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208
V. Kavarthapu and J. A. Sánchez
and partial ray amputation including the metatarsal head are the available surgical options.
Plantar or dorsal approach can be used for
removing the metatarsal head or the metatarsal
phalangeal joint [52]. Conservative surgery
consisting of resection of metatarsal head is
also widely used [23, 58–64]. A group of
authors retrospectively compared the outcomes
of both approaches and reported that there were
no differences regarding time to healing but
patients operated by dorsal approach experienced a higher rate of postoperative complications [65]. Transfer ulcers due to biomechanical
changes in the foot are very common when a
metatarsal head is removed either as part of ray
amputation or in isolation. That is especially
true in cases in which the rst metatarsal head
is removed [66]. First ray amputation is associated with severe biomechanical disturbances of
the foot, subsequent amputations [67–71], and
even the development of Charcot
Neuroarthropathy [72]. It has been suggested
that a more proximal level amputation, such as
a balanced transmetatarsal, might provide a
better functional and reliable residual weightbearing foot [71]. Conservative approaches
leading to save the hallux could be an alternative but there is no long-term follow-up of these
procedures. One-stage resection and pin stabilisation [73] or the use of external xation after
removing the infected bone [74] has been
described in a short series. Another group
reported a cohort including 28 patients with
osteomyelitis of the rst ray treated by a technique requiring a one-stage surgical approach
[75]. After surgical debridement with removal
of the infected bone, the authors placed antibiotic-loaded bone cement and stabilised the
treated area with an external xator [75]. Four
patients (14.2%) developed a relapse of the
ulceration after the procedure. No ulceration
recurrences, transfer ulcerations, shoe t problems, or gait abnormalities were detected in the
other 24 patients (85.8%) [75]. Bone debridement and antibiotic-impregnated cement spacer
may be another option [58]. However, it is necessary to highlight that additional controlled
trials are required to evaluate this further.
Surgical Treatment ofInfected Heel
Ulcers
Infected plantar heel ulcers in people with diabetic peripheral neuropathy carry a high risk of
major amputation as these not only result in
osteomyelitis of calcaneal body, but also lead to
destruction of plantar heel pad. Heel is the second most common anatomical location for pressure ulcers [76]. The reported outcomes of
surgical management of heel ulcers are variable,
as the earlier studies showed healing rates ranging from 35% to 74% [77], but the most recent
ones revealed better outcomes with 97–100%
limb salvage reported from treating centres
[78–80].
Various surgical techniques have been reported
on the surgical management of calcaneal osteomyelitis to achieve limb salvage. These include
partial or total calcanectomy. Cook etal., in 2007,
reported a 71.4% healing rate during the rst year
in their series of 50 partial calcanectomies for
chronic non-healing ulcers. However, they found
a high rate of ulcer recurrence after 1 year, with
higher negative outcomes in the presence of
MRSA infection, vascular compromise, low
albumin levels, and higher grade of preoperative
ulcer [77]. Paola et al. reported a 100% ulcer
healing rate, within their follow-up period of
12months, in their cohort of 18 patients treated
with open partial calcanectomy and application
of circular external xator [78]. Ngwe et al.,
more recently, reported the outcomes of surgical
management of 30 diabetic neuropathic heel
ulcers with no critical limb ischemia, managed
with ulcer debridement without partial calcanectomy when COM was present [80]. At a mean
follow-up period of 28 months (12–83), 50%
achieved full ulcer healing and 97% had limb salvage. A mortality rate of 38% was observed in
this cohort. Only 9 out of 24 ulcers with calcaneal
osteomyelitis (p value 0.044) achieved full ulcer
healing. Local antibiotic delivery as an adjunct
during partial calcanectomy can help eradicate
any residual infection and promote complete
infection eradication. Antibiotic-loaded injectable bone substitute is injected in multiple channels created by making drill holes in the residual
16 Surgical Management ofDiabetic Foot Infection andOsteomyelitis
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209
calcaneal body to achieve this [80]. This provides
high tissue concentration of antibiotic for several
weeks that eradicates any residual pathogens [81,
82]. Dramploas et al. reported 100% infection
eradication and healing rate using similar technique in their series of 12 patients with infected
heel ulcers and calcaneal osteomyelitis [79].
Principles ofExostectomy
An infected plantar ulcer, as a result of peak plantar pressures due to underlying bone prominence,
requires exostectomy in addition to ulcer debridement, to achieve eradication of infection and
ulcer healing. The ulcer rst is excised and thoroughly debrided down to the oor, exposing full
area of exostosis. The bone prominence is marked
by careful palpation, cross checking under uoroscopy. The edