The Foot 26 (2016) 714

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The Foot
journal homepage: www.elsevier.com/locate/foot

Review

Current concepts of Charcot foot in diabetic patients

Javier La Fontaine a, , Lawrence Lavery a , Edward Jude b
a
b

UT Southwestern Medical Center, Department of Plastic Surgery, Dallas, TX, USA

Tameside Hospital NHS Foundation Trust, Lancashire, UK

h i g h l i g h t s

Charcot neuroarthropathy is uncommon but it leads to ulceration and amputation when is not detect early.
A new classication system has been suggested to help in early diagnosis.
New insights for pathological process exist and are covered in this article.
Medical and surgical managements have been further studied and a better recommendation is suggested.

a r t i c l e

i n f o

Article history:
Received 27 June 2014
Received in revised form 20 August 2014
Accepted 12 November 2015
Keywords:
Diabetes
Charcot
Neuroarthropathy
Foot
Ankle

a b s t r a c t
The Charcot foot is an uncommon complication of neuropathy in diabetes. It is a disabling and devastating
condition. The etiology of the Charcot foot is unknown, but it is characterized by acute inammation with
collapse of the foot and/or the ankle. Although the cause of this potentially debilitating condition is not
known, it is generally accepted that the components of neuropathy that lead to foot complications must
exist. When it is not detected early, a severe deformity will result in a secondary ulceration, infection,
and amputation. Immobilization in the early stages is the key for success, but severe deformity may
still develop. When severe deformity is present, bracing may be attempted but often patients will need
surgical intervention. Good success has been shown with internal and external xation. In patients with
concomitant osteomyelitis, severe deformity, and/or soft tissue infection, a high amputation may be the
best treatment of choice.
2015 Elsevier Ltd. All rights reserved.

1. Epidemiology
In 1868, Jean-Martin Charcot described neuroarthropathy in the
foot in relation to tabes dorsalis [1]. The author proposed the rst
theory in how this process may occur. In 1936, Jordan was the
rst to describe Charcot in diabetes [2]. Charcot neuroarthropathy
(CN) is a disabling and devastating condition. Although the cause of
this potentially debilitating condition is not known, it is generally
accepted that the components of diabetic neuropathy that lead to
foot complications must exist. Untreated CN may lead to a rocker
bottom foot which will lead to increase plantar pressure in the neuropathic foot. This cascade may lead to an ulceration and possible
amputation. A recent study shows, however, that CN alone may

not pose a risk for amputation, but CN along with ulceration has 12
times higher risk of having an amputation [3].
The incidence of CN is about 0.1 to 5% in diabetic neuropathy
[46]. Since neuropathy is a common complication of diabetes, 80%
of the cases occur in patients with diabetes for over 15 years, and
60% of the cases in patients with diabetes for over 10 years. The
prevalence of CN ranges from 0.08% to 8.5% [6]. Lee et al. found a
prevalence of 7.5% of CN in patients with diabetes, and 29% of those
had neuropathy [7]. Frequently, this pathology occurs between the
5th and 6th decade with a mean age of 50.3, and no difference
between genders [8]. Although it is more common unilaterally,
it can involve both extremities in up to 39% of the cases and the
incidence of ulceration is 17% per year [9].

2. Classication and staging

Correspondence to: UT Southwestern Medical Center, Department of Plastic Surgery, 5323 Harry Hines Blvd, Dallas, TX 75390, USA. Tel.: +1 214 648 9103;
fax: +1 214 648 2550.
E-mail addresses: Javier.lafontaine@utsouthwestern.edu,
javierlafontaine@gmail.com (J. La Fontaine).
http://dx.doi.org/10.1016/j.foot.2015.11.001
0958-2592/ 2015 Elsevier Ltd. All rights reserved.

