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17 Charcot Foot Syndrome: Aetiology andDiagnosis
219
mal artery disease were associated with decreased
likelihood of the Charcot syndrome [36].
It is recognised that there are changes in distal
limb blood ow associated with diabetic neuropathy [37, 38] and these are associated with alterations of distal capillary function [39]. The
distribution of blood to the periphery—and the
integrity of its normal regulation—is thus dependent on multiple processes in people with diabetes including cardiac function (including the
effect of any medications on pulse and blood
pressure), patency of larger arteries, changes in
peripheral vascular resistance, effective constriction and relaxation of smaller vessels and changes
in capillary and extravascular structure and
function.
Other Predisposing Factors inDiabetes
While the clinical presentation of the Charcot
syndrome may be broadly similar in all underlying pathologies, there are particular features of
diabetes that may make it more likely.
Skeletal Fragility inDiabetes
It is known that both type 1 and type 2 diabetes
are associated with increased risk of fracture
[40].
Chronic Renal Failure
Chronic renal failure may predispose to the
development of the syndrome because of the
osteopenia it causes.
Simultaneous Pancreas-Kidney Transplant
(SPKT) inType 1 Diabetes
The incidence of active Charcot syndrome is very
high in the months following transplantation:
affecting between 5% and 15% within a year or
two in recent published series [41–44]. The cause
is likely to be multifactorial. Both neuropathy
and renal osteodystrophy are very likely in the
treated population, while those with overt macrovascular disease will have been excluded prior to
transplantation. It is also possible that posttransplant Charcot syndrome was particularly
common when higher doses of glucocorticoid
immunosuppression were used and that the incidence is now falling—even though it remains far
higher than in any other at risk group. Of interest
is the observation by Valabhji [45] that the use of
immunosuppressants may modify the clinical
presentation.
Obesity
It is commonly thought that increased body mass
index (BMI) predisposes to the onset of the syndrome in diabetes [9] but the evidence is not
strong and it is possible that it is the difculties
posed by obesity in the management of particular
individuals that encourages the belief in clinical
practice. There is one small study that which
found no difference in BMI between matched
groups with and without Charcot syndrome [46].
Genetic Predisposition
A small number of groups have reported associations with differing candidate genes but the evidence is not currently strong [47–49].
Aetiology: Permissive Factors
The frequency with which neuropathy complicates diabetes contrasts with the relative rarity of
the Charcot syndrome, with available data suggesting it might affect between 0.1 and 1.0 people per thousand with diabetes [50]. This indicates
that while the presence of one or more components of nerve dysfunction is essential, the syndrome will not occur without one or more key
permissive factors.
Of these, it is likely that the most important
factor required for the expression of the syndrome is the capacity to mount an adequate
inammatory response by increasing blood ow
to the affected area. One piece of evidence in tangential support is provided by the occasional
reports of the syndrome being triggered by revascularisation of a major proximal artery [51].
More important evidence is provided by the
observations made by two groups that people
who have had an episode of active Charcot foot
can be distinguished from other people with neuropathy by the fact that they have been shown to
retain patterns of pedal blood ow and they retain
the capacity for it to increase [52, 53].
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W. Jecoate and F. Game
Aetiology: Precipitation
What Triggers theOnset
ofInammation at theTime That
theCharcot Process Becomes Active?
While affected individuals may have underlying
predisposition arising from any of the above processes, it seems that the onset of the active
Charcot syndrome is usually triggered by an
external event and by trauma in particular—even
though the severity of the trauma may often have
been thought to be trivial at the time it occurred.
Other important triggers are foot ulceration,
infection, surgery to the foot [11, 12] but in many
cases there is no identied precipitant.
Once triggered, the capacity to mount an
exaggerated and persistent inammatory reaction may be limited to those who produce a more
intense response of pro-inammatory cytokines
such as TNF-alpha, IL-1beta and IL-6 [54, 55] or
there may be an inadequate capacity to terminate
an inammatory response that has already
occurred.
Aetiology: Presentation
suggested the involvement of a pathway other
than that of RANKL and OPG.There is a possibility that this pathway is that centred on the
Wnt/β- catenin pathway for which Folestad has
since provided independent evidence [58]. High
levels of Wnt ligand prevent the breakdown of
catenin which in turn promotes osteoblast maturation and therefore bone formation. Low levels
therefore would be consistent with bone breakdown. Folestad and colleagues have also conrmed the involvement of TNF-alpha in active
Charcot foot, as well as IL-Iβ, IL-6 and other
interleukins [59, 60].
Eects ofClinically Overt Inammation
onBone
Worsening inammation is associated with
increased osteocytic osteolysis with increased
bone fragility. In this respect it is worth reecting
that osteolysis is normally a prelude to new bone
formation and is a key component of the early
phase of a protective response to skeletal injury.
The exaggerated osteolysis of the Charcot syndrome must occur only in those in whom the
capacity for auto-regulation is defective.
The onset of an active Charcot foot is marked by
overt clinical inammation. This will result from
increasing activation of pro-inammatory cytokine pathways and is most likely to be centred on
the RANKL/OPG/NFKappaB pathway or, alternatively, the Wnt/β-catenin pathway. The resultant clinical inammation will only occur if the
local microvasculature is capable of responding
with the necessary vasodilatation and hence is
restricted it to a small minority.
Changes inPro-inammatory Cytokine
Expression When theCharcot Foot
Syndrome Is Active
Active Charcot is associated with increased osteolysis. Baumhauer et al. [56] demonstrated
increased expression of the pro-inammatory
cytokines IL-1, IL-6 and TNF-alpha in histological specimens. Mabilleau [57] conrmed these
observations in a follow-up study, which also
Aetiology: Perpetuation
Once the process is triggered, the person who is
already predisposed to an exaggerated inammatory reaction then enters a phase whereby
the inammation further worsens bone fragility
and capsular laxity with the increasing risk of
skeletal damage which is itself made more
likely by loss of protective sensation and continued weight- bearing [61]. The bone of people
with active Charcot syndrome shows inammatory inltration with reduced quality of the trabeculae [62].
The process will eventually prove self- limiting
and the foot will stabilise once the inammation
settles—provided that irreversible skeletal damage does not lead to limb loss. Expert teams manage the condition by minimising trauma by
ensuring effective off-loading as well as management of complications (including secondary
17 Charcot Foot Syndrome: Aetiology andDiagnosis
221
deformity, ulceration and infection). Currently,
there is no effective systemic therapy to either
prevent or reduce the causative processes or to
minimise their effects.
Studies ontheExpression ofProinammatory Cytokines During
theCourse ofActive Charcot Syndrome
Folestad etal. [58–60] conducted a detailed analysis of changes in the expression of circulating
cytokines in samples collected from 24 to 28
people following the introduction of off-loading
for active Charcot syndrome. They were able to
demonstrate that changes in the expression of
IL-6, IL-8, IL-1β and TNF-alpha were all lower
than in controls at the time of presentation with
active disease but that IL-6 and TNF-alpha rose
slowly and steadily after the introduction of offloading—suggesting an increased in bone lysis
as a prelude to remodelling [58]. In contrast, the
concentrations of IL-17A and IL-17E were no
different from controls at presentation and then
rose slowly over 2–4 months, while those of
IL-17F were low at presentation and rose during
follow-up to be no different from controls [59].
Finally, they observed that sclerostin, Dkk-1 and
Wnt-1 were all low at presentation and rose over
2years of follow-up and, while concentrations of
OPG and RANKL were higher than controls at
presentation and fell during follow-up, the ratio
of OPG/RANKL did not change [60]. Current
knowledge of the detailed interaction of the measured substances is insufcient to allow detailed
interpretation to explain these fascinating
observations.
Resolution
It is common clinical practice to accept a difference in the temperature of the skin over the area
of interest of <2°C when compared with the noninvolved foot as sign of clinical resolution
although the data to support this is poor.
Magnetic resonance imaging (MRI), repeated
X-rays, repeated bone scans and infrared thermometry have been used to evaluate remission
but the lack of validated protocols, standardisation of equipment and high quality studies mean
that uncertainty remains about the effectiveness
for any [19].
Prognosis
Recurrence
As noted above, some 20% of individuals with
Charcot foot syndrome complicating diabetes
will have or will develop similar changes on the
contralateral foot before, during or after the index
presentation. Long term relapse is, however, very
rare and this is most likely because the factors
that predisposed to or permitted the original
attack no longer exist.
Mortality
In one single centre series of 117 cases in the UK,
survival was shown to be reduced to a median
7.9years with a reduction in overall life expectancy of 14.4years. This reduction in life expectancy was not, however, signicantly different
from a matched control sample managed for neuropathic foot ulcer and hence is not related to the
Charcot syndrome per se [63] but more to the
population which is at risk of it.
