med 6:97–138,
1886.
7. Cole WH: The treatment of claw foot, J Bone Joint Surg Am
22:895–908, 1940.
8. Dhillon MS, Sandhu HS: Surgical options in the management
of residual foot problems in poliomyelitis, Foot Ankle Clin
5:327–347, 2000.
9. Duchenne GB: The physiology of motion (trans EB Kaplan),
Philadelphia, 1959, WB Saunders.
10. Dwyer FC: Osteotomy of the calcaneum for pes cavus, J Bone
Joint Surg Br 41:80–86, 1959.
11. Dwyer FC: The present status of the problem of pes cavus, Clin
Orthop 106:254–275, 1975.
12. Dyck PJ, Lambert EH: Lower motor and primary sensory neuron
diseases with peroneal muscular atrophy. I. Neurologic, genetic,
and electrophysiologic findings in hereditary polyneuropathies,
Arch Neurol 18:603–618, 1968.
13. Fortin PT, Guettler J, Manoli A: Idiopathic cavovarus and lateral
ankle instability: recognition and treatment implications relat-
ing to ankle arthritis, Foot Ankle Int 23:1031–1037, 2002.
14. Guyton GP: Peroneal nerve branching suggests compression
palsy in the deformities of Charcot-Marie Tooth disease, Clin
Orthop Relat Res 451:167–170, 2006.
15. Guyton GP, Mann RA: The pathogenesis and surgical manage-
ment of foot deformity in Charcot-Marie-Tooth disease, Foot
Ankle Clin 5:317–326, 2000.
16. Halgrimsson S: Pes cavus, seine Behandlung und einige
Bemerkungen uber seing Aetiologie, Acta Orthop Scand 10:73,
1939.
17. Henderson CP, Parks BG, Guyton GP: Lateral and medial plantar
pressures after split versus whole anterior tibialis tendon trans-
fer, Foot Ankle Int 29:1038–1041, 2008.
18. Huber H, Dutoit M: Dynamic foot-pressure measurement in the
assessment of operatively treated clubfeet, J Bone Joint Surg Am
86-A:1203–1210, 2004.
19. Ibrahim K: Pes cavus. In Evarts CM, editor: Surgery of the muscu-
loskeletal system, New York, 1990, Churchill Livingstone, pp
4015–4034.
20. Irwin TA, Anderson RB, Davis WH, Cohen BE: Effect of ankle
arthritis on clinical outcome of lateral ankle ligament recon-
struction in cavovarus feet, Foot Ankle Int 31:941–948, 2010.
21. Japas LM: Surgical treatment of pes cavus by tarsal V-osteotomy.
Preliminary report, J Bone Joint Surg Am 50:927–944, 1968.
22. Jones R: An operation for paralytic calcaneocavus, Am J Orthop
Surg 5:371, 1908.
23. Knupp M, Horisberger M, Hintermann B: A new Z-shaped cal-
caneal osteotomy for 3-plane correction of severe deformity of
the hindfoot, Tech Foot Ankle Surg 7:90–95, 2008.
1382
24. Krause F, Windolf M, Schwieger K, Weber M: Ankle joint pressure
in pes cavovarus, J Bone Joint Surg Br 89:1660–1665, 2007.
25. Krause FG, Henning J, Pfander G, et al: Cavovarus foot realign-
ment to treat anteromedial ankle arthrosis, Foot Ankle Int 34:54–
64, 2013.
26. Krause FG, Klammer G, Benneker LM, et al: Biochemical T2*
MR quantification of ankle arthrosis in pes cavovarus, J Orthop
Res 28:1562–1568, 2010.
27. Krause FG, Pohl MJ, Penner MJ, Younger AS: Tibial nerve palsy
associated with lateralizing calcaneal osteotomy: case reviews
and technical tip, Foot Ankle Int 30:258–261, 2009.
28. Krause FG, Sutter D, Waehnert D, et al: Ankle joint pressure
changes in a pes cavovarus model after lateralizing calcaneal
osteotomies, Foot Ankle Int 31:741–746, 2010.
29. Krause FG, Wing KJ, Younger AS: Neuromuscular issues in cav-
ovarus foot, Foot Ankle Clin 13:243–258, vi, 2008.
30. Kremli MK: Fixed forefoot adduction after clubfoot surgery,
Saudi Med J 24:742–744, 2003.
31. Kroon M, Faber FW, van der Linden M: Joint preservation surgery
for correction of flexible pes cavovarus in adults, Foot Ankle Int
31:24–29, 2010.
32. Malerba F, De Marchi F: Calcaneal osteotomies, Foot Ankle Clin
10:523–540, vii, 2005.
33. Mann DC, Hsu JD: Triple arthrodesis in the treatment of fixed
cavovarus deformity in adolescent patients with Charcot-Marie-
Tooth disease, Foot Ankle 13:1–6, 1992.
34. Manoli A, Graham B: The subtle cavus foot, “the underprona-
tor,” Foot Ankle Int 26:256–263, 2005.