There are different types of classications to describe CN. Most

classications are inconsistent since they have a wide spectrum of
description using radiographical changes, clinical locations, and/or
pattern of destruction. None of the classication suggests possible

J. La Fontaine et al. / The Foot 26 (2016) 714

Table 1
Clinical and radiological description for Charcot neuroarthropathy.
Stage 0:
Stage 1:
Stage 2:
Stage 3:

Clinically, there is joint edema, but radiographs are negative

Osseous fragmentation with joint dislocation
Decreased local edema, with coalescence of fragments
No local edema, with consolidation and remodeling of fracture
fragments. The foot is now stable and a rocker bottom type
foot may be seen

treatments or prognostic factors. The rst classication describe

was by Eichenholtz in 1966 [10]. This classication uses three
clinical and radiological stages of progression: the stage of development, stage of coalescence, and stage of reconstruction. The stage
of development or stage 1 is dened by periarticular debris formation and fragmentation of subchondral bone, and joint subluxation
and dislocation. Clinically, the foot is warm, erythematous, edematous, painful and with bounding pulses. In most occasions, the
affected limb needs to be compared to the contralateral limb to
appreciate the erythematous changes. During the coalescent stage,
or stage 2, the large bone fragments become fused and unite with
bone adjacent bones. Absorption of small debris is noticeable as
well. Clinically, this foot will present with decreased warmth, and
swelling, but instability of the joints may continue. Finally, the stage
of reconstruction, or stage 3 is characterized by bone consolidation, and rounding of bone fragments. As revascularization occurs,
decrease in sclerosis is appreciated. A stage 0 or pre-CN stage has
been proposed where a sudden onset, warmth and erythema occurs
in the neuropathic patient. Normal anatomy or joint distention may
be observed radiologically [11,12] (Table 1).
The most common locations involved in the foot are midfoot
joints (50%), hindfoot joints (28%), followed by ankle joint (19%),
and forefoot joints (3%) [13]. Other classications by location have
been described, but resemble previous ones, and have been in small
sample studies [5,16,17]. Most recently, Chanteleau and colleagues
described an MRI classication of acute CN [14,15]. The best study
describing pattern of destruction and proposing risk factors for
poor outcomes is the prospective study done by Herbst et al. in
2004 [13]. They followed 55 patients prospectively and classied
patients by injury (fracture, dislocation, or combination), and by
location (ankle, hind foot, midfoot, and forefoot). They also measured bone mineral density with dual energy X-ray absorptiometry
(DEXA). They found that poor outcomes noticed where associated
with fracture pattern located at ankle and forefoot.
3. Clinical assessment and imaging
The general consensus is that in order to develop CN the patient
has to be neuropathic. Currently, diabetes is the main cause for
neuropathy in the lower extremity in industrialized countries [16].
Factors such as osteopenia, equinus, peripheral vascular disease,
and nephropathy, have also been described as risk factors for CN
[4].
Although the cause of this potentially debilitating condition is
not known, a number of theories have been proposed:
Following the development of autonomic neuropathy there is an
increased blood ow to the extremity, resulting in increased bone
reabsorption and osteopenia.
Following sensori-motor neuropathy, the resulting sensory loss
and muscle imbalance induces abnormal stress in the bones and
joints of the affected limb, leading to bone destruction [17].
Stretching of the ligaments due to joint effusion, may lead to joint
subluxation [18].
The most common presentation is the neuropathic patient
which sustains an unperceived, injury, continues to walk until

a severe inammatory process leads to osteopenia, distention of

joint, and end stage foot and/or ankle dislocation [19]. In the CDUK
audit of Charcot foot by Frame and colleagues, 12% of patients
had surgery in the index limb prior to registration of the study.
Also, 7% of patients presented with an ulcer were complicated with
osteomyelitis [20]. There are two etiological theories to the development of CN. The Neurovascular Theory or French Theory was
developed by Charcot in 1868 [1]. After studying more than 5000
chronically ill patients, the author concluded that the profound
joint destruction and deformities were secondary to changes in the
trophic centers of the spinal cord, specically the diseased anterior
horn cells which resulted in neurogenic and circulatory disruption
may result in osteopenia.
In an attempt to support the French theory, Edelman et al. [21]
described 3 cases in which CN develops after the lower extremity was revascularized. Subsequently, in a study by Shapiro et al.
[22], blood ow was measured with laser Doppler owmetry with
local skin warming in patients with CN, neuropathy, and healthy
patients. Increasing local skin temperature increased skin blood
ow and vasomotion in healthy and CN patients, but not in diabetes
mellitus (DM) with neuropathy alone. The authors concluded that
blood ow in the controls and CN patients, despite the extent of
neuropathy, is intact. The neurotraumatic theory or German Theory was described in 1870. The theory is based on unperceived
trauma or injuries to an insensate joint will lead to stress fractures.
This results in progressive and permanent damage to the bone and
joints in the foot forming a problematic biomechanical foot. CN
feet develop an increase in vertical pressures and shear stress due
to deformity and equinus [23].
Most commonly, an acute presentation of the patient presents
with erythematous, warm, edematous foot. The most common
complaint is pain [19]. Usually, patients will not recall an
injury. Clinically, patients demonstrate signicant neuropathy
with bounding pulses. If the patient does not seek treatment
immediately, the foot will collapse giving the appearance of
rocker bottom. When presentation is chronic, a midfoot ulcer
may become evident as well the patient continues to ambulate.
Although, the classic description is rocker-bottom foot, other deformities such as ankle dislocation abduction of the forefoot, and
swollen MPJs can be evident (Fig. 1).
There are few diagnostic modalities that could be used clinically to assist in the diagnosis of this entity. The infrared cutaneous
temperature monitor to detect skin temperature changes is the
most accurate tool for diagnosis and monitor progression (Fig. 2).
Patients with acute CN experience increased temperature in the
affected foot when compared to the contralateral foot. Briey, the
monitor is closely placed to areas in the forefoot, midfoot, and
hindfoot, to record the temperature and compare it to the contralateral side at the same location. Skin temperature differences
of 4 F (2 C) when compared with the contralateral side indicate
an active CN, and should be ofoaded until normalization of temperature [24]. Laboratory studies are helpful when the diagnosis of
CN is not clear. White blood cell count (WBC) with differential will
help to distinguish between acute CN and an acute soft tissue or
acute osteomyelitis. However, it is a nonspecic marker and may
be elevated in CN. C-reactive protein (CRP) could be used to distinguish between acute CN and osteomyelitis and often elevated in
infection, but it is a nonspecic marker for inammation [25].
3.1. Imaging
Radiographs are the most useful in diagnosing the pathology,
locate the area of involvement, evaluate quality of bone, and identify if the process is acute or chronic. If an infection is suspected,
foreign body and soft tissue emphysema can be identied. Also,
radiographs are helpful in correlating the ulcer location and the

J. La Fontaine et al. / The Foot 26 (2016) 714

Fig. 1. Charcot neuroarthopathy of the rst metatarsophalangeal joint.

area of osteomyelitis. Nuclear medicine is a modality that can be

used to assist in the diagnosis. It is more sensitive and can conrm
pathology earlier, but it is not required for every patient. Triphasic
technetium-99 bone scan detects bone activity early in the process. It is not very helpful differentiating between acute CN and
osteomyelitis because the specicity is very low [26]. Indium111
WBC is more specic for infection than technetium-99 scan since
white blood cells accumulate in the area where infective process
is present. When an infectious process is suspected in an area of
chronic CN, this imaging technique may be helpful. However, in the
presence of acute CN, the signicant inammatory response around
the soft tissue will make the diagnosis difcult [27]. Tc-99 HMPAO
(aka Ceretec) labeled leukocyte scan is a non-invasive means of
determining osteomyelitis. Blume et al. [28] found Tc-99 HMPAO
WBC sensitive for osteomyelitis at 90% and a specicity at 86%. Boc
et al. found that false positives do occur using the Tc-99 HMPAO test
even though it is a reliable modality [29]. Sulfur colloid scanning
is innovative and useful modality for the differentiation between
osteomyelitis and acute CN by using leukocytes scintigraphy and
bone marrow scanning. Labeled leukocytes will not accumulate in
regions where bone infection is present as infection infarcts bone
marrow elements. During the process of bone resorption and bone
formation in acute CN, labeled leukocytes will accumulate and the
diagnosis of CN can be made [30]. Magnetic resonance imaging
(MRI) is a modality commonly used for the diagnosis of CN. One of
the key ndings to identify bone involvement in MRI is the presence
of bone edema, and subchondral cysts [31]. However, it is important
to realize that MRI often fail to differentiate adequately between
Charcot and osteomyelitis [32]. In acute CN, a decrease in signal

is observed in T1 and T2. Other groups tried to compare MRI, and

nuclear medicine techniques as described previously, and showed
MRI being somewhat superior [33]. Bone biopsy with bone culture
is the most denitive diagnosis. By harvesting the bone in question,
sampling for culture and biopsy can be obtained. The area of biopsy
should be obtained away from any chronic wound. Polymorphonuclear cells (PMN) are found in patients with CN, and presence of
bacteria and leukocytes are found in patients with bone infection.
It is common where either the bone culture or bone biopsy may
have different results. The clinician will require making a decision
based on history and physical examination.
4. Pathogenesis
Charcot concluded that the profound joint destruction and
deformities were secondary to changes in the trophic centers of
the spinal cord, specically the diseased anterior horn cells which
resulted in neurogenic and circulatory disruption. Most textbooks
suggest that CN primarily occurs in patients with adequate blood
ow to the foot. Other studies suggest that there is usually adequate
large vessel perfusion to the foot with arterial venous shunting
associated with autonomic neuropathy that alters the microcirculation [11]. In addition, metabolic and vascular insulin resistance in
CN patients is thought to lead to early changes in endothelial function. A dysfunctional endothelium compromises the regulation of
blood ow and pressure, facilitates cell migration, and proliferation
and an inammatory response ensues. Lipid deposition and formation of reactive oxygen species contribute to enhance this process
and structural changes progress to plaque formation.

Fig. 2. Infrared cutaneous thermometry.

10

J. La Fontaine et al. / The Foot 26 (2016) 714

An autonomic nervous system dysfunction causes a hyperemic demineralization leading to osteopenia. The loss of peripheral
blood ow and vasomotion in DM neuropathy could be protective against CN. Even though, for a CN to develop, signicant
sensory loss must exist. It has been speculated that loss of vascular tone may lead to decrease bone mineralization as a result
of increased bone turnover, similar to that of osteoporosis, that
has been demonstrated in diabetic patients [34]. The extent to
which abnormal vasodilatation and inappropriate micro-vascular
tone control contribute to the development of the CN has not
yet been dened. These investigators found that there was a
signicant reduction in the bone mineral density of the lower
limbs with CN, and that this was greater in the affected limb.
Also, it has been reported that patients with type 1 and type 2
diabetes have decreased bone mineral density when compared
to agesex matched control subjects and this might predispose
to increased fracture risk [35]. Therefore, a decrease in vascular tone and decrease in bone mineral density may predispose
neuropathic patients to develop CN. The relationship between
bone mineral density and CN is not clear. Osteopenia, prolonged
inammatory response has been advocated [3638]. Therefore,
further research is necessary to assess the role of OPG/RANKL
pathway, and other pathways involved in the development
of CN.
Several authors have suggested that an exaggerated inammatory response in diabetes may be associated with CN [37,39].
Sinacore suggested that the prolonged inammatory response
observed in CN contributes to osteolysis and loss of BMD in the
calcaneus [39].
The most accepted pathway is the RANKL/OPG axis. Jeffcoate
and Mabilleau have advocated using the RANKL/OPG pathway to
identify and evaluate therapies for fracture complications and CN
[40]. Most of the work that evaluates RANKL and OPG expression
in diabetic bone has been done in streptozotocin induced type 1
animal models. RANKL and its decoy receptor, (OPG) were identied in 1997. The system is a key mediator of bone metabolism,
and it has been used to evaluate osteoclastogenesis and osteolytic
processes in a number of disease states such as rheumatoid arthritis, osteoarthritis, bone tumors, prosthetic failure, and periodontal
disease [4143]. RANKL is part of the TNF- superfamily. Proinammatory cytokines (tumor necrosis factor and interleukins)
and calciotropic hormones (parathyroid hormones, calcitonin, and
CGRP) mediate RANKL and the acute inammatory responses following fracture. The process of bone resorption and formation is
controlled by the level of RANKL and OPG. When RANKL expression
is higher in relation to OPG, it increases osteoclastogenesis. On the
other hand, if OPG concentrations are high in relation to RANKL,
OPG prevents binding with RANKL receptors. Thus bone resorption will not increase. In diabetes, CN is exemplied by prolonged
inammation and osteolysis that may be similar to the osteolysis observed in rheumatoid arthritis, periodontal disease, and hip
implant failure.
There is emerging evidence that the nervous system and neuropeptides effect bone metabolism [44]. One such neuropeptide is
calcitonin gene-related peptide (CGRP). In the peripheral nervous
system CGRP can be demonstrated in motor, sensory and autonomic nerve bers, particularly unmyelinated C type and small
myelinated A- bers. Sensory bers contribute to the maintenance of trabecular bone integrity through mechanisms mediated
by CGRP and/or substance P, another neuropeptide product of sensory nerve bers. In addition, ablation of CGRP results in osteopenia
due to reduced osteoblastic bone formation. To investigate this possibility, La Fontaine and colleagues [45] studied bone samples from
normal subjects, subjects with diabetic neuropathy, and subjects
with diabetes and CN. They investigated the differences of cellular
components (osteoblasts and osteoclasts) in hematoxylin and eosin

stains, and used immunohistochemical techniques to immunolocalize CGRP and endothelial nitric oxide synthase (eNOS) in bone
samples.
Hematoxylin and eosin stains demonstrated increased numbers of osteoblasts and osteoclasts in bone samples from subjects
with CN and diabetic neuropathy compared to those from normal
subjects. In CN specimens, immunolocalization of CGRP and eNOS
intensies at the margin of trabecular bone, osteocytes, and osteoclasts cytoplasm compared to normal bone. No difference of CGRP
and eNOS immunolocalization was noticeable between CN and DN
specimens. The authors concluded that CGRP and eNOS may regulate osteoblastic and osteoclastic activity in neuropathy [46].
5. Treatment
The success for the conservative management will depend on
how early the Charcot is diagnosed. We consider a red, hot, swollen
foot in presence of diabetes and neuropathy to be a Charcot even
in the presence of negative radiographs. Immobilization is the
mainstay of conservative management. The following are the most
common devices used for immobilization.
5.1. Ofoading
Based on our current knowledge of the pathologic process, the
goal of the treatment is to maintain a plantigrade foot, with minimal deformity and hence no areas of increased pressure. The gold
standard treatment for CN has been immobilization [47]. For example, treatment with the total contact cast is lengthy, and may lead
to contra-lateral CN development [19,47]. Despite adequate immobilization, severe and unstable deformities may be unavoidable
in some patients. More recently, in a study by Pinzur, 60% of the
CN patients studied reach the end point without surgical intervention [48]. However, a variety of different types of treatment
has been studied for this entity. As mentioned above, the gold
standard for the treatment of acute CN is immobilization with
total contact cast (TCC) (Fig. 3). Most of the medical evidence supporting TCC is retrospective and lacks signicant detailed results
[24,47]. Another modality used commonly is the Charcot Restraint
Orthotic Walker (CROW) (Fig. 4). The CROW is advocated mostly as
a transition device from cast immobilization, and very effective in
controlling lower extremity edema. Although it is commonly used,
the evidence is minimal to support effectiveness [49]. The patellar
tendon-bearing brace (PTB) (Fig. 5) has been used for the management of CN, mostly when it involves the midfoot, rearfoot, or the
ankle [50]. The PTB works by using the knee as a weight bearing
structure to transfer weight in the foot to the knee. A removable cast
walker (RCW) is another common device to ofoad the foot (Fig. 6).
Removable cast walker has the advantage of allowing wound care to
a concomitant ulcer while providing immobilization to the injured
limb. RCW have been shown to reduce time of immobilization when
provided as an initial treatment [20].
5.2. Medical management
The medical management of CN has been evolving in the past
few years with emphasis on drugs that regulates osteoclastic activity. Historical, descriptive data demonstrated radiological osseous
changes radiographs [5153]. These changes include vascular calcications, fragmentations, dislocations, periarticular lytic lesions,
and sclerosis. Furthermore, osteopenia has been shown to be more
prevalent in patients with diabetic neuropathy and CN [34,5456].
Bisphosphonates have been proposed as a treatment for this entity
since they slow down osteoclastogenesis [35,57,58]. However, a
recent systematic review concluded that there is not enough evidence to support the use of these drugs in the management of CN

