Clin Podiatr Med Surg

19 (2002) 391 – 409

The effect of ankle equinus upon

the diabetic foot
Carl C. Van Gils, DPM, MSa,*, Brett Roeder, DPMb
a
Foot & Ankle Institute of Utah and Diabetic Foot Center of Southern Utah, 754 South Main Street,
St. George, UT 84770, USA
b
Phoenix Indian Medical Center, 4212 North 16th Street, Phoenix, AZ 85016, USA

Root et al state that ‘‘the worst foot is the one with the fully compensated
equinus deformity’’ [1]. The association between ankle equinus and common foot
pathologies such as Achilles tendinitis, metatarsalgia, Morton’s neuroma, hallux
abductovalgus, and plantar fasciitis has been described [2,3]. However, the
association between ankle equinus and diabetic foot pathology has only been
recognized recently.
Over half of the nontraumatic amputations occurring in the United States are
related to complications of diabetes. It is imperative that risk factors for lower
extremity ulceration and amputation are identified and addressed. Important risk
factors for lower extremity amputation include neuropathy, foot ulceration or
history of amputation, Charcot deformity, and peripheral vascular disease [4]. The
association between high plantar pressures and the development of ulceration in
the diabetic foot has also been well established [5]. Recently, clinicians have
begun to discuss the effect of ankle equinus on diabetic foot deformity, plantar
pressure, ulceration, and ultimately amputation. This article reviews the effect of
ankle equinus deformity on the diabetic foot and the available treatment options.
New data on the prevalence of equinus in a population of patients with diabetes
are also presented.
Ankle equinus is measured as a sagittal plane relationship of the foot to the leg
with maximum ankle joint dorsiflexion. Ankle equinus is generally accepted as
an inability to dorsiflex the foot at the ankle a minimum of 10 degrees during the
propulsive period of gait [1,2]. McGlamry and Kitting described five types of
equinus in 1973: talipes equinus, osseous equinus, gastrocnemius soleus equinus,
metatarsal equinus, and forefoot equinus [6]. Whitney and Green later narrowed
this classification into muscular forms of ankle equinus (gastrocnemius and
gastrocsoleus) and osseous forms of ankle equinus (osseous equinus and

* Corresponding author.
E-mail address: cvangils@yahoo.com (C.C. Van Gils).

0891-8422/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved.
PII: S 0 8 9 1 - 8 4 2 2 ( 0 2 ) 0 0 0 1 0 - 1
392 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409

pseudoequinus) [7]. Downey subdivides the muscular forms of equinus to include

spastic and nonspastic (congenital, idiopathic, or acquired shortness) etiologies
[2]. Acquired contracture of the gastrocenemius soleus complex can result from a
prolonged or repeated plantarflexed position of the ankle. Prolonged casting with
the ankle joint plantarflexed, frequent use of high heeled shoes, chronic excessive
pronation, and trauma are examples of factors that can lead to acquired nonspastic
ankle equinus [2,8]. This article predominantly discusses acquired ankle equinus
of a neuromuscular origin in the diabetic lower extremity. A full discussion of the
anatomy, etiology, classification, and treatment of equinus can be found else-
where [2,9].

Ankle equinus as a deforming force

Without the necessary range of motion at the ankle during the gait cycle, ankle
equinus becomes a deforming force, and can affect the function and position of
the foot, leg, knee, hip, and spine. In the absence of 10 degrees of dorsiflexion of
the foot on the leg, the body must compensate for this reduced range of motion in
other ways. Common methods of compensation in gait include excessive foot
pronation, early heel off at midstance of gait, knee flexion or hyperextension at
midstance, and a shortened stride by decreased hip extension. Three categories of
compensation have been described for ankle equinus: noncompensated, partially
compensated, and fully compensated. Noncompensated equinus includes less
than 1% of all equinus patients and usually affects those with severe neuro-
muscular disease. We again refer the reader to other references for a more
complete review of this type of compensation [2,9]. In the partially compensated
equinus, dorsiflexion is combined from the ankle and the midtarsal joint to permit
heel contact during the early part of the stance phase of gait. However, early heel
off is common due to lack of dorsiflexion in the later stages of stance.
Inadequate dorsiflexion of the ankle requires compensation within the foot.
Perhaps the most common type of ankle equinus is the fully compensated
equinus, which requires subtalar joint pronation to allow the midtarsal joint to
pronate and dorsiflex the foot. Abnormal compensatory midtarsal joint pronation,
or excessive and persistent subtalar joint pronation, are common causes of
pathology within the foot [1]. Due to the maximally everted position of the heel
during gait, there is a marked decrease in the ability to absorb the shock forces of
weightbearing [9]. In addition, the leg is forced into excessive internal rotation,
which can create an increased lordotic attitude of the spine and an excessive
amount of transverse plane mobility in the knee joint. Therefore, in addition to
foot pathology, sequella of equinus can include low back pain, chondromalacia of
the knee, exaggerated genu valgum, and muscular fatigue [9].
With fully compensated ankle equinus, the foot becomes abnormally unstable,
and hypermobility results when the foot is weightbearing. Muscular imbalance of
the foot causes the extensor muscles to compete against the deforming force of the
tight Achilles tendon, creating hammertoe contracture [10]. Long standing ham-
mertoe deformity results in rigid digits that are predisposed to ulcer formation. Foot
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pathologies such as hallux abductovalgus, second metatarsophalgeal joint sub-

luxation, plantar fasciitis, and posterior tibial tendon insufficiency are common
findings in fully compensated ankle equinus. Hypermobility can also cause ab-
normal movement of the metatarsal heads on the plantar soft tissues that are fixed
by friction between the skin and the ground. This shearing about the metatarsal
heads results in increased forefoot tissue trauma and thick callus buildup.
Soft tissue plantar to the forefoot is normally subjected to vertical ground
reactive and shear forces during the stance phase of gait. Healthy tissue is capable
of withstanding this degree of trauma without developing symptomatology. The
ability of skin to withstand trauma from abnormal shearing forces is decreased
primarily by age, loss of viability of tissue, and a decrease in the amount of
subcutaneous fat. In those cases in which propulsive phase pronation is great,
minute hemorrhages develop in the skin at points of the greatest concentration of
force. Deeper areas of callus develop in the hemorrhagic areas, and have the
potential to continue on to ulceration. Thus, hypermobility due to ankle equinus
causes microtrauma to the soft tissues of the forefoot with each step.

Diabetes in the lower extremity

A common complication of diabetes is polyneuropathy of the lower extremity.
Sensory neuropathy results in a decreased ability to sense painful stimuli.
Autonomic neuropathy results in a decreased ability to regulate blood flow and
control sweating. Motor neuropathy results in atrophy of the intrinsic musculature
of the foot, and anterior muscle group weakness. Diabetic neuropathy also
degrades muscle sensory function, which may contribute to impaired balance
and unsteadiness of gait [11]. In the lower extremity, neuropathy contributes an
underlying neurological mechanism of ankle equinus deformity when the
peroneal nerve is involved. Peroneal nerve atrophy allows the posterior muscle
group to overpower the weakened anterior muscles [12].
Perhaps the greatest complication linked to diabetic neuropathy is the
relationship to pedal ulceration and subsequent amputation. Sensory loss is
considered to be the permissive factor in foot ulceration [13] and a common
factor in the pathway leading to lower extremity amputation [14]. The Semmes-
Weinstien 10-g monofilament is widely accepted as an inexpensive and sensitive
screening instrument in detecting loss of protective sensation [15 – 17]. Loss of
protective sensation limits an individual’s ability to discern injury, and often leads
to a delay in seeking treatment. Patients unable to feel the 10-g monofilament
should be considered at risk for foot injury and amputation.

Limited joint mobility

Cheiroarthropathy is the syndrome of limited joint mobility associated with
diabetes, and is most frequently described in the hand and upper extremity. This
394 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409

syndrome is becoming increasingly recognized as an early and common com-

plication of diabetes mellitus. Range of motion is reduced and skin is usually
described as swollen, thick, tight, waxy, and difficult to bend [18]. The extent of
joint involvement in the hand is easily evaluated by the ‘‘prayer sign,’’ the
approximation of the palmar surfaces of the IP joints in the praying position with
the fingers fanned [19]. Cheiroarthropathy occurs in 4 to 14% of the nondiabetic
population, with the incidence ranging widely from 8.4 to 55% with Type 1
diabetes, and 4.2% to 76% with Type 2 diabetes [20]. Limited joint mobility has
also been linked to other chronic complications of diabetes, including coronary
heart disease, vascular disease, retinopathy, and nephropathy [19,21 – 23].
There is growing support to suggest that limited joint mobilty is a widespread
phenomenon in diabetic patients, and is not restricted to the hand. Recently,
limited joint mobility has been described in the lower extremity of patients with
diabetes [24 – 29]. In fact, it has been suggested that as changes in the hand
increase in severity, a progressive decline in foot mobility can be expected [28].
The presence of hardened flexor tendons in the feet of patients with diabetes has
also been reported [30].
The pathogenesis of limited joint mobility is complex and multifactorial, but is
likely related to the nonenzymatic glycosylation of collagen, resulting in
thickening of skin, tendons, ligaments, and joint capsules, and thus a reduction
in tissue flexibility [18,23,25– 27,31]. Electron microscopic investigation found
increased packing density of collagen fibers, decreased fibrilar diameter, and
abnormal fibril morphology in the Achilles tendons of diabetic patients with
gastrocnemius soleus equinus. These structural abnormalities are thought to be
related to nonenzymatic glycosylation of the tendon, and presumably contribute
to the tightening of the Achilles tendon [32]. Microangiopathy, neuropathy,
increased hydration of collagen, and abnormalities in the aldose reductase
pathways are additional mechanisms and etiologic factors related to impaired
joint mobility in patients with diabetes [23,31].
As is the case with other chronic complications of diabetes, presence and
severity of limited joint mobility appear to be related to duration of diabetes and
glycemic control [21,22,27,33]. More precisely, it is the degree of long-term
glycemic control that is most closely linked with connective tissue dysfunction.
HbA1c levels above 8% have been shown to double or triple the risk of limited
joint mobility. Every 1% increase in the HbA1c level represents a 250% increase
in the risk of limited joint mobility [33].
Limited joint mobility may predispose the diabetic foot to ulceration. Del-
bridge and colleagues found that diabetic patients with a history of neuropathic
ulceration have a marked limitation of subtalar joint range of motion, especially
in the ulcerated foot [26]. A strong association has been made between limited
joint mobility and elevated plantar pressures in the diabetic foot [28]. The same
study identified limited joint mobility as a contributing risk factor for neuropathic
ulceration. It has also been shown that racial differences exist in joint mobility.
Subtalar joint mobility was more reduced in white diabetic patients than in white
non-diabetics, black diabetics, and non-diabetic black patients [34].
 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409 395

A limited number of studies have compared differences in ankle joint range of

motion in diabetic and non-diabetic patients and the subsequent association with
neuropathic ulceration. In two studies, ankle joint dorsiflexion was more reduced
in diabetic patients with history of ulceration than in non-diabetic controls
[24 – 29]. Limitation of both passive and active dorsiflexion of the ankle was
found in diabetic patients with sensory deficit of the foot [35]. These studies
suggest that in cases of acquired ankle equinus in patients with diabetes, limited
joint mobility must be considered a strong etiologic factor, providing yet another
reason to optimize glycemic control.

Role of equinus in diabetic foot pathology

As previously described, ankle equinus contributes to many foot deformities.
In patients without diabetes, these deformities can result in pain, poor fitting
shoes, and cosmetic complaints. In the diabetic foot, these deformities can result
in ulceration and amputation.
The role of plantar foot pressure and ulceration in individuals with diabetes is
becoming increasingly obvious. The combination of high plantar pressures and
sensory neuropathy has been well linked to plantar ulceration [36,37]. Diabetic
feet with a history of ulceration have been shown to have higher plantar pressures
than feet without a history of ulceration [38]. It has also been established that
there is an increase in plantar pressure after great toe amputation or following
partial foot amputation [39,40]. Furthermore, the combination of foot deformity,
limited joint range of motion, and neuropathy has been linked to ulceration [41].
Because high plantar pressure is associated with ulceration, the added effect of
ankle equinus may precipitate further ulceration and amputation. As discussed
earlier, the pathology of ankle equinus results from the compensation of equinus.
This is also true when considering plantar ulceration. Limited ankle dorsiflexion
will increase or prolong forefoot stress during walking [42,43]. When the forefoot
is in pronation, as with a fully compensated equinus foot, we can predict higher
plantar pressure under the first metatarsal head, especially if a hallux limitus
develops [44]. Hypermobility of the foot, commonly found with ankle equinus,
leads to increased shearing forces about the forefoot, causing soft tissue
deterioration and skin lesions. The authors have frequently observed recurrent
forefoot ulceration in the diabetic foot that we believe is due to the increased
stress of ankle equinus.
Nowhere is the effect of equinus on plantar pressure more obvious than in the
Charcot foot (Fig. 1). Charcot arthropathy is characterized by chronic repetitive
trauma or stress to the neuropathic foot, which leads to bone and joint
subluxation, fragmentation, and destruction.Although no conclusive data exist,
some observers have theorized that ankle equinus deformity, high peak plantar
pressure, and sensory neuropathy combine in the development of Charcot
arthropathy [45,46]. They suggest that the deforming force of the Achilles
tendon increases load on the forefoot and predisposes a patient to the sequella
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Fig. 1. Charcot foot with ankle equinus, rockerbottom foot, and history of plantar foot ulceration.

of Charcot arthropathy. Biomechanical compensation for equinus, as discussed

above, includes midtarsal joint pronation, which contributes to the formation of
the classic Charcot rockerbottom foot. Uncontrolled jamming of the neuropathic
foot that has lost its sense of proprioception is part of the Charcot process; this
can also produce limited joint range of motion secondary to bony remodeling.

Treatment of equinus
‘‘the treatment of neuropathic foot ulcerations is (a matter of) mechanics not
medicine.’’ Paul W. Brand, MD [47]
The first step in treating equinus is recognizing it. Dorsiflexion should be
measured with the knee straight and the knee flexed in all diabetic patients. Ankle
joint dorsiflexion is then measured with the subtalar joint held in neutral and the
midtarsal joint fully pronated (Fig. 2). Ankle equinus is present when less than 5
degrees of dorsiflexion past perpendicular is noted with the knee straight, and less
than 15 degrees is noted with the knee flexed [48]. Limitation of dorsiflexion
with the knee straight, but normal dorsiflexion with the knee flexed, represents an
isolated gastrocnemius equinus. This maneuver is called the Silfverskiold test,
and can quickly differentiate gastrocnemius equinus from other types of ankle
equinus [49]. If there is limitation of ankle joint dorsiflexion with the knee flexed
and extended, then both the gascrocnemius and soleus muscles may be involved.
Radiographs of the ankle should be performed in all patients to evaluate for a
bony cause of equinus that would not repond to the treatments that are discussed.
There are several nonsurgical methods of treating ankle equinus. Stretching for
at least 30 seconds per day increases flexibility and clinically lengthens the
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Fig. 2. Measuring for ankle equinus with the subtalar joint in neutral position.

gastrocnemius [50]. A study performed in individuals without diabetes found that

manual manipulation of the ankle increases ankle dorsiflexion twice as well as
stretching [51]. Studies in the treatment of plantar fascitis have demonstrated that
nightsplints increase ankle joint dorsiflexion [52]. In the sensate foot, this method
of treatment can be safely used. A pilot study of 11 patients demonstrated that a
physical therapy program of two sessions a week produces a significant
improvement of foot and ankle joint mobility in diabetic patients with limited
joint mobility and neuropathy. Three months after therapy ended, range of motion
at the ankle, subtalar joint, and first metaralophalangeal joint were still signific-
antly improved [53].
Modification to shoe gear is another type of treatment for ankle equinus and
related deformities. Sensate diabetics can use functional orthosis to limit the
deformities of ankle equinus. Insensate diabetics typically use accommodative
orthosis to protect the deformities that have resulted from ankle equinus. Rock-
erbottom soles allow for an artificial increase in ankle joint dorsiflexion and
decrease metatarsal head pressure. Padded ankle foot orthosis can be used to
support feet that have an ankle equinus deformity without the ability to dorsiflex
the ankle. To prevent skin ulceration, insensate feet are better served with braces
that attach to the shoe than those which rest against the skin [54].
Ankle equinus should be considered when treating diabetic foot ulceration.
Methods of addressing ankle equinus in ulceration treatment include walking
boots that have a rockerbottom sole, or total contact casts that redistribute
pressure and limit ambulation to a shorter stride length. Mueller demonstrated
a case of 21-month-old plantar second-metatarsal head ulceration secondary to
equinus that healed 85 days after total contact casting was initiated. The patient
subsequently was placed in rockerbottom shoes to decrease forefoot pressure
from the ankle equinus [55]. The effectiveness of total contact casting as a
treatment for planter ulceration can be improved through the use of percutaneous
Achilles tendon lengthening [56].
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Role of Achilles tendon lengthening

Surgical intervention that addresses ankle equinus deformity is now being
recognized as a very important component in the treatment of the diabetic foot.
Achilles tendon lengthening, gastrocnemius recession, or tendon advancement
procedures have long been used in the treatment of equinus deformity in the
nondiabetic [9,48,57,58]. The importance of these procedures in the treatment of
the diabetic foot is becoming increasingly evident. A recent case study recorded
an 83% reduction of in-shoe peak plantar pressure immediately after an Achilles
tendon lengthening. The in-shoe plantar forefoot pressure was still 55% reduced
seven months after the procedure. Barefoot plantar pressures initially decreased
46% after the Achilles tendon lengthening, but were only 14% decreased after
seven months [59]. The authors of this study attribute the noticeable difference in
barefoot and in-shoe pressures to the existence of longstanding forefoot deform-
ity that is better controlled in shoe gear. This case report closely parallels work
done by Armstrong and colleagues, who found a 27% reduction in peak plantar
pressures in the forefoot of 10 diabetics after percutaneous lengthening of the
Achilles tendon [60].
Generally, surgical treatment of muscular ankle equinus aims to restore ankle
range of motion by decreasing excessive passive moment, while maintaining the
active force-generating capacity of the muscles. If the Achilles tendon, for
example, is lengthened too much, the active force-generating capacity of the
gastrocsoleus muscle group can be greatly reduced, resulting in a poor outcome.
Computer simulations reveal that equinus due to isolated gastrocnemius con-
tracture can be treated effectively by lengthening the gastrocnemius aponeurosis
[61]. This same study suggested that lengthening of the Achilles tendon is not as
desirable as lengthening the gastrocnemius aponeurosis, because of the effect on
active moment-generating capacity about the ankle. While both procedures
restore normal passive moments about the ankle, lengthening of the Achilles
tendon may decrease the strength of these muscles too much, and reduce the
active moment-generating capacity about the ankle. With combined contracture
of the gastocnemius and soleus, independent lengthening of the gastrocnemius
and soleus aponeurosis, instead of lengthening their common tendon, has been
shown in computer simulation to be an effective way of maintaining plantar
flexion strength [62]. This underscores the importance of performing the Silver-
skiold test to differentiate isolated gastrocnemius contracture versus combined
muscular contracture.

TAL and forefoot amputations

Equinus deformity after forefoot amputation is common. After transmetatarsal
amputation, extensor tendon function is significantly diminished, and dorsi-
flexory power is greatly reduced. The gasctrocnemius soleus complex over-
powers the dorsiflexors of the foot, resulting in equinus deformity. Varus
deformity often accompanies equinus in the patient with a forefoot amputation,
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due to the unopposed pull of the posterior and anterior tibialis muscles and the
natural bone contours of the arch. The shorter the midfoot amputation, the more
likely the patient is to develop an equinovarus deformity [62]. Often a short
transmetatarsal amputation or more proximal foot amputation is bypassed in
favor of a below-knee amputation, due to fear of stump breakdown or ulceration
(Fig. 3). This fear can be alleviated by addressing the postoperative deforming
force of equinus with a tendoAchilles lengthening. A 91% healing rate of
transmetatarsal amputation stump ulceration with Achilles tendon surgery and
revisional transmetatarsal amputation has been demonstrated [63]. The authors
perform tendoAchilles lengthenings whenever possible on all transmetatarsal and
more proximal forefoot amputations. In the transmetatarsal amputation, extensor
tendon function is significantly diminished. The gastrocnemius soleus complex
subsequently overpowers the dorsiflexors of the foot, with equinus deformity
frequently developing. A tendoAchilles lengthening is an excellent operative
choice, because it decreases both the passive and active moments about the ankle
from the Achilles tendon. The shorter the midfoot amputation, the more likely the
patient is to develop an equinovarus deformity [62].
The Chopart amputation (calcaneocuboid-talonavicular level) also creates a
muscular imbalance and equinus deformity that can lead to stump ulceration and
possible below-knee amputation. However, like the transmetatarsal amputation,
when the deforming force of the Achilles tendon is addressed, amputation at the
Chopart level can give a good functional result. Lieberman and colleagues
reported on successful Chopart amputations performed with simultaneous per-
cutaneous heel cord lengthening [64]. Anterior tibial tendon transfer combined
with Achilles tendon lengthening has been recently suggested to counter

Fig. 3. Equinovarus deformity and rcurrent ulceration after LisFranc’s amputation.

400 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409

equinovarus deformity after Chopart’s amputation [62]. These results encourage

the use of proximal forefoot amputations in lieu of below-knee amputation.