Footnote
Why Is theCharcot Syndrome
SoUncommon?
Given that distal neuropathy is currently thought
to affect between a third and a half and of all
people with diabetes, it is very remarkable that a
syndrome that is thought to be primarily the consequence of neuropathy is so rare. It may be that
the primary cause is some particular facet of neuropathy which is itself rare or, as suggested here,
that the condition only occurs when a variety of
predisposing and potentiating factors co-exist
and that such co-existence is uncommon.
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W. Jecoate and F. Game
Diagnosis ofActive Disease
Diagnosis ofActive Disease: Clinical
If a health care professional is asked over the
phone about a patient who has developed unexplained warmth and swelling of the midfoot, his
or her rst thought should be to ask two questions: has the person got diabetes and have they
got distal neuropathy? If the answer to either is
Yes, then active Charcot syndrome must be considered. Early suspicion is essential—not least to
minimise weight-bearing until it has been
excluded. The single most important stage in the
diagnosis of the Charcot foot is to think of it.
Most people do not think of it as a possibility
because they believe it is rare and that they are
unlikely ever to see a case. The Charcot syndrome is uncommon but it is not rare.
Diagnosis ofActive Disease:
Investigations
Imaging
Once the diagnosis of Charcot syndrome is considered, a plain X-ray should be done immediately and the result reviewed. The foot must be
protected by off-loading until a diagnosis is
made. Signs that may be seen on a plain lm
include osteopenia and osteolysis, associated
fragmentation of subchondral bone, fractures,
dislocations, subluxations and later bony consolidation [64]. Subtle dislocations, joint deformity
and collapse may be better visualised on weightbearing views. The sensitivity of plain X-ray to
exclude acute Charcot is not good even on
weight-bearing lms particularly in the early
stages [65].
More advanced imaging techniques have been
proposed including MRI, radiolabelled bone
scans and more recently 18F-uorodeoxyglucose
positron emission tomography (FDG-PET). MRI
is noninvasive and has much better sensitivity for
the detection of early stage acute active Charcot
[66] with reported sensitivities of (77–100%) and
specicities (80–100%) for the diagnosis [67].
However, the main limitation of MRI lies in its
inability to distinguish bone oedema caused by
infection (osteomyelitis) from active Charcot,
particularly if the two co-exist. A recent retrospective review suggests that if bone infection is
suspected in addition, then white blood cell
(WBC) scintigraphy had a higher accuracy for
the detection of osteomyelitis as long as standardised protocols are used [13] and so may be
useful where there is clinical doubt. Other tests
involving radiolabelled isotopes such as triple
phase bone scans have good sensitivity but lack
the specicity of MRI scans for early diagnosis
[67]. 18F-uorodeoxyglucose positron emission
tomography (FDG-PET) scanning may be useful
for differentiating acute Charcot from osteomyelitis [64] but a recent large series suggests that it
lacks the accuracy of WBC scintigraphy and so it
is not currently recommended [13].
Other Investigations
There are no other investigations that are useful
for the positive diagnosis of active Charcot,
unless the intention is to look for other causes of
inammation. While changes in inammatory
cytokines have been described above, none is
specic to active Charcot and will be raised in
almost any cause of inammation, whether this
be infective or metabolic, as in acute gout, for
example.
Diagnosis ofActive Disease:
Education ofthePerson
withDiabetes
Any person with diabetes and peripheral neuropathy should know that they are at risk of future
foot problems. Their risk of foot ulcers far
exceeds the risk of developing an active Charcot
but it is most important that they know how to
contact someone with the necessary expertise
should they develop an unexplained red hot swollen foot. It is just as important that the health care
professional should think of the diagnosis and
make appropriate referrals for investigation and
off-loading without delay.
17 Charcot Foot Syndrome: Aetiology andDiagnosis
223
The Bottom Line
The Charcot syndrome is uncommon but not rare
and it is important that it is considered in any person with neuropathy who presents with unexplained inammation of the foot. When
considered, the foot should be protected against
unnecessary trauma until the diagnosis has been
either proved or excluded. If the diagnosis is
conrmed, long term off-loading is the current
mainstay of management 1.
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Care. 2022;45:1691–7.
Charcot Foot: Conservative
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Management
ArminKoller
18
Introduction
Conservative treatment in Charcot neuroarthropathy (CN) on the one hand represents an alternative to surgical treatment; on the other hand it is
always used before or after operations and therefore an integral part of the treatment algorithm.
Goals of conservative therapy are reduction of
inammation by shielding the foot skeleton from
mechanical stress, preservation of foot shape
until consolidation of CN, and redressment of
foot deformity prior to stabilization.
There are several conceivable scenarios in
which conservative treatment would be preferable to surgery. A very morbid patient with highgrade limitation of walking distance due to his
medical conditions is not a good candidate for
complex and high-risk operative reconstructions.
In general, functional improvement from reconstructive surgery has to justify the possibly substantial risk of operation or anesthesia. A foot
with mild to moderate deformity which is plantigrade and capable of full weight-bearing in a
shoe or an orthosis does not necessarily need
operative treatment [1].
Drug treatment is discussed as a complementary anti-inammatory therapy. There is growing
A. Koller (*)
Department of Technical Orthopedics, Hospital Dr.
Guth, Hamburg, Germany
e-mail: info@arminkoller.de
evidence of a link between neuropathy, bone
turnover, inammation, and mechanical stress in
Charcot neuroarthropathy [2].
Since neuropathy cannot be reversed and
mechanical stress is within the scope of casts and
orthoses, different drugs have been utilized to
normalize bone turnover and reduce inammation. Medication can never be a standalone treatment but is intended to shorten time to resolution
of the active neuroarthropathic process in combination with standard treatment by means of total
contact cast or orthosis. However, none of the
drug treatments so far has supplied scientic evidence of a therapeutic effect that would justify
unequivocal recommendation. Even adverse
effects could be noticed with signicant prolongation of the time to resolution using bisphosphonates [3].
Edema typically coming along with the active
stages of CN interferes with proper t of orthotic
devices and compromises wound healing. In
return, treatment with effective immobilization
of foot and lower leg leads to edema regression,
unless that is not a consequence of venous, lymphatic, renal, or cardiac insufciency. Antiedematous therapy includes compression
bandages, Unna boot, or semi-rigid casts (Photo
18.1). Additionally, patients should exert com-
plete off-loading of the affected limb, in the sense
of completely refraining from weight-bearing, by
means of crutches, wheelchair, or even bed rest in
the very acute stage of CN, when massive edema
© Springer Nature Switzerland AG 2023
C. E. Attinger, J. S. Steinberg (eds.), Functional Limb Salvage,
https://doi.org/10.1007/978-3-031-27725-2_18
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Photo 18.1 Regression of the previously massive edema
of the foot and lower leg after only 1 day of at positioning and application of a semi-rigid cast (3M™
Scotchcast™ Soft Cast Casting Tape)
with erythematous vulnerable skin makes
weight- bearing in a cast or splint impossible anyway. When there is only mild to moderate swelling of foot and lower leg, treatment with casts or
orthoses can start.
Charcot neuroarthropathy quite often comes
along with pressure ulcers. Both conditions are
usually treated by so-called off-loading, but the
biomechanical principles of treatment are fundamentally different in both cases. That is quite
understandable, since one condition affects the
soft tissue, the other one the skeleton. Neuropathic
ulcers are caused by pressure exceeding a certain
threshold, and treatment basically implies reversal of that process. As complete pressure elimination is not always feasible, redistribution of
forces acting on the plantar surface has to effect
pressure reduction at the ulcer site to a subthreshold level.
Regarding only the mechanical aspects of the
complex etiology, CN is not induced or aggravated by forces acting on the skin surface, but by
A. Koller
external (walking, standing, and sitting!) and
internal (tendon pull) forces acting on the foot
skeleton. The result is strain of bones and ligaments. This deformation can only be eliminated
or minimized by a device that allows for a permanent rigid three-dimensional xation of foot and
lower leg. With this ensured, weight-bearing and
subsequent pressure on soft tissue is not a major
obstacle. Not recommended, however, is leaving
the device off even for the shortest walk.
Charcot Foot withFractures
Beyond the contribution of inammation and
deregulated bone metabolism to the multifaceted
etiology of CN, the disease has a lot in common
with fractures due to repetitive stress or trauma.
The basic principles of conservative fracture
treatment have been laid down nearly one hundred years ago. Lorenz Böhler (1885–1973) [4],
one of the godfathers of modern trauma surgery,
emphasized that accurate reduction of the displaced fragment is only sensible if subsequent
measures are taken to keep the reduced bone
fragments in a good position—without any
interruption!
Fractures lead to deformity with resulting
abnormal plantar pressure and repetitive microtraumata, which in turn are responsible for
inammation, osteoclast activation, and osteopenia, increasing again the risk for further fractures.
Casts and orthoses are valuable tools to accommodate deformity and abnormal loading patterns,
since it is paramount to interrupt that vicious circle [5].
Since CN rather is a syndrome than a specic
nosological entity, orthotic treatment cannot be
uniform. Active CN requires permanent stabilization, whereas inactive CN is treated sufciently
with protected weight-bearing. The presence of a
plantar ulcer requires additional local pressure
relief by plantar insoles or by load transfer to the
tibial condyles or patella. A mild to moderate
deformity basically can be treated with an offthe- shelf walker, a pronounced deformity must
be tted with a cast or a custom-made orthosis.
The plane of the deformity also has to be taken
18 Charcot Foot: Conservative Management
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229
into consideration. Sagittal plane deformity is
easy to accommodate; transverse plane or frontal
plane deformity, in particular, makes orthotic tting and compensation of static alignment quite
challenging. Circadian uctuations of edema due
to cardiac or renal insufciency are usually
treated with compression stockings or bandages,
but those are not always applicable together with
orthoses. As a consequence, the orthotic design
should have an adjustment mechanism that
enables containment of a lower leg with volume
variations without losing proper t.
Of course, the foot cannot be regarded quite
apart from the patient, who will demonstrate different body weight and activity level. Heavy use
of an orthosis must be countered with a heavy
duty construction.
Orthotic Treatment
General requirements for orthoses in treating
Charcot feet include accommodation of any
deformity, protection of vulnerable soft tissue,
and volume control. Patients should be able to
don and doff the orthosis without an auxiliary
person to keep their autonomy. Mobility needs
range from a few steps at home to long distances
in the community. Hence, design of the rocker
sole is either geared to stability or to dynamics.
Geriatric patients need more safety and active
patients more agility.
Specic requirements for orthoses in treating
CN depend on the respective pathology to be
treated. Activity of the neuroarthropathic process
needs rigid three-dimensional xation comprising foot and lower leg. Activity nds its expression in inammatory signs having a mechanical
component due to fracture or joint dislocation
which in turn are treated comparable to a skeletal
trauma. Ground reaction force during walking
and standing is not the major concern, but movements of the foot within the device.
Rotation around the long axis of the leg does
not only occur at the hip joint. At the same time
the subtalar joint complex accomplishes an
inversion- eversion movement which has to be
compensated by a contrarotating pronation-
supination movement of the midfoot against the
hindfoot. This torsion also involves the tarsal
bones, so that rigid xation of that area of the
foot skeleton does not only call for a stiff rocker
sole, but also for an orthotic design able to control lower leg rotation. The triangular shape of
the proximal tibia is the place where rotation can
be restricted by an accordingly molded pretibial
shell of the orthosis. Counter-pressure at the calf
muscles must keep the proximal tibia in the
desired position. Large area pressure helps to
avoid undue proximal constriction of venous and
lymphatic drainage.
The concept of immobilization of foot joints is
not new. It was introduced by Morgan in 1993
[6]. A long time ago protection from cumulative
microtrauma was recognized to be the keynote
for orthotic treatment of Charcot feet.
Subsequently, this idea had been replaced by a
focus on relief of plantar pressure [7]. Orthoses
were designed to reduce load transmission to the
midfoot or forefoot [8]. Indeed, measurement of
high plantar pressure within an orthosis may
serve as an indirect proof of mechanical instability or insufcient anatomical t of the respective
device. However, it remains difcult to draw
clear conclusions from plantar pressure measurement to joint or fragment movements. The effect
of tibial rotation on movement of foot joints cannot be detected by means of plantar pressure
measurement. The concept of joint immobilization is consistent with up-to-date hypotheses
about the etiology of neuro-arthropathy, but there
is still a need for well-designed studies on the
mechanical effects of orthoses in a larger cohort
of Charcot feet [9].
Deformity of the Charcot foot of a certain
extent does not only call for individual fabrication of the ankle foot orthosis, but also has negative impact on biomechanics of walking and
standing. Frontal plane deformity at the hindfoot,
that is medial or lateral displacement of the calcaneus, calls for an opposed enlargement of the
orthotic heel, so that the physiological plumbline
of the leg is restored. A deformed but stiff foot is
often easier to accommodate with an orthosis
than a Charcot foot with instability. In particular,
when only partial redressment of the deformity is
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