J. La Fontaine et al. / The Foot 26 (2016) 714

11

proposed ve reasons to take into consideration when operating

the CN foot. The ve reasons are:

Fig. 3. Total contact cast.

[59]. Other methods such as intranasal calcitonin, bone stimulation have been studied, however, randomized controlled trial are
still needed to be conducted [60].
5.3. Surgical management
The surgical treatment for CN has become popularized in the
recent years, although it was advocated in early 1990s. Eichenholtz

Unknown role of neuropathy in bone healing.

Compression is not indicated.
Similar Charcot process after a fracture of a long bone is observed.
Prolonged non-weight bearing is required.
Bone grafting indicated.

Outcomes from studies in 1980s, and early 1990s were short of

good outcomes. Often, subjects included in the studies had different stages of CN, different methods of xation joint involvement
at different locations in the foot or ankle, and inclusion of patients
with and without ulcerations. Also, the denition of success varies
among studies. Some investigators dened radiographic healing as
a successful outcome; meanwhile others described return to ambulation as a successful outcome. Tendo-Achilles lengthening (TAL) is
a common adjunctive procedure for the surgical management of
CN. High peak pressures in the forefoot may serve as a lever forcing the collapse of the midfoot [23]. Exostectomy or planning is
commonly used by surgeons to relieve pressure in areas at risk for
ulcerations especially in patient with long standing, rigid rockerbottom deformities. Exostectomy was rst described in 4 cases
by Leventen in 1986 [61]. Several case series has suggested good
outcomes for the stable, rigid chronic CN foot [5,62].
One of the principal controversies is the use of internal xation
or external xation.
Many surgeons have suggested internal xation as a technique
to prevent or correct severe deformities in the late stages of CN
[6366]. In general, all patients regained the level of walking ability and all procedures were successful. In the majority of these case
series, the staging of CN has not been dened clearly, no details on
unstable or xed deformities, and therefore, difcult to reach any
conclusion in what is the best surgical treatment. External xation
has become popular. The medical literature is compiled of mostly
review articles, expert opinions, and retrospective review [6770].
It is important to mention that studies, all case series, involving
surgical correction of CN often conclude that outcomes are successful even though, patients had complications such as repeat
surgeries, recurrent of ulcer, bracing, and stable nonunion. In any

Fig. 4. CROW.

12

J. La Fontaine et al. / The Foot 26 (2016) 714

Fig. 6. RCW.

