2 ½ DAY
COURSE
2nd International Course on
The Neuropathic
Osteoarthropathic Foot (Charcot)
Advanced Postgraduate Course
Rheine, Germany · 3 -5 July 2014
General information
The course is supported by
Dates: 3-5 July 2014
Venue, Practical part:
Mathias-Spital, Interdisciplinary Diabetic Foot Centre, Rheine, Germany
Venue, Theoretical part:
Mathias-Spital, University of Applied Sciences, Rheine, Germany
Form:
Lectures combined with hands-on workshops / training in clinic
Language: English
More information: www.charcotfootcourses.org
Social events
The course offers participants and faculty members plenty of
opportunity to network and exchange knowledge during the social
events. During the course, the following social events are included:
3 July, 19:30: Welcome dinner, Restaurant Casa Gonzales
(located close to Hotel Lücke). Address: Tiefern Straße 28.
4 July, 20:00: Course dinner, Restaurant Gottesgabe
Address: Salinenstraße 101.
Bus from Hotel Lücke to the restaurant.
5 July, 15:00: Excursion to Münster and dinner
at 18:30 at Pinkus Müller (local brewery).
Train to Münster from Rheine train station at 15:29.
www.charcotfootcourses.org
Faculty
Nina Petrova, London, UK
Alberto Piaggesi, Pisa, Italy
Klaus Kirketerp-Møller, Copenhagen, Denmark
Stephan Morbach, Soest, Germany
Oleg Udovichenko, Moscow, Russia
Ludwig Schwering, Dubai, UAE
Ernst Chantelau, Bremen, Germany
Maximillian Spraul, Rheine, Germany
Armin Koller, Rheine, Germany
Herr Damer, Rheine, Germany
Raimund Fiedler, Rheine, Germany
Guido Schomacher, Rheine, Germany
Dirk-Theodor Schraeder, Rheine, Germany
Swetlana Schnar, Rheine, Germany
Martina Broer, Rheine, Germany
2
Scientific Responsibility:
Maximilian Spraul, Prof. Dr. med.
Armin Koller, Dr. med.
Mathias-Spital
Frankenburgstr. 31
48431 Rheine
Nordrhein-Westfalen
Germany
Contact Information:
Course Secretariat:
CAP Partner
Nordre Fasanvej 113, 2nd floor
2000 Frederiksberg C
Denmark
Tel: +45 70200305
[email protected]
Programme
THURSDAY 3 JULY
17:00-17:15 Welcome and outline of the course
Koller/Spraul
17:15-17:45 New findings in the Pathogenises of Charcot Osteoarthropathy
Petrova
17:45-19:00 Operative therapy of the active Charcot
Koller
19:30-21:30 Drinks and Welcome dinner, Restaurant Casa Gonzales
FRIDAY 4 JULY
09:00-09:30 Early diagnosis and conservative treatment of the Charcot Foot
Piaggesi
09:30-10:00 Is the Eichenholtz Classification still valid for the diabetic Charcot foot?
Chantelau
10:00-10:30 Principles of deformity correction with external fixation
Schwering
10:30-11:00 Coffee break
11:00-12:30 Practical Sessions 1:
A:Early diagnosis and conservative treatment (Case presentation)
Petrova/Piaggesi
B: Technical details for external fixation
Koller/Schwering
C:TCC (application of soft and rigid casts)
Schnar/Schomacher
12:30-13:30 Lunch
13:30-15:00 Practical Sessions 2:
A:Ward round with case discussions
Spraul/Fiedler
B: Clinical orthopedic foot examination
Schwering
C:Prosthetics and Orthotics in daily practice
Koller/Damer
15:00-15:30 Coffee break
15:30-17:00 Practical Sessions 3:
A:Handling of osteomyelitis in the Charcot Foot
Kirketerp-Møller/Koller
B: Ward round with case discussions
Spraul/Fiedler
C:Vacuum therapy in TCC
Broer/Schnar/Morbach
20:00-23:00 Course dinner, Restaurant Gottesgabe
SATURDAY 5 JULY
09:00-09:45 Rehabilitation and orthotic fitting
Koller
09:45-10:15 Update on relevant studies concerning the Charcot foot
Spraul
10:15-10:45 Coffee break
10:45-11:30 How to diagnose osteomyelitis in the Charcot foot
Kirketerp-Møller
11:30-12:00 The Charcot Foot in Russia
Udovichenko
12:00-13:00 Lunch
13:00-14:30 Practical Sessions 4:
A:Prosthetics and Orthotics in daily practice
Koller/Damer
B: Clinical orthopedic foot examination
Schwering
C:Conservative treatment and follow-up
Morbach/Piaggesi
14:30-15:00 Summary and farewell
15:00-18:00 Optional Excursion to Münster with informal discussions
18:00-21:00 Optional dinner in Münster
3
DIABETIC FOOT
& ANKLE
Diabetic Foot & Ankle is a peer-reviewed international Open Access journal
created as a forum for the dissemination of information on the latest advances pertinent
to diabetic foot and ankle pathology and its related areas of prevention, clinical care,
pathophysiology, epidemiology, and surgical and cardiovascular management.
The journal is essential to all educators, researchers, clinicians, and other health care
professionals engaged in patients with diabetes mellitus.
Editor-in-Chief: Thomas Zgonis, DPM, FACFAS, UT Health Science Center, San Antonio, Texas, United States
Join Diabetic Foot & Ankle on
All content freely available on www.DiabeticFootandAnkle.net
MEDICINE & HEALTH
S E R I E S
Design: [email protected]
Diabetic Foot & Ankle
Reviews/Commentaries/ADA Statements
C O N S E N S U S
R E P O R T
The Charcot Foot in Diabetes
LEE C. ROGERS, DPM1
ROBERT G. FRYKBERG, DPM, MPH2
DAVID G. ARMSTRONG, DPM, PHD3
ANDREW J.M. BOULTON, MD4
MICHAEL EDMONDS, MD5
GEORGES HA VAN, MD6
AGNES HARTEMANN, MD6
FRANCES GAME, MD7
WILLIAM JEFFCOATE, MD7
ALEXANDRA JIRKOVSKA, MD8
EDWARD JUDE, MD4
STEPHAN MORBACH, MD9
WILLIAM B. MORRISON, MD10
MICHAEL PINZUR, MD11
DARIO PITOCCO, MD12
LEE SANDERS, DPM13
DANE K. WUKICH, MD14
LUIGI UCCIOLI, MD15
The diabetic Charcot foot syndrome is a serious and potentially limb-threatening lower-extremity
complication of diabetes. First described in 1883, this enigmatic condition continues to challenge even the most experienced practitioners. Now considered an inflammatory syndrome, the
diabetic Charcot foot is characterized by varying degrees of bone and joint disorganization
secondary to underlying neuropathy, trauma, and perturbations of bone metabolism. An international task force of experts was convened by the American Diabetes Association and the
American Podiatric Medical Association in January 2011 to summarize available evidence on the
pathophysiology, natural history, presentations, and treatment recommendations for this entity.
Diabetes Care 34:2123–2129, 2011
T
he Charcot foot in diabetes poses
many clinical challenges in its diagnosis and management. Despite
the time that has passed since the first
publication on pedal osteoarthropathy in
1883, we have much to learn about the
pathophysiology, and little evidence exists on treatments of this disorder. The
international task force was convened in
January 2011 at the Salpêtrière Hospital
in Paris, France, to review the literature
and report on the definition, pathogenesis, diagnosis, and treatment of the diabetic Charcot foot. Recommendations in
this report are solely the opinions of the
authors and do not represent the official
positions of the American Diabetes Association or the American Podiatric Medical
Association.
DEFINITION—Charcot neuropathic
osteoarthropathy (CN), commonly referred to as the Charcot foot, is a condition affecting the bones, joints, and soft
tissues of the foot and ankle, characterized by inflammation in the earliest phase.
The Charcot foot has been documented to
occur as a consequence of various peripheral neuropathies; however, diabetic neuropathy has become the most common
etiology. The interaction of several component factors (diabetes, sensory-motor
neuropathy, autonomic neuropathy,
trauma, and metabolic abnormalities of
bone) results in an acute localized inflammatory condition that may lead to
varying degrees and patterns of bone
destruction, subluxation, dislocation,
and deformity. The hallmark deformity
c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c
From the 1Amputation Prevention Center at Valley Presbyterian Hospital, Los Angeles, California; the 2Carl T.
Hayden Veterans Affairs Medical Center, Phoenix, Arizona; the 3Southern Arizona Limb Salvage Alliance (SALSA), University of Arizona College of Medicine, Tucson, Arizona; the 4Department of Medicine,
University of Manchester, Manchester, U.K.; the 5Diabetic Foot Clinic, King’s College Hospital, London,
U.K.; the 6Diabetes and Metabolic Diseases Department, Pitié-Salpêtrière University Hospital, Paris, France;
the 7Department of Diabetes and Endocrinology, Nottingham University Hospitals NHS Trust, Nottingham,
U.K.; the 8Institute for Clinical and Experimental Medicine, Diabetes Centre, Prague, Czech Republic; the
9
Department of Diabetes and Angiology, Marienkrankenhaus, Soest, Germany; the 10Department of Radiology,
Thomas Jefferson University Hospital, Philadelphia, Pennsylvania; the 11Department of Orthopedic Surgery,
Loyola University Health System, Maywood, Illinois; the 12Diabetes Center and Foot Care Unit A, Gemelli
Hospital, Catholic University, Rome, Italy; the 13Podiatry Service, Veterans Affairs Medical Center, Lebanon,
Pennsylvania; the 14Department of Orthopedic Surgery, University of Pittsburgh Medical Center, Pittsburgh,
Pennsylvania; and the 15Department of Internal Medicine, University of Rome Tor Vergata, Rome, Italy.
Corresponding author: Lee C. Rogers, [email protected].
DOI: 10.2337/dc11-0844
This article is copublished in Diabetes Care and the Journal of the American Podiatric Medical Association, under
joint copyright.
© 2011 by the American Diabetes Association and the American Podiatric Medical Association. Readers may
use this article as long as the work is properly cited, the use is educational and not for profit, and the work is
not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
care.diabetesjournals.org
associated with this condition is midfoot
collapse, described as a “rocker-bottom”
foot (Fig. 1), although the condition appears in other joints and with other presentations. Pain or discomfort may be a
feature of this disorder at the active
(acute) stage, but the level of pain may
be significantly diminished when compared with individuals with normal sensation and equivalent degrees of injury.
The set of signs and symptoms that
occur together with CN qualifies this
condition as a syndrome, the “Charcot
foot syndrome.”
Definition and classification
recommendations
c Nomenclature should be standardized
to CN or the Charcot foot.
c Existing classifications do not provide
prognostic value or direct treatment.
Active or inactive should be used to
describe an inflamed or stable CN, respectively. Acute and chronic can also
be used in this regard, but there is
no accepted measure that defines the
transition point.
PATHOGENESIS—There is no singular cause for the development of the
Charcot foot, but there are factors that
predispose to its development, as well as
a number of likely precipitating events.
The current belief is that once the disease
is triggered in a susceptible individual,
it is mediated through a process of uncontrolled inflammation in the foot. This
inflammation leads to osteolysis and is
indirectly responsible for the progressive
fracture and dislocation that characterizes
its presentation (1). The evidence to support this hypothesis is largely circumstantial. A neurally mediated vascular reflex
leading to increased peripheral blood
flow and active bone resorption has
been proposed as an etiological factor in
the development of bone and joint destruction in neuropathic patients. However, the relationship between increased
blood flow to bone and active bone resorption has not been conclusively defined.
Uncontrolled inflammation
When a bone is fractured, the release of
proinflammatory cytokines including tumor
necrosis factor-a and interleukin-1b leads
to increased expression of the polypeptide receptor activator of nuclear factor-kB
DIABETES CARE, VOLUME 34, SEPTEMBER 2011
2123
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Consensus Report
Figure 1—The typical appearance of a laterstage Charcot foot with a rocker-bottom deformity.
ligand (RANKL) from any of a number of
local cell types. RANKL triggers the synthesis of the nuclear transcription factor
nuclear factor-kb (NF-kb), and this in
turn stimulates the maturation of osteoclasts from osteoclast precursor cells. At
the same time, NF-kb stimulates the production of the glycopeptide osteoprotegerin
(OPG) from osteoblasts. This “decoy receptor” acts as an effective antagonist of
RANKL (2). The fracture will also be associated with pain, and this leads to splinting
of the bone, and the rise in proinflammatory cytokines is usually relatively shortlived. In the person who develops an acute
Charcot foot, however, the loss of pain sensation allows for uninterrupted ambulation,
with repetitive trauma. It has been suggested that this results in continual production
of proinflammatory cytokines, RANKL,
NF-kb, and osteoclasts, which in turn
leads to continuing local osteolysis (1).