35. Morcuende JA, Dolan LA, Dietz FR, Ponseti IV: Radical reduction
in the rate of extensive corrective surgery for clubfoot using the
Ponseti method, Pediatrics 113:376–380, 2004.
36. Pandolfo M: Friedreich ataxia, Semin Pediatr Neurol 10:163–172,
2003.
37. Pareyson D: Differential diagnosis of Charcot-Marie-Tooth
disease and related neuropathies, Neurol Sci 25:72–82, 2004.
38. Roper BA, Tibrewal SB: Soft tissue surgery in Charcot-Marie-
Tooth disease, J Bone Joint Surg Br 71:17–20, 1989.
39. Samilson RL: Crescentic osteotomy os calcis for calcaneovarus
feet. In Bateman JE, editor: Foot science, Philadelphia, 1976, WB
Saunders, p 18.
40. Sammarco GJ, Taylor R: Combined calcaneal and metatarsal
osteotomies for the treatment of cavus foot, Foot Ankle Clin
6:533–543, vii, 2001.
41. Schmalbruch H, Haase G: Spinal muscular atrophy: present
state, Brain Pathol 11:231–247, 2001.
42. Simbak N, Razak M: Residual deformity following surgical
treatment of congenital talipes equinovarus, Med J Malaysia
53(Suppl A):115–120, 1998.
43. Steindler A: Operative treatment of pes cavus: stripping of the
os calcis, Surg Gynecol Obstet 24:612–615, 1917.
44. Tooth HH: The peroneal type of progressive muscular atrophy,
London, 1886, HK Lewis.
45. Tynan MC, Klenerman L, Helliwell TR, et al: Investigation of
muscle imbalance in the leg in symptomatic forefoot pes cavus:
a multidisciplinary study, Foot Ankle 13:489–501, 1992.
46. Valderrabano V, Hintermann B, Horisberger M, Fung TS: Liga-
mentous posttraumatic ankle osteoarthritis, Am J Sports Med
34:612–620, 2006.
47. Ward CM, Dolan LA, Bennett DL, et al: Long-term results of
reconstruction for treatment of a flexible cavovarus foot in
Charcot-Marie-Tooth disease, J Bone Joint Surg Am 90:2631–
2642, 2008.
48. Wetmore RS, Drennan JC: Long-term results of triple arthrodesis
in Charcot-Marie-Tooth disease, J Bone Joint Surg Am 71:417–
422, 1989.
 Part V ■ Soft Tissue Disorders of the Foot and Ankle
Foreign Body Injuries
134. Yang ZN, Shih HR, Chao L, et al: Free transplantation of sub-
axillary lateral thoraco-dorsal flap in burn surgery, Burns
10:164–169, 1984.
135. Banerjee B, Das RK: Sonographic detection of foreign bodies
of the extremities, Br J Radiol 64:107–112, 1991.
136. Bostman OM: Osteolytic changes accompanying degradation
of absorbable fracture fixation implants, J Bone Joint Surg Br
73:679–682, 1991.
137. Frey C: Marine injuries: prevention and treatment, Orthop Rev
23:645–649, 1994.
138. Gooding GA, Hardiman T, Sumers M, et al: Sonography of the
hand and foot in foreign body detection, J Ultrasound Med
6:441–447, 1987.
139. Inaba AS, Zukin DD, Perro M: An update on the evaluation and
management of plantar puncture wounds and Pseudomonas
osteomyelitis, Pediatr Emerg Care 8:38–44, 1992.
140. Krych SM, Lavery LA: Puncture wounds and foreign body reac-
tions, Clin Podiatr Med Surg 7:725–731, 1990.
141. Markiewitz AD, Karns DJ, Brooks PJ: Late infections of the foot
due to incomplete removal of foreign bodies: a report of two
cases, Foot Ankle Int 15:52–55, 1994.
142. Mizel MS, Steinmetz ND, Trepman E: Detection of wooden
foreign bodies in muscle tissue: experimental comparison of
computed tomography, magnetic resonance imaging, and
ultrasonography, Foot Ankle Int 15:437–443, 1994.
143. Montano JB, Steele MT, Watson WA: Foreign body retention
in glass-caused wounds, Ann Emerg Med 21:1360–1363,
1992.
144. Pelto-Vasenius K, Hirvensalo E, Vasenius J, et al: Osteolytic
changes after polyglycolide pin fixation in chevron osteotomy,
Foot Ankle Int 18:21–25, 1997.
145. Rockett MS, Gentile SC, Gudas SJ, et al: The use of ultraso-
nography for the detection of retained wooden foreign
bodies in the foot, J Foot Ankle Surg 34:478–484, 510–511,
1995.
146. Rokkanen P, Bostman O, Vainionpaa S, et al: Absorbable
devices in the fixation of fractures, J Trauma 40(Suppl 3):S123–
S127, 1996.