Fig. 5. Patellar tendon brace.

other pathology studied in the lower extremity, same outcomes

would be considered as complications.
There is only one comparative study between surgical and
accommodative treatment. One hundred and ninety-eight patients
(201 feet) with CN were followed up to a 6-year period. One hundred and forty-seven feet had collapsed midfoot. The endpoint
for the study was time to return to extra depth shoe with custom inlays. At minimum 1 year follow-up, 87/147 (59.2%) had
plantigrade foot posture without surgery. Forty-two of 147 feet
with midfoot involvement required corrective surgery (40.8%)
[48]. Therefore, more than half of the limbs were managed successfully with accommodative measures. Combination of therapy
to ease the foot into weight bearing is a must for the successful treatment of CN. In a retrospective study, Fabrin and
colleagues followed 115 subjects (140 limbs) for a median of
48 months. All subjects were diabetic patients and maintained
a non-weight bearing status with protective shoes or crutches
until temperature were normal. One hundred and thirty-two
out of the 140 feet healed. However, late complications were
observed. Forty-seven percent of the subjects developed new onset
of CN or neuropathic ulcer [71]. Almost half of the population

developed late complications. It is possible that the method of

treatment utilized may not prevent the development of deformity
and provide no stability to the foot. A single treatment protocol has
been shown to be an effective treatment for CN. In a retrospective
study of 115 subjects (127 limbs), subjects were treated surgically or conservatively for CN. A comprehensive program included
immediate immobilization with casting, transfer to CROW, and
then to custom full-contact inserts. All types of CN deformities
were included. At median of 3.8 years, the limb survivorship was
90%. Thirty-six limbs (31%) that presented initially with ulceration
went into some type of amputation, compared to 6% of those without chronic ulceration. Eleven percent (15 limbs) went in to a below
knee amputation. Sixty-two limbs (49%) had ulcers recurrence. The
authors suggested that improved care for patients with CN is necessary [72]. A systematic review demonstrated that uncontrolled
retrospective case series and case reports guide the use of exostectomy, fusion, and Achilles tendon lengthening for CN, but there
is inconclusive evidence concerning timing of treatment and use
of different xation methods. The authors suggested that more
prospective series and randomized studies are necessary to support
and strengthen current practice [73]. Surgical management of CN
may lead to undesirable outcomes such as above the ankle amputations. Surgeons take upon CN surgical correction with the goal
of saving a functional limb. Self-reported outcomes of 13 patients
after transtibial amputations secondary to CN and osteomyelitis
were studied by Wukich and Pearson [74]. In this selected group
with CN patients and chronic osteomyelitis, trans-tibial amputation
resulted in improvement in self-reported outcomes.
6. Conclusion
The Charcot foot is an uncommon complication of neuropathy
in diabetes. It is a disabling and devastating condition. The etiology

J. La Fontaine et al. / The Foot 26 (2016) 714

of the CN is unknown, but it is characterized by acute inammation with collapse of the foot and/or the ankle. Although the
cause of this potentially debilitating condition is not known, it is
generally accepted that the components of neuropathy that lead
to foot complications must exist. When it is not detected early,
a severe deformity will result in a secondary ulceration, infection, and amputation. In the early stages, immobilization is the
key for success, but severe deformity may still develop. When
severe deformity is present, bracing may be attempted but often
the patients will need surgical intervention. According to expert
opinions, surgery should be delayed until the acute process has
been dissipated. Good success has been shown with internal and
external xation. Patients with concomitant osteomyelitis, severe
deformity, and and/or soft tissue infection, a high amputation may
be the best treatment of choice. The importance of aggressive cardiovascular management should not be underestimated. CN has
been signicantly associated with higher mortality risk than diabetes alone and with lower risk than foot ulcer [75]. In a study
by Young and colleagues demonstrated 5 year mortality reduction
from 485 to 26.8% when an aggressive management was instituted
on those patients with a rst incident of foot ulcer [76]. Thus, an
aggressive management of cardiovascular risk factors may need to
be also incorporated in patients CN.

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