TAL technique
The percutaneous Achilles tendon lengthening is the most commonly per-
formed procedure to address equinus deformity in the diabetic. Advantages of
this procedure include simple technique, short operative time, small incisions
with few wound-healing complications, and a decrease in both the passive tone
and the active strength of the Achilles tendon. Several methods of tenotomy, or
lengthening, of the Achilles tendon have been described; the authors perform this
procedure modeled after the triple hemisection slide lengthening as described by
Hoke [2]. It should be noted that this procedure is only performed in patients with
proper blood supply. If the procedure is performed in isolation, the patient is in a
prone position. When tenotomy is performed in conjunction with other proce-
dures, the patient is in a supine position, with the leg elevated and externally
rotated by an assistant (Fig. 4). The procedure is typically performed under
sedation with local anesthesia. To limit complications, an external tourniquet is
discouraged. Three incisions approximately 1 cm long are made perpendicular to
the long axis of the leg, and parallel to the relaxed skin tension lines (Fig. 5). The
first incision is made on the medial aspect of the Achilles tendon, approximately
3 cm proximal to the Achilles tendon insertion on the calcaneus. A second
incision is made on the medial aspect of the Achilles tendon, approximately 3 cm
distal to the musculotendonous junction. The third incision is performed on the
lateral aspect of the Achilles tendon, at the midpoint between the other two

Fig. 4. TendoAchilles lengthening in the prone position, preoperative.

 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409 401

Fig. 5. TendoAchilles lengthening, incisional approach.

incisions. Blunt dissection with a hemostat then frees the tendon from soft tissue
attachments (Fig. 6). Using a #11 blade, a hemisection of the tendon is performed
in each incision (Fig. 7). Deep structures are protected from inadvertent trauma
by cutting from deep to superficial. The foot is then dorsiflexed in a controlled
manner to create an increase in tendon length and ankle dorsiflexion of at least
10 degrees (Fig. 8). The skin is then reapproximated with nylon suture without
any deep closure. Postoperatively, the patient must be maintained in a posterior
splint, night splint, cast, or other immobilization device, with the ankle at least

Fig. 6. Visualizing the Achilles tendon.

402 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409

Fig. 7. Contolled sectioning of the Achilles tendon.

10 degrees dorsiflexed to prevent healing in a contracted position. Patients are

typically kept braced with limited weightbearing for three to four weeks. Patients
placed in total contact casts postoperatively are allowed to bear full weight at
24 hours (Fig. 9). In a study of rats and children, a percutaneous Achilles tendon
lengthening took three weeks to heal [65]; therefore we prefer to immobilize our
diabetic patients for at least this long.
Overlengthening of the Achilles tendon can occur with this procedure. Loss of
Achilles tendon strength results in compensation by the posterior tibialis, flexor

Fig. 8. Controlled dorsiflexion to lengthen the Achilles tendon.

 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409 403

Fig. 9. TendoAchilles lengthening, postoperative.

hallucis, and flexor digitalis muscles, which produces secondary deformity.

Excessive lengthening of the Achilles tendon can also result in a dorsiflexed
position of the foot, due to the extensor muscles overpowering the Achilles
tendon. This complication may result in a calcaneal gait with heel ulceration and
hammertoe development. Achilles transection has been suggested for trans-
metatarsal and more proximal amputations [63]. Therefore, the authors are not
overly concerned with an overlengthened tendon in partial foot amputations, and
we perform aggressive tendoAchilles lengthening in this circumstance. When the
complete foot is still present, an isolated gastrocnemius recession is sometimes
considered in lieu of the tendoAchilles lengthening, to preserve active strength
and limit the chance of overlengthening. Under these circumstances, the authors
use a distal inverted tongue-in-groove recession, as described by Downey [2].

Authors’ experience
The authors are unaware of any studies that record the prevalence of ankle
equinus in a high-risk diabetic population. From July 1, 2000 to June 1, 2001, all
patients who presented to the Diabetic Foot Center of Southern Utah for the
fitting of therapeutic or custom-molded shoes and insoles were screened for ankle
equinus, neuropathy, history of ulceration or amputation, and history of Charcot
arthropathy. Under the Medicare program guidelines, patients qualify for thera-
peutic shoes and inserts if they have Type 1 or Type 2 diabetes, and one or more
of the following conditions: previous amputation of the foot or part of the foot,
history of previous foot ulceration, history of pre-ulcerative callus formation,
peripheral neuropathy with evidence of callus formation, foot deformity of either
foot, or poor circulation in either foot.
404 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409

Determination of ankle joint range of motion was performed by a single nurse

investigator in all patients with the subtalar joint in neutral, the midtarsal joint
maximally pronated, and the knee extended. Maximum passive ankle joint
dorsiflexion was determined by measuring the angle formed by the intersection
of a line parallel to the lateral aspect of the fifth ray and a line parallel to the
longitudinal axis of the leg. Sensory neuropathy was defined as a vibration-
perception threshold of greater than 25 volts or insensitivity to a 10-g Semmes-
Weinstein monofilament [5,66].

Results
One hundred and fifty-one consecutive Medicare patients who qualify for
therapeutic shoes and inserts were screened by the same nurse investigator. The
patient age ranged from 51 to 95. The mean age was 72. Equinus deformity was
found in 138 of the 151 patients (91%). One hundred and thirty-three of the 151
patients had neuropathy and loss of protective sensation. Forty-five patients had
history of diabetic foot ulceration. Of these 45 patients, 43 (95%) were found to
have ankle equinus. Six of the 151 patients had history of Charcot arthropathy.
All of these patients had an ankle equinus deformity.

Discussion
These data suggest that the prevalence of ankle equinus among individuals
with diabetes is quite common. By common inclusion criteria, all patients
screened had some form of musculoskeletal, neurological, or vascular foot
pathology. Neuropathy was a dominant characteristic of this group of diabetic
patients. Therefore, the high prevalence of equinus found may only apply to
diabetic individuals with existing lower extremity complications. Further studies
are needed to compare the prevalence of ankle equinus among diabetic patients
with and without foot pathology.