147. Schneider HJ, Weiss MA, Stern PJ: Silicone-induced erosive
arthritis: radiologic features in seven cases, AJR Am J Roentgenol
148:923–925, 1987.
148. Schwab RA, Powers RD: Conservative therapy of plantar punc-
ture wounds, J Emerg Med 13:291–295, 1995.
149. Talley JH: Fluoroquinolones: new miracle drugs? Postgrad Med
89:101–103, 106–108, 111–113, 1991.
Blisters
150. Verdile VP, Freed HA, Gerard J: Puncture wounds to the foot,
J Emerg Med 7:193–199, 1989.
151. Akers WA: Measurements of friction injuries in man, Am J Ind
Med 8:473–481, 1985.
152. Berkley SF, McNeil JG, Hightower AW, et al: A cluster of blister-
associated toxic shock syndrome in male military trainees and
a study of staphylococcal carriage patterns, Mil Med 154:496–
499, 1989.
153. Carragee EJ, Csongradi JJ, Bleck EE: Early complications in the
operative treatment of ankle fractures. Influence of delay before
operation, J Bone Joint Surg Br 73:79–82, 1991.
154. Darrigrand A, Reynolds K, Jackson R, et al: Efficacy of antiper-
spirants on feet, Mil Med 157:256–259, 1992.
748
155. Giordano CP, Koval KJ: Treatment of fracture blisters: a pro-
spective study of 53 cases, J Orthop Trauma 9:171–176, 1995.
156. Knapik JJ, Hamlet MP, Thompson KJ, et al: Influence of boot-
sock systems on frequency and severity of foot blisters, Mil Med
161:594–598, 1996.
157. Knapik JJ, Reynolds KL, Duplantis KL, et al: Friction blisters:
pathophysiology, prevention and treatment, Sports Med
20:136–147, 1995.
158. Patterson HS, Woolley TW, Lednar WM: Foot blister risk factors
in an ROTC summer camp population, Mil Med 159:130–135,
1994.
159. Reynolds K, Darrigrand A, Roberts D, et al: Effects of an anti-
perspirant with emollients on foot-sweat accumulation and
blister formation while walking in the heat, J Am Acad Dermatol
33:626–630, 1995.
160. Varela CD, Vaughn TK, Carr JB, et al: Fracture blisters: clinical
and pathological aspects, J Orthop Trauma 7:417–427, 1993.
Foot Odor and Sweating
161. Aluminum chloride for hyperhidrosis, Drug Ther Bull 19:101–
102, 1981.
162. Campanati A, Bernardini ML, Gesuita R, Offidani A: Plantar
focal idiopathic hyperhidrosis and botulinum toxin: a pilot
study, Eur J Dermatol 17:52–54, 2007.
163. Critchley M: The citadel of the senses, New York, 1986, Raven.
164. Fitzpatrick TB, Eisen AZ, Wolff K, et al: Dermatology in general
medicine, ed 4, New York, 1993, McGraw-Hill, pp 753–755.
165. Darrigrand A, Reynolds K, Jackson R, et al: Efficacy of antiper-
spirants on feet, Mil Med 157:256–259, 1992.
166. Gibbons B: The intimate sense of smell, National Geographic
170:324–361, 1986.
167. Grice K: Hyperhidrosis and its treatment by iontophoresis,
Physiotherapy 66:43–44, 1980.
168. Hurley HJ: Disorders of the eccrine sweat gland. In Moschella
SL, Pillsbury DM, Hurly HJ, editors: Dermatology, Philadelphia,
1975, WB Saunders, pp 1165–1190.
169. Kanda F, Yagi E, Fukada M, et al: Elucidation of chemical com-
pounds responsible for foot odor, Br J Dermatol 122:771–776,
1990.
170. Kern U, Kohl M, Seifert U, Schlereth T: Botulinum toxin type
B in the treatment of residual limb hyperhidrosis for lower
limb amputees: a pilot study, Am J Phys Med Rehabil 90:321–
329, 2011.
171. Kobayashi S: Relationship between an offensive smell given
from human foot and Staphylococcus epidermidis, Jpn J Dermatol
45:797–800, 1990.
172. Levit F: Simple device for treatment of hyperhidrosis by ionto-
phoresis, Arch Dermatol 98:505–507, 1968.
173. Pedowitz WJ: The malodorous foot, Foot Ankle Int 17:54–55,
1996.
174. Ramsey ML: Foot odor: how to clean the air, Physician Sports
Med 24:91–92, 1996.
175. Rook A, editor: Textbook of dermatology, Boston, 1986, Blackwell
Scientific, pp 1894–1895.
176. Strauss EJ, Petrucelli G, Bong M, et al: Blisters associated with
lower-extremity fracture: results of a prospective treatment pro-
tocol, J Orthop Trauma 20:618–622, 2006.
177. Vergilis-Kalner IJ: Same-patient prospective comparison of
botox versus dysport for the treatment of primary axillary
hyperhidrosis and review of literature, J Drugs Dermatol
10:1013–1015, 2011.