This has subsequently been shown by an
increase in proinflammatory phenotypes of
monocytes in those with active Charcot
foot when compared with diabetic control
subjects (3).
Osteoclasts generated in vitro in the
presence of macrophage colony-stimulating
factor and RANKL from patients with
active CN have been shown to be more
aggressive and exhibit an increase in their
resorptive activity compared with control
subjects. However, these changes are only
partially inhibited by OPG, indicating that
other cytokines may also be important (4).
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6
Predisposition
Neuropathy is a universal feature of the
affected limb. Although it has been suggested that people with a Charcot foot
may have particular patterns of sensory
loss reflecting involvement of different
fibers (5,6), this is not generally accepted.
Nevertheless, three groups have shown
that people who have had an acute Charcot foot exhibit retention of vasodilatory
reflexes in contrast to diabetic individuals
with distal symmetrical neuropathy without CN (7–9).
Despite these observations, it should
be noted that the syndrome might also
occur in patients with a spectrum of
unrelated diseases complicated by nerve
damage. These include distal neuropathies
caused by toxins (ethanol, drug related)
and infection (leprosy), as well as diseases
of the spinal cord and nerve roots (tabes
dorsalis, trauma, syringomyelia) and a
number of other conditions (Parkinson’s
disease, HIV, sarcoidosis, rheumatoid disease, and psoriasis). Although the neuroarthropathy is typically more proximal in
those with disease of the spinal cord, the
presentation may be otherwise indistinguishable.
Loss of protective sensation will increase the likelihood of trauma to the foot,
while motor neuropathy could result in
altered structure of the foot (with exaggeration of the plantar arch and clawing)
and changed gait with resultant abnormal
loading.
Finally, it is possible that peptides
normally secreted from nerve terminals
are also important in the underlying
pathophysiology. Of these, calcitonin
gene–related peptide (CGRP) is a likely
candidate because it is known to antagonize the synthesis of RANKL. Hence, any
reduction of CGRP through nerve damage
will result in an increase in RANKL expression. It is of particular interest that
CGRP has been reported to be necessary
for the maintenance of the normal integrity of joint capsules, and it follows that
any reduction in CGRP release by nerve
terminals could facilitate joint dislocation (10).
Because it is not possible to identify
those most likely to develop the Charcot
syndrome, it is impossible to determine
with any degree of confidence whether
preexisting osteopenia is a significant
predisposing factor. One group has, however, reported an apparent reduction in
bone mineral density (BMD) of the femoral neck in the contralateral (unaffected) limb at the time of presentation.
DIABETES CARE, VOLUME 34, SEPTEMBER 2011
The researchers also reported an association between BMD and the relative prevalence of fracture and of dislocation in the
affected foot (11).
Diabetes may be associated with osteopenia, but the available evidence suggests that reduction of BMD is a feature of
type 1 diabetes more so than type 2 diabetes (12). Any reduction of BMD in type
1 diabetes may relate to loss of islet peptides such as insulin and amylin (IAPP),
both of which act as growth factors for
bone. Despite this, the fracture risk in
type 2 diabetes may be no less than in
type 1 diabetes (12), and this would explain the fact that the presentation does
not appear to differ between the two types
of the disease. Any associated deficiency
of vitamin D—with or without renal failure
and secondary hyperparathyroidism—
would increase the possibility of reduced
BMD in diabetes. The use of thiazolidinediones could theoretically increase the likelihood of an acute Charcot foot through an
effect on bone density, but this has not yet
been reported. The use of corticosteroids
as immunosuppressants in people with diabetes who have had a renal and/or pancreatic transplant (13) may explain the
apparent high incidence of the Charcot
foot in this group.
Although the Charcot syndrome may
occur in a variety of conditions, diabetes
is ostensibly the most common worldwide. Diabetes may predispose to its
occurrence through a number of mechanisms. Apart from the presence of neuropathy and possible osteopenia, these
include the effects of advanced glycation
end products, reactive oxygen species,
and oxidized lipids, which may all enhance
the expression of RANKL in diabetes
(10). The effect of local inflammation
on this pathway would similarly compound the expression of RANKL. Furthermore, a single study has reported
an apparent association between two
OPG-related polymorphisms in people
with a history of an acute Charcot foot
in diabetes (14).
Many patients recall that the onset of
the condition was precipitated by trauma
that is often minor in nature (15). Other
cases may be triggered by different causes
of local inflammation, including previous
ulceration, infection, or recent foot surgery. In this respect the occurrence of an
acute Charcot foot as a complication of
osteomyelitis is increasingly recognized
in people with diabetes. Very occasionally, the onset of an acute Charcot foot
may follow successful revascularization.
care.diabetesjournals.org
Rogers and Associates
DIAGNOSIS—The initial manifestations of the Charcot foot are frequently
mild in nature, but can become much
more pronounced with unperceived repetitive trauma. Diagnostic clinical findings include components of neurological,
vascular, musculoskeletal, and radiographic abnormalities. There have been
no reported cases of CN developing in the
absence of neuropathy. Accordingly, peripheral sensory neuropathy associated
with reduced sensation of pain is the
essential predisposing condition that permits the development of the arthropathy
(16–19). Because of the very presence of
insensitivity, a personal history concerning antecedent trauma is often unreliable
(18,20,21). Typical clinical findings
include a markedly swollen, warm, and
often erythematous foot with only mild
to modest pain or discomfort (16,18–
20,22). Acute local inflammation is often
the earliest sign of underlying bone and
joint injury (23). This initial clinical picture
resembles cellulitis, deep vein thrombosis,
or acute gout and can be misdiagnosed as
such. There is most often a temperature
differential between the two feet of several
degrees (20,24). The affected population
typically has well preserved or even exaggerated arterial blood flow in the foot.
Pedal pulses are characteristically bounding unless obscured by concurrent
edema. Patients with chronic deformities,
however, can develop subsequent limbthreatening ischemia. Musculoskeletal
deformity can be very slight or grossly
evident most often due to the chronicity
of the problem and the anatomical site of
involvement (16,17,19,25). The classic
rocker-bottom foot, with or without
plantar ulceration, represents a severe
chronic deformity typical for this condition (16,26,27). Radiographic and other
imaging modalities can detect subtle
changes consistent with active CN.
Imaging of the Charcot foot
Radiographs are the primary initial imaging method for evaluation of the foot in
diabetic patients. Easily available and inexpensive, they provide information on
bone structure, alignment, and mineralization. X-rays may be normal or show
subtle fractures and dislocations or later
show more overt fractures and subluxations. In later stages, the calcaneal inclination angle is reduced and the talo-first
metatarsal angle is broken (Fig. 2). Medial calcification of the arteries is present
in most Charcot feet and is a frequent
secondary finding on radiographs (25).
care.diabetesjournals.org
However, radiographic changes of CN
are typically delayed and have low sensitivity (28).
Magnetic resonance imaging (MRI)
allows detection of subtle changes in the
early stages of active CN when X-rays
could still be normal. MRI primarily
images protons in fat and water and can
depict anatomy and pathology in both
soft tissue and bone in great detail. Because of its unique capability of differentiating tissues with high detail, MRI has a
high sensitivity and specificity for osteomyelitis and has become the test of choice
for evaluation of the complicated foot in
diabetic patients (29). Although not required for diagnosis when X-rays are diagnostic for Charcot bone and joint
changes, MRI is very useful in making the
diagnosis at its earliest onset before such
changes become evident on plain films.
Nuclear medicine includes a number
of exams based on the use of radioisotopic
tracers. Three-phase bone scans, based on
technetium-99m (99mTc), are highly sensitive for active bone pathology. However, diminished circulation can result
in false-negative exams and, perhaps
more importantly, uptake is not specific
for osteoarthropathy. Labeled white blood
cell scanning (using 111In or 99mTc) provides improved specificity for infection in
the setting of neuropathic bone changes
(30), but it can be difficult to differentiate
soft tissue from bone. Therefore, this exam
can be combined with a three-phase bone
scan or sulfur colloid marrow exam when
superimposed osteomyelitis is suspected
(31). More recently, positron emission tomography scanning has been recognized
as having potential for diagnosis of infection and differentiating the Charcot foot
from osteomyelitis (32,33). However,
this remains investigational at this time.
Evaluation of bone density may be
useful in those with diabetes to assess
onset of CN as well as fracture risk. BMD
can be assessed using dual-energy X-ray
absorptiometry or calcaneal ultrasound.
BMD has been related to the pathological
pattern of CN, whereby joint dislocation
is more prevalent in those with normal
mineralization versus fracture in those
with diminished BMD (11).
Experts agree that radiographs are
important as the first exam in virtually
all settings (33,34). However, a negative
result obviously should not offer any confidence regarding lack of disease. In a
patient with low clinical suspicion of
osteomyelitis and no sign of CN on radiographs, either three-phase bone scan or
Figure 2—Lateral X-ray of a Charcot foot
deformity showing a dislocation of the tarsometatarsal joint with break in the talo-first
metatarsal line (dashed lines) and a reduced
calcaneal inclination angle (solid lines).
noncontrast MRI is very effective at excluding osseous disease. If the patient
has an ulceration with a high likelihood
of deep infection, MRI is the best diagnostic modality. Nonetheless, one test may
not be adequate for full evaluation. In
this setting where MRI diagnosis is indeterminate, a subsequent labeled white
blood cell scan can provide more specificity and should be correlated with clinical findings. The decision of nuclear
imaging versus MRI is largely based on
personal preference, availability, and local
experience. In general, if metal is present
in the foot, nuclear medicine exams are
preferred, whereas diffuse or regional ischemia makes MRI the preferred exam.
Diagnostic recommendations for
active CN
c The diagnosis of active Charcot foot is
primarily based on history and clinical
findings but should be confirmed by
imaging.
c Inflammation plays a key role in the
pathophysiology of the Charcot foot
and is the earliest clinical finding.
c The occurrence of acute foot/ankle fractures or dislocations in neuropathic
individuals is considered active CN
because of the inflammatory process of
bone healing, even in the absence of
deformity.
c X-rays should be the initial imaging
performed, and one should look for
subtle fractures or subluxations if no
obvious pathology is visible.
c MRI or nuclear imaging can confirm
clinical suspicions in the presence of
normal-appearing radiographs.
MEDICAL TREATMENT—The medical treatment of CN is aimed at offloading the foot, treating bone disease, and
DIABETES CARE, VOLUME 34, SEPTEMBER 2011
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7
Consensus Report
preventing further foot fractures (34). Because of the various etiologies of increased
local bone resorption and/or secondary osteoporosis in patients with CN and limited
randomized placebo-controlled trials in
this area, treatment guidelines are largely
based on professional opinion rather than
the highest level of clinical evidence.
Offloading
Offloading at the acute active stage of the
Charcot foot is the most important management strategy and could arrest the
progression to deformity. Ideally, the
foot should be immobilized in an irremovable total contact cast (TCC), which is
initially replaced at 3 days, then checked
each week. Edema reduction is often
remarkable in the first few weeks of treatment. The cast should be changed frequently to avoid “pistoning” as the edema
subsides. If possible, the patient should
use crutches or wheelchair and should
be encouraged to avoid weight bearing
on the affected side. The casting is continued until the swelling has resolved and
the temperature of the affected foot is
within 2°C of the contralateral foot (35).
An alternative device for offloading the
acute active stage of CN is a prefabricated
removable walking cast or “instant TCC”
technique, which transforms a removable
cast walker to one that is less easily removed (36,37). It is important to take
into consideration that TCC may actually
have unfavorable consequences on the
non-Charcot limb and induce unnatural
stress patterns causing ulcerations and
even fractures. Furthermore, patients
with CN have increased instability and
risk for falling and fracture as a result
of multiple comorbidities including loss
of proprioception and postural hypotension. Nonetheless, it should be noted that
total immobility has disadvantages in itself
with a loss of muscle tone, reduction in
bone density, and loss of body fitness.
Duration and aggressiveness of offloading (nonweight bearing vs. weight
bearing, nonremovable vs. removable
device) are guided by clinical assessment
of healing of CN based on edema, erythema, and skin temperature changes
(34,35). Evidence of healing on X-rays
or MRI strengthens the clinical decision
to transition the patient into footwear.
To prevent recurrence or ulceration on
subsequent deformities, various devices
are recommended after an acute or active
episode has resolved, including prescriptive shoes, boots, or other weight-bearing
braces. Frequent monitoring is required.
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Antiresorptive therapy
Treatment by antiresorptive drugs has
been proposed because bone turnover in
patients with active CN is excessive.
However, there is little evidence to support their use, but both oral and intravenous bisphosphonates (38) have been
studied in the treatment of CN in small
randomized, double-blind, controlled
trials (39,40) or in retrospective controlled studies (41). Some patients cannot tolerate oral bisphosphonates but
may benefit from intravenous therapy using pamidronate or zoledronic acid (42).
Intranasal calcitonin is another antiresorptive agent that has been studied in CN.
This treatment was associated with a significantly greater reduction in crosslinked carboxy-terminal telopeptide of
type I collagen and bone-specific alkaline phosphatase than standard treatment
in the control group that received only
calcium supplementation and offloading.
Calcitonin has a safer profile in renal failure when compared with bisphosphonate
therapy (43–46). However, a single dose
of intravenous bisphosphonate generally
does not require renal adjustment. There
is no conclusive evidence for using bisphosphonates in active Charcot foot,
and our understanding is evolving as
more trials are currently underway.
Bone growth stimulation
There is limited evidence for the use of
external bone stimulation in CN. Ultrasonic bone stimulation was reported for
the treatment of CN of the ankle and for
the healing of fresh fractures. Direct current electrical bone growth stimulators
have been used specifically in CN patients
undergoing arthrodesis and clinically
tested to promote healing of fractures
in the acute phase of CN in small case
series. Although these findings are promising, there have been no subsequent
studies to validate this method, and its
use has been supported only as an adjunct therapy during the postsurgical
period (45–49).
Recommendations for medical
therapy
c Offloading the foot and immobilization
are the most important treatment recommendations in active CN and can
prevent further destruction.
c There is little evidence to guide the use
of available pharmacological therapies
to promote the healing of CN.
c Protective weight bearing is required
after an active episode, involving
DIABETES CARE, VOLUME 34, SEPTEMBER 2011
c
weight-bearing devices such as prescription shoes, boots, or braces.
Lifetime surveillance is advised to monitor for signs of recurrent or new CN
episodes as well as other diabetic foot
complications.
SURGICAL TREATMENT—Surgical treatment of Charcot arthropathy of
the foot and ankle is based primarily on
expert opinion. Surgery has generally
been advised for resecting infected bone
(osteomyelitis), removing bony prominences that could not be accommodated
with therapeutic footwear or custom
orthoses, or correcting deformities that
could not be successfully accommodated
with therapeutic footwear, custom anklefoot orthoses, or a Charcot Restraint Orthotic Walker (50). This clinical approach
is based on expert opinion and small, uncontrolled retrospective case series. There
has been an increasing trend in the literature to advise earlier surgical correction of
deformity and arthrodesis, based on the assumption that surgical stabilization would
lead to an improved patient-perceived
quality of life (51).
Several investigators have suggested
that Achilles tendon lengthening combined with total contact casting has the
potential to decrease the deforming forces
at the midfoot and decrease the morbidity
associated with CN (52–57). Exostectomy offers the potential to reduce pressure caused by bony prominences. This
treatment is often combined with accommodative bracing and appears to obtain
more favorable results in patients without
associated ulcers (58–60).
Surgery has generally been avoided
during the active inflammatory stage because of the perceived risk of wound infection or mechanical failure of fixation.
Two recent case series would suggest potentially favorable outcomes with early
correction of deformity combined with
arthrodesis (61,62). Most case series have
focused on reconstruction of the deformity
by reduction and arthrodesis using standard methods of internal fixation. Because
of the poor bone quality, expert opinion
has advised an extended period of nonweight bearing after surgery to account
for the poor bone healing and inherent
weakness of the underlying osseous structures. Early surgical series showed improvement in restoring a plantigrade foot
and preventing recurrence of ulceration, although nonunion, failure, and loss of initial
correction were common (63–67). The concept of an internal fixation “superconstruct”
care.diabetesjournals.org
Rogers and Associates
that extends internal fixation beyond the
zone of fusion has evolved to address these
issues (68). The combination of poor bone
quality and a tenuous soft tissue envelope
in a relatively immune-impaired population has led many surgeons to use a modification of the external fixation method
of Ilizarov to correct deformity with a
limited risk for surgical-associated morbidity (69–74).
Charcot arthropathy of the ankle
Given the common failures of nonsurgical
management of CN of the ankle, the task
force members agree that surgical management could be considered a primary
treatment. Surgical correction of deformity at the level of the ankle is likely more
necessary due to the poor tolerance of
deformity in the coronal plane (i.e., ankle
varus or valgus) and the resultant prominence of the malleoli and their vulnerability to pressure-induced ulceration.
Several small uncontrolled series have
recommended augmented internal fixation followed by prolonged periods of
immobilization and nonweight bearing in
neuropathic patients who sustain acute
ankle fractures (75–77). Acute ankle fractures in patients with complicated diabetes are associated with significantly higher
rates of noninfectious complications and
need for surgical revision when compared
with diabetic patients without other organ
system comorbidities (78). Numerous
techniques have been reported without
comparative effectiveness (79–82). All of
the surgical studies are retrospective in
nature without a control group and are
based on a limited number of patients.
While a strong, stable construct is required,
inconclusive data exist to recommend one
form of fixation over another (i.e., internal, external, or combined) in the surgical
reconstruction of the foot and ankle in patients who are not infected.
Recommendations for surgical
treatment
c Surgical treatment is beneficial in CN
cases refractory to offloading and immobilization or in the case of recalcitrant
ulcers.
c The initial management of acute neuropathic fractures and dislocations should
not differ from other fractures.
c Exostectomy is useful to relieve bony
pressure that cannot be accommodated
with orthotic and prosthetic means.
c Lengthening of the Achilles tendon or
gastrocnemius tendon reduces forefoot
pressure and improves the alignment of
care.diabetesjournals.org
Figure 3—An algorithm depicting the basic approach to the Charcot foot. *Osteomyelitis can be
difficult to distinguish from the Charcot foot. The reader is referred to the “Imaging of the Charcot
foot” section of the article for techniques to improve specificity of various imaging modalities.
c
c
the ankle and hindfoot to the midfoot
and forefoot.
Arthrodesis can be useful in patients
with instability, pain, or recurrent ulcerations that fail nonoperative treatment, despite a high rate of incomplete
bony union.
For severe CN of the ankle, surgical
management could be considered a
primary treatment.
CONCLUSIONS—The Charcot foot
syndrome is a complex complication of
diabetes and neuropathy. Its destructive
effects on the foot and ankle begin with a
cycle of uncontrolled inflammation. The
classic rocker-bottom foot deformity is a
late stage of the syndrome and can be
avoided by early recognition and management. Offloading is the most important initial treatment recommendation.
Surgery can be helpful in early stages
involving acute fractures of the foot or
ankle or in later stages when offloading is
ineffective. An algorithm summarizing
the approach to the Charcot foot can be
seen in Fig. 3.
Acknowledgments—The American Diabetes
Association/American Podiatric Medical Association Task Force meeting was supported
by unrestricted educational grants from Small
Bone Innovations, sanofi-aventis, and Integra
LifeSciences. No other potential conflicts of
interest relevant to this article were reported.
The authors thank Cécile Swiatek, chief
librarian, from the J.-M. Charcot library at the
Hospital Pitié-Salpêtrière for her assistance
with the site preparation for the task force and
references in this article.
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PERSPECTIVES
German-Austrian consensus on
operative treatment of Charcot
neuroarthropathy: a Perspective by the
Charcot task force of the German
Association for Foot Surgery
Armin Koller, MD1*, Ralph Springfeld, MD2,
Gerald Engels, MD3, Raimund Fiedler, MD1,
Ernst Orthner, MD4, Stefan Schrinner, MD5 and
Alexander Sikorski, MD6
1
Department of Technical Orthopaedics, Mathias-Hospital, Rheine, Germany; 2Clinic Dr. Guth, Hamburg,
Germany; 3Surgical Group Practice, Cologne, Germany; 4Foot Center Althofen, Austria; 5Nuremberg
Hospital, Germany; 6Malteser Foot Center, Rheinbach, Germany
Accepted: 3 October 2011; Published: 9 November 2011
number of published guidelines exist on the
diabetic foot, yet the sections on Charcot neuroarthropathy (CN) focus mainly on diagnosis
and conservative therapy. Surgical aspects, if ever present,
are addressed very briefly and are very limited on surgical
information and guidelines (1). For this reason, a group
of German and Austrian foot surgeons who are well
acquainted with the operative treatment of CN established a consensus statement despite a plethora of
existing diverging opinions. The following proposal is
far from scientific evidence, but may be the basis for an
ongoing discussion and further research opportunity.
A
Etiology of Charcot neuroarthropathy
Charcot neuroarthropathy is characterized by a predominantly painless destruction of pedal bones and joints in
which the etiology is not entirely understood. A complex
compound of neuropathy, repeated trauma, hypervascularization, and molecular-biological alterations of bone
metabolism may result in dramatic deterioration of the
foot skeleton. A distal symmetric polyneuropathy (PNP)
is conditio sine qua non for the development of neuroarthropathy. Diabetes mellitus is the most frequent underlying disease, yet sequelae of long-term alcohol abuse or
idiopathic cases should not be overlooked. Perhaps 80%
of all patients suffering from PNP have long-standing
diabetes mellitus. An additive effect of diabetic metabolism and alcohol or nicotine as neurotoxins has not yet
been examined. Ischemic or idiopathic PNP are prevalent
in a small percentage of patients.
Neuropathy may affect different efferent and afferent
nerve fibers; first, sensory neuropathy interfering with the
receptor-activated nuclear factor kappa-ligand/osteoprotegerin (RANK-L/OPG) system as a possible explanation
for an unleashed inflammatory response to a minor
trauma or repetitive stress (2). Secondly, autonomic
neuropathy with dysfunctional vascular control and
opened arteriovenous shunts as a possible reason for
local osteoporosis and lastly, motor neuropathy with
paresis of intrinsic foot musculature and consequent
development of foot deformity (claw toes, high arched
foot) as a reason for increased static and dynamic
loading.
The diabetic foot syndrome comprises three clinical
subgroups: peripheral vascular disease (PVD) in 25%,
PNP in 25%, and a combination of PVD and PNP in 50%.
CN, where PNP is always present (although not always
noticeable on clinical examination), has an estimated
incidence of 7% per year among diabetics with PNP, as
recently published by a major German health insurer on
the basis of data collected in 2007. In the German
situation, this translates to about 5,000 cases emerging
every year (3). Stuck et al. (4) reported an annual
incidence of 1.2% in a cohort of diabetics with increasing
incidence of CN in the presence of PNP or obesity.
Coexistence of PVD may occur with long-standing CN
Diabetic Foot & Ankle 2011. # 2011 Armin Koller et al. This is an Open Access article distributed under the terms of the Creative Commons AttributionNoncommercial 3.0 Unported License (http://creativecommons.org/licenses/by-nc/3.0/), permitting all non-commercial use, distribution, and reproduction
in any medium, provided the original work is properly cited.
Citation: Diabetic Foot & Ankle 2011, 2: 10207 - DOI: 10.3402/dfa.v2i0.10207
1
(page number not for citation purpose)
13
Armin Koller et al.
in up to 30% of cases. Nevertheless, the low incidence of
CN in the general population is comparable to malignancies and makes the high frequency of misdiagnosis
understandable. Sohn reported a 5-year mortality rate of
28.3% among patients with CN (5).
Classification of Charcot neuroarthropathy
Charcot neuroarthropathy is classified based on the
topography of affected joints, course of the disease, and
patterns of destruction. In this consensus, localization is
classified according to the Sanders system (6). The
simplicity and practicality of this system implies its
limitations, when more than one joint line is involved
or when the topographic pattern deviates from anatomical lines (e.g. Lisfranc, Chopart). The Sanders classification system does not allow for deduction of a specific
operative procedure based on a given radiological CN
pattern.
Another important classification was established by
Eichenholtz in 1966 describing destruction as well as
repair of joints and bone in the course of time (7). This
clinical and radiographic staging system has been well
accepted internationally, delineating three distinct stages:
(1) destruction, (2) resolution, and (3) coalescence.
A prodromal Stage 0 could represent a sensible modification in cases of bone bruise apparent on magnetic
resonance imaging (MRI) without manifest changes on
plain film radiographs. The denomination ‘Stage 0’ might
underestimate a serious problem; therefore, another
proposal is to subdivide Stage 1 into ‘1a’ with clinical
signs of inflammation and bone bruise on MRI plus ‘1b’
with additional osseous destruction visible on conventional radiographs.
Ulcers often accompanying CN are best classified
using the University of Texas Wound Classification
System that describes ulcer depth and the presence of
inflammation, ischemia, and/or PNP (8). Risk of amputation correlates well with the more severe stages (3D).
Category E should be introduced in case of dialysis, as
practical experience shows a high failure rate of conservative ulcer treatment when end stage renal disease is
present. An ulcerated CN foot should be characterized by
means of Sanders, Eichenholtz, and the University of
Texas Wound Classification System.
Diagnosis of Charcot neuroarthropathy
Combination of medical history, clinical examination,
and conventional radiography (anteroposterior, lateral,
and mortise views) is sufficient for making the diagnosis
of CN. Affected bones and the extent of bone bruise can
be identified precisely with the help of MRI. Any
suspicion of Eichenholtz Stage 0 or 1a, respectively,
must include MRI or scintigraphy in addition to plain
film radiographs. Clinical significance of bone bruise as
incidental findings in patients with diabetic PNP remains
2
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14
unclear, in particular with regard to potential development of CN. Uncertainty also exists in terms of estimating safe loading capacity of Charcot feet with the help of
MRI, as many of those feet with destructed joints will
retain a life-long inflammatory activity due to degenerative changes. Last but not the least, distinction between
CN and osteomyelitis remains difficult on the basis of
radiological examination alone.
Specimen for microbiological testing should be taken
from deep tissue, preferably from bone and through
intact, non-contaminated skin under sterile conditions.
Laboratory testing does not always facilitate a distinction
between acute CN and osteomyelitis or abscess formation, as on the one hand acute CN is often accompanied
by leukocytosis and elevated C-reactive protein. On the
other hand, osteomyelitis may demonstrate only vague
signs of inflammation due to ischemia or immunodeficiency (HbA1c 11%).
As a complex correction of a deformed Charcot foot
may turn into a catastrophe in the presence of relevant
ischemia, the absence of palpable pulses must imply
vascular examination ranging from Doppler sonography
to invasive arteriography.
Therapy of Charcot neuroarthropathy
principles
basic
Therapy of CN is often conservative. A deformed but
plantigrade foot capable of full weight bearing in a shoe
or orthosis and without increase of deformity is not a
candidate for surgery. There are a variety of devices
available for conservative treatment. Each device, such as
total contact cast (TCC), prefabricated walker, Charcot
Restraint Orthotic Walker (CROW), or individual ankle
foot orthosis (AFO), has a different risk-benefit profile
and has to be selected by the treating physician. Injuries
due to ill-fitting orthoses or shoes may create an immense
medical and financial burden.
An acute Charcot foot may call for in-patient treatment
or off-loading by means of a wheelchair over a period of
68 weeks. After decrease in the acute inflammatory stage,
total weight relief may be replaced by orthotic treatment
with particular emphasis on rigid three-dimensional
fixation of the foot and lower leg including elimination
of tibial rotation. Physical load is gradually increased
according to clinical parameters monitoring swelling,
redness, and sensible heat. Resumption of walking as
soon as possible protects against loss of bone mineral
density, thereby reducing cadence and walking speed when
using the orthosis. Partial weight bearing is not feasible in
the presence of PNP. Thus, guidance of weight bearing
takes place by limitation of walking time and speed.
Knowledge on the field of rehabilitation with shoes and
orthoses is extremely helpful.
Citation: Diabetic Foot & Ankle 2011, 2: 10207 - DOI: 10.3402/dfa.v2i0.10207
German-Austrian consensus on operative treatment of Charcot neuroarthropathy
Principles of operative treatment of Charcot feet
Operative therapy of Charcot feet
Closed reduction and retention by means of casting is
ineffective in cases of acute CN with joint dislocation and
significant instability. This subtype of CN can only be
managed by open reduction with internal or external
fixation (ORIF or OREF).
From a biomechanical point of view, the two-column
model of the foot has to be taken into account. Fusion of
the lateral column should be considered, even if the
problem is confined to the medial column only. As soon
as conservative treatment signals an unfavorable outcome, reconstructive surgery should take place without
waiting for Eichenholtz Stage 3, where deformity has
become fixed and rigid. Ulcers are not necessarily an
obstacle to surgery. An infected ulcer, however, should be
treated first with debridement, moist dressings, and
antibiotics. Bony prominences with high risk of ulcer
occurrence or reoccurrence should be excised, preferably
via a direct surgical approach or from the lateral or
medial foot border. Vast soft tissue defects are treated in
the scope of plastic surgery. Infected Charcot feet are the
worst case scenario. To be precise, treatment is no longer
targeted to neuroarthropathy but has to follow the rules
of septic surgery. Even amputations or wide internal
resections may be necessary.
The aim of surgery is to correct deformities in all three
planes. The frontal and transverse planes are more
important than the sagittal plane. Mild equinus position
of the foot may even be useful to correct for a shortened
limb due to loss of bone stock. On the other hand, CN of
the tarsal bones may be in part a result of a shortened
Achilles tendon. In this case and in the presence of a
mobile ankle joint, tendoachilles lengthening (TAL)
should be considered. Adequate technique, for example
intramuscular lengthening, is important to avoid calcaneal foot position with the risk of heel ulcers. Preferably,
osseous corrections are performed in a subtractive rather
than in an additive fashion. Allogenic cancellous bone or
synthetic bone substitutes cannot be recommended without reservation, although use of autologous graft is not
stringently required.
To avoid disuse osteoporosis, total off-loading should
be reduced to an unavoidable duration of 68 weeks. The
use of circular frames may even permit early weight
bearing with the appliance. Bone fusion can be evaluated
by computed tomography or conventional radiographs.
After internal fixation or after removal of an external
fixation device, the foot has to be protected from bending
and torque forces by means of an AFO that is generally
worn over a period of 36 months. The device is designed
for rigid fixation of the foot and full weight bearing, as
patients with PNP cannot practice partial weight bearing.
Eichenholtz’s or Sanders’ classification does not enable a
clear association of deformity patterns and operative
techniques. Nevertheless, the Sanders classification is
very common, therefore it is used for the following
overview.
Citation: Diabetic Foot & Ankle 2011, 2: 10207 - DOI: 10.3402/dfa.v2i0.10207
Sanders I
Type I affects the metatarsophalangeal (MTP) and the
interphalangeal joints. The natural course of this type is
different from the other four. The percentage of patients
with PVD is significantly higher, whereas body mass
index is not so much elevated. When the MTP joints are
involved, bone changes are predominantly resorptive
leading to the so-called candy stick deformity of the
metatarsals. Reconstructive surgery in these cases is
rarely indicated. Dislocation of the first MTP joint may
require repositioning and fusion. For the most part,
resections of bone in this type are performed due to
severe destructions or superimposed infections.
Sanders II
Type II frequently affects the tarsometatarsal articulations (Lisfranc). A rather common variation is perinavicular involvement, and sometimes the neuroarthropathic changes are restricted to the medial or the lateral
column. Diverging dislocations are seen as well as
deviations of all metatarsals to the medial or lateral
side. A frequent pattern of deformity with this type of
CN is forefoot abduction together with a flattened medial
arch and heel valgus. In case of Eichenholtz Stage 3 and
stable tarsal joints, realignment is possible by means of
two- or three-dimensional wedge resection. Pure medial
fusion may be indicated if the lateral column is spared.
Repositioning and achievement of stable fusion may be
technically demanding in case of dislocation of all five
metatarsals in all directions. Another common pattern is
naviculo-cuneiform dislocation with plantar flexion of
the talus with the navicular and dorsal dislocation of the
first metatarsal with the medial cuneiform. Unresisted
pull of the anterior tibial muscle may lead to progressive
fragmentation and displacement making conservative
treatment even under strict non-weight bearing conditions ineffective, so that early operative intervention may
be indicated to restore stability of the medial column.
Disagreement exists with respect to the optimal method
of fixation, be it a frame, internal osteosynthesis, or a
combination of both. There is a consensus that a
particular stable fixation is necessary just as for Charcot
surgery in general and different from traditional trauma
surgery. As any operation in case of Eichenholtz Stage 3
may lead to an acute exacerbation of neuroarthropathy,
postoperative immobilization is obligatory by means of a
cast or an AFO over a period of several months.
3
(page number not for citation purpose)
15
Armin Koller et al.
Sanders III
By definition, Stage III involves the midtarsal (Chopart)
joint line. Presentation in combination with type II is
quite common. A typical deformity pattern for isolated
type III is a rocker bottom foot with the cuboid being the
lowest lying part of the foot skeleton. As the talonavicular joint holds a key role for biomechanics, coupling
the movements of foot and lower leg, exact reduction and
fixation are challenging as much as essential. Even if the
talonavicular joint shows the most evident extent of
dislocation, reduction and fusion of this joint alone is
hardly ever sufficient. At the very least, inclusion of the
subtalar joint is advisable to minimize rotational forces
acting on the talus. In cases of doubt, triple arthrodesis is
a guarantor for successful stabilization. Length compensation between medial and lateral column requires
subtractive arthrodeses.
Sanders IV
In Sanders IV, the ankle joint and subtalar joint are
impaired. Frontal plane deformities in the region of the
hindfoot are hard to manage conservatively, particularly
in cases of instability. Surgery aims at solid ankle fusion
with broad contact area. Talectomy may be a valuable
option in the event of an extensive and rigid deformity to
overcome soft tissue contracture. Tibio-calcaneal arthrodesis requires a months-long duration of orthotic
after treatment with axial loading of the hindfoot. In
terms of functionality, stable fibrous ankylosis is not
necessarily inferior to complete bony fusion, as PNP
allows pain-free walking in custom-made shoes.
Sanders V
Sanders V involves the calcaneus and constitutes the
rarest type of CN. As long as the deformity is stagnant,
conservative therapy is favorable, in particular in case of
poor calcaneal bone quality with no support for screws or
pins. If fragment distance of a calcaneal fracture is
increasing due to pull of the Achilles tendon, treatment
in a CROW or an AFO is ineffective or leads to a marked
deformity. Again, surgery can be performed with a frame
or with internal osteosynthesis, in particular with an
intramedullary nail. If a nail has caused complications
like septic or aseptic loosening with or without fracture,
revision surgery can be done with external fixation. In
case of impaired skeletal anchorage due to loss of bone
4
(page number not for citation purpose)
16
substance, external fixation surgery may be considered as
the primary treatment option.
Conclusion
This perspective is not a scientific review, nor the least
common denominator within a group of diabetic foot
surgeons. It is an attempt to develop a future-oriented
consensus based on existing scientific literature as well as
personal experience. As additional studies continue to
expand the knowledge available for operative treatment
of CN and its outcomes, more definitive evidence-based
recommendations may be established.
Conflict of interest and funding
The authors have not received any funding or benefits
from industry to conduct this study.
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Diabetic Foot (2007) Prepared by the International Working
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2. Jeffcoate WJ, Game F, Cavanagh PR. The role of proinflammatory cytokines in the cause of neuropathic osteoarthropathy
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3. Chantelau E, ed. Diabetic feet and their shoe supply [in German].
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4. Stuck RM, Sohn MW, Budiman-Mak E, Lee TA, Weiss KB.
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E. Mortality risk of Charcot arthropathy compared with that of
diabetic foot ulcer and that of diabetes alone. Diab Care 2009; 32:
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6. Sanders LJ, Frykberg R. Diabetic neuropathic osteoarthropathy:
the Charcot foot. In: Frykberg RG, ed. The high risk foot in
diabetes mellitus. New York, NY: Churchill Livingstone; 1993,
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*Armin Koller
Department of Technical Orthopaedics Mathias-Hospital
Rheine, Germany
Email: [email protected]
Citation: Diabetic Foot & Ankle 2011, 2: 10207 - DOI: 10.3402/dfa.v2i0.10207
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