Case report 1
A 55-year-old white woman with Type 1 diabetes, hypertension, and neuro-
pathy presented in December of 1995 with an infected ulceration plantar to the
first metatarsophalangeal joint. With regular debridement, culture-directed anti-
biotics, and wound care, the ulcer healed quickly. However, the ulceration
recurred multiple times. Dr. Van Gils began treating this patient, now aged 60,
19 months after one such recurrence. On physical exam, the patient had palpable
pedal pulses, absent protective sensation, and an ulceration measuring 2 cm in
diameter. Initial treatment began with weekly subcutaneous ulcer debridement,
felt and foam offload, and daily dressing changes with becaplermin platelet-
derived growth-factor gel. After two months of treatment, the patient was placed
 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409 405

in a total contact cast. Repeat subcutaneous ulcer debridement was performed at

each cast change, and the wound size decreased to 1.1 cm in diameter. After two
months of casting, an Achilles tendon lengthening was performed as described
above, and graftskin (Apligraf, Organogenesis, Inc. and Novartis Pharmaceu-
ticals, East Hanover, NJ) was applied to the ulcer site. Ankle joint range of
motion improved from perpendicular to eight degrees past perpendicular. The
patient was placed in a below-knee cast walker boot and instructed to follow
limited weightbearing instructions. Four weeks post-operatively the ulcer was
completely closed. One year later, the patient continues with weightbearing
responsibilities at work, and there has been no plantar callus formation, and no
recurrence of ulceration indicative of continued increased plantar pressure.

Case report 2
A 61-year-old obese white male with Type 2 diabetes, hypertension, and a
history of Charcot arthropathy initially presented with an infected full thickness
ulcer plantar to the first metatarsophalangeal joint on the right foot (Fig. 10). The
ulcer measured 1.5 cm in diameter with full-thickness depth, pedal pulses were
regular and palpable, and protective sensation was absent. The patient had no
previous history of ulceration, but was wearing four-year-old, custom-molded
shoes prescribed after the initial development of Charcot deformity. With local
wound care, felt and foam offload, and weekly debridement, the ulcer reached
full epithelization and complete closure. However, upon return to normal activity,

Fig. 10. Recurrent diabetic ulcer, preoperative.

406 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409

Fig. 11. Healed diabetic foot ulcer.

thick callus tissue developed, followed by ulcer recurrence. This pattern repeated
itself three times despite new custom-molded shoes and plastizote insoles.
Eleven months after initial presentation, the patient was scheduled for Achilles
tendon lengthening. Preoperative evaluation of his right ankle joint demonstrated
an ankle equinus deformity with dorsiflexion measured at two degrees less than
perpendicular in relation to the long axis of the leg. Percutaneous Achilles tendon
lengthening was performed as described above, and the patient was placed in a
below-knee cast walker boot for four weeks. Postoperatively, the patient’s right an-
kle dorsiflexion increased to five degrees past perpendicular. The ulcer was healed
at the patient’s two week follow-up visit and remains healed twelve months after
surgery (Fig. 11).

Conclusion
Root was not referring to the diabetic foot when he stated that the worst foot
is the one with a fully compensated equinus [1], but it is becoming increasingly
evident that he could have been. The effects of ankle equinus on the lower
extremity are well documented. The effects of ankle equinus in the patient with
diabetes are now being more commonly recognized and treated. Ankle equinus
in the diabetic foot increases deformity, plantar pressure, and the risk of
 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409 407

ulceration, and complicates healing of plantar foot ulcers. We suggest that health
care providers include screening for ankle equinus when determining risk factors
for ulceration. Care of the diabetic foot, and especially the ulcerated, partially
amputated, or Charcot foot, would benefit from the diagnosis and treatment of
ankle equinus.

References
[1] Root ML, Orien WP, Weed JH. Forces acting upon the foot during locomotion. Abnormal
motion of the foot. In: Root ML, Orien WP, Weed JH, editors. Normal and abnormal function
of the foot, clinical biomechanics, vol. 2. Los Angeles: Clinical Biomechanics Corp.; 1977.
p. 165 – 79, 295 – 348.
[2] Downey MS. Ankle equinus. In: McGlamery ED, Banks AS, Doney MS, editors. Comprehen-
sive textbook of foot surgery, vol. 1. Baltimore: Williams & Wilkins; 1992. p. 687 – 730.
[3] Hill RS. Ankle equinus: prevalence and linkage to common foot pathology. J Am Podiatr Med
Assoc 1995;85(6):295 – 300.
[4] Boyko EJ, Ahroni JH, Stensel V, Forsberg RC, Davignon DR, Smith DG. A prospective study of
risk factors for diabetic foot ulcer. Diabetes Care 1999;22(7):1036 – 42.
[5] Frykberg RG, Lavery LA, Pham H, et al. Role of neuropathy and high foot pressures in diabetic
foot ulceration. Diabetes Care 1998;21(10):1714 – 9.
[6] McGlamry ED, Kitting RW. Equinus foot: an analysis of the etiology, pathology and treatment
techniques. J Am Podiatr Assoc 1973;63:165 – 84.
[7] Whitney AK, Green DR. Pseudoequinus. J Am Podiatr Assoc 1982;72:365 – 71.
[8] Kent MH. Ankle equinus related to trauma and its surgical treatment: a preliminary report of
three cases. J Foot Surg 1978;17(2):75 – 9.
[9] Feehery RV. Surgery of the Achilles tendon and posterior muscle group. Clin Podiatr Med Surg
1991;8(3):513 – 42.
[10] Green DR, Brekke M. Anatomy, biomechanics and pathomechanics of lesser digit deformities.
Clin Podiatr Med Surg 1996;13(2):179 – 200.
[11] Van Deursen RWM, Sanchez MM, Ulbrecht JS, Cavanagh PR. The role of muscle spindles in
ankle movement perception in human subjects with diabetic neuropathy. Exp Brain Res
1998;120:1 – 8.
[12] Frykberg RG. The high risk foot in diabetes mellitus. New York: Churchhill Livingstone, 1991.
[13] Boulton AJM. Peripheral neuropathy and the diabetic foot. Foot 1992;2:67 – 72.
[14] Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation: basis for preven-
tion. Diabetes Care 1990;13:513 – 21.
[15] American Diabetes Association. Foot care in patients with diabetes mellitus. Diabetes Care
1998;21:S54.
[16] Lavery LA, Armstrong DG, Vela SA. Practical criteria for screening patients at high risk for
diabetic foot ulceration. Arch Intern Med 1998;158:157 – 62.
[17] Simeone LR, Veves A. Screening techniques to identify the diabetic patient at risk of ulceration.
J Am Podiatr Med Assoc 1997;87:313 – 7.
[18] Rosenbloom AL, Silverstein JH. Connective tissue and joint disease in diabetes mellitus. Endo-
crinol Metab Clin North Am 1996;25(2):473 – 83.
[19] Rosenbloom AL, Silverstein JH, Lezotte DC, et al. Limited joint mobility in childhood diabetes
mellitus indicates increased risk for microvascular disease. N Engl J Med 1981;305:191 – 4.
[20] Aljahlan M, Lee KC, Toth E. Limited joint mobility in diabetes. Postgrad Med 1999;105(2):
99 – 106.
[21] Arkkila PET, Kantola IM, Viikari JSA. Limited joint mobility in type 1 diabetic patients:
correlation to other diabetic complications. J Int Med 1994;236:215 – 23.
[22] Arkkila PET, Kantola IM, Viikari JSA. Limited joint mobility in non-insulin-dependent diabetic
408 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409

(NIDDM) patients: correlation to control of diabetes, atherosclerotic vascular disease, and other
diabetic complications. J Diabetes Complications 1997;11(4):208 – 17.
[23] Fitzcharles MA, Duby S, Waddell RW, et al. Limitation of joint mobility (cheiroarthropathy) in
adult noninsulin-dependent diabetic patients. Ann Rheum Dis 1984;43:251 – 7.
[24] Birke JA, Franks BD, Foto JG. First ray joint limitation, pressure, and ulceration of the first
metatarsal head in diabetes mellitus. Foot Ankle Int 1995;16(5):277 – 84.
[25] Campbell RR, Hawkins SJ, Maddison PJ, Reckless JPD. Limited joint mobility in diabetes
mellitus. Ann Rheum Dis 1985;44:93 – 7.
[26] Delbridge L, Perry P, Marr S, et al. Limited joint mobility in the diabetic foot: relationship to
neuropathic ulceration. Diabet Med 1988;5:333 – 7.
[27] Duffin AC, Donaghue KC, Potter M, et al. Limited joint mobility in the hands and feet of
adolescents with type 1 diabetes mellitus. Diabet Med 1999;16:125 – 30.
[28] Fernando DJS, Masson EA, Veves A, Boulton AJM. Relationship of limited joint mobility to
abnormal foot pressures and diabetic foot ulceration. Diabetes Care 1991;14:8 – 11.
[29] Mueller MJ, Diamond JE, Delitto A, Sinacore DR. Insensitivity, limited joint mobility, and
plantar ulcers in patients with diabetes mellitus. Phys Ther 1989;69:453 – 62.
[30] Ramirez LC, Raskin P. Diabetic foot tendinopathy: abnormalities in the flexor plantar tendons in
patients with diabetes mellitus. J Diabetes Complications 1998;12:337 – 9.
[31] Kapoor A, Sibbitt WL. Contractures in diabetes mellitus: the syndrome of limited joint mobility.
Semin Arthritis Rheum 1989;18(3):168 – 80.
[32] Grant WP, Sullivan R, Sonenshine DE, et al. Electron microscopic investigation of the effects of
diabetes mellitus on the Achilles tendon. J Foot Ankle Surg 1997;36(4):272 – 8.
[33] Silverstein JH, Gordon G, Pollock BH, Rosenbloom AL. Long-term glycemic control influences
the onset of limited joint mobility in type 1 diabetes. J Pediatr 1998;132:944 – 7.
[34] Veves A, Sarnow MR, Giurini JM, et al. Differences in joint mobility and foot pressures between
black and white diabetic patients. Diabet Med 1995;12:585 – 9.
[35] Simmons RW, Richardson C, Deutsch K. Limited joint mobility of the ankle in diabetic patients
with cutaneous sensory deficit. Diabetes Res Clin Pract 1997;37:137 – 43.
[36] Boulton AJM, Veves A, Young MJ. Etiopathogenesis and management of abnormal foot pres-
sures. In: Levin ME, O’Neal LW, Bowker JH, editors. The diabetic foot. St. Louis: Mosby Year
Book; 1993. p. 233 – 46.
[37] Veves A, Murray HJ, Young MJ, Boulton AJM. Do high pressures lead to ulceration: a pro-
spective study. Diabetologia 1992;35:660 – 3.
[38] Stess R, Jensen SR, Mirmiran R. The role of dynamic plantar pressures in diabetic foot ulcers.
Diabetes Care 1997;20(5):855 – 8.
[39] Armstrong DG, Lavery LA. Plantar pressures are higher in diabetic patients following partial
foot amputation. Ostomy/Wound Management 1998;44(3):30 – 9.
[40] Lavery LA, Lavery DC, Quebedeax-Farnham TL. Increased foot pressures after great toe am-
putation in diabetes. Diabetes Care 1995;18(11):1460 – 2.
[41] Birke JA, Cornwall MW, Jackson M. Relationship between hallux limitus and ulceration of the
great toe. J Orthop Sports Phys Ther 1988;11:172 – 6.
[42] Hunt GC, Brocato RS, Cornwall MW. Gait: foot mechanics and neurobiomechanics. In: Hunt
GC, McPoil TG, editors. Physical therapy of the foot and ankle. 2nd edition. New York:
Churchill Livingstone; 1995. p. 47 – 80.
[43] Morag E, Cavanagh P. Structural and functional predictors of regional peak pressures under the
foot during walking. J Biomech 1999;32:359 – 70.
[44] Cavanagh PR, Ulbrecht JS. Biomechanics of the foot in diabetes mellitus. In: Levin ME,
O’Neal LW, Bowker JH, editors. The diabetic foot. St. Louis: Mosby Year Book; 1993.
p. 199 – 232.
[45] Armstrong DG, Lavery LA. Elevated peak plantar pressures in patients who have Charcot
arthropathy. J Bone Joint Surg 1998;80A:365 – 9.
[46] Sanders LJ, Frykberg RG. Charcot foot. In: Levin ME, O’Neal LW, Bowker JH, editors. The
diabetic foot. St. Louis: Mosby Year Book; 1993. p. 149 – 80.
 C.C. Van Gils, B. Roeder / Clin Podiatr Med Surg 19 (2002) 391–409 409

[47] Birke JA, Patout CA, Foto JG. Factors associated with ulceration and amputation in the neuro-
pathic foot. J Ortho Sports Phys Ther 2000;30(2):91 – 7.
[48] Strecker WB, Via MW, Oliver SK, Schoenecker PL. Heel cord advancement for treatment of
equinus deformity in cerebral palsy. J Pediatr Orthop 1990;10:105 – 8.
[49] Silfverskiold N. Reduction of the uncrossed two-joints muscles of the leg to one-joint muscles in
spastic conditions. Acta Chir Scand 1924;56:316.
[50] Grady JF, Saxena A. Effects of stretching the gastrocnemius muscle. J Foot Surg 1991;30(5):
465 – 9.
[51] Dananberg HJ, Shearstone J, Guillano M. Manipulation method for the treatment of ankle
equinus. J Am Podiatr Med Assoc 2000;90(8):385 – 9.
[52] Powell M, Post WR, Keener J, Wearden S. Effective treatment of chronic plantar fasciitis with
dorsiflexion night splints: a crossover prospective randomized outcome study. Foot Ankle Int
1998;19(1):10 – 8.
[53] Dijs HM, Roofthooft JMA, Driessens MF, et al. Effect of physical therapy on limited joint
mobility in the diabetic foot. J Am Podiatr Med Assoc 2000;90(3):126 – 32.
[54] Sobel E, Levitz SJ, Caselli MA. Orthosis in the treatment of rearfoot problems. J Am Podiatr
Med Assoc 1999;89(5):220 – 33.
[55] Mueller MJ, Diamond JE. Biomechanical treatment approach to diabetic plantar ulcers: a case
report. Phys Ther 1988;68(12):1917 – 20.
[56] Lin SS, Lee TH, Wapner KL. Plantar forefoot ulceration with equinus deformity of the ankle in
diabetic patients: the effect of tendo-Achilles lengthening and total contact casting. Orthopedics
1996;19(5):465 – 75.
[57] Katz K, Arbel N, Apter N, Soudry M. Early mobilization after sliding Achilles tendon length-
ening in children with spastic cerebral palsy. Foot Ankle Int 2000;21(12):1011 – 4.
[58] Downey MS, Banks AS. Gastrocnemius recession in the treatment of nonspastic ankle equinus. J
Am Podiatr Med Assoc 1989;79(4):159 – 74.
[59] Hastings MK, Mueller MJ, Sinacore DR, et al. Effects of a tendo-Achilles lengthening procedure
on muscle function and gait characteristics in a patient with diabetes mellitus. J Orthoped &
Sports Phys Ther 2000;30(2):85 – 90.
[60] Armstrong DG, Stacpoole-Shea S, Nguyen H, Harkless L. Lengthening of the Achilles tendon in
diabetic patients who are at high risk for ulceration of the foot. J Bone Joint Surg 1999;81A:
535 – 8.
[61] Delp SL, Statler K, Carroll NC. Preserving plantar flexion strength after surgical treatment for
contracture of the triceps surae: a computer simulation study. J Orthop Res 1995;13:96 – 104.
[62] Reyzelman AM, Hadi S, Armstrong DG. Limb salvage with Chopart’s amputation and tendon
balancing. J Am Podiatr Med Assoc 1999;89(2):100 – 3.
[63] Barry DC, Sabacinski KA, Habershaw GM, et al. Tendo Achillis procedures for chronic ulcer-
ations in diabetic patients with transmetatarsal amputations. J Am Podiatr Med Assoc 1993;
83(2):96 – 100.
[64] Lieberman JR, Jacobs RL, Goldstock L, et al. Chopart amputation with percutaneous heel cord
lengthening. Clin Orthop 1993;296:86 – 91.
[65] Blasier RD, White R. Duration of immobilization after percutaneous sliding heel-cord length-
ening. J Ped Ortho 1998;18(3):299 – 303.
[66] Armstrong DG, Lavery LA, Harkless LB. Who is at risk for diabetic foot ulceration? Clin
Podiatr Med Surg 1998;15(1):11 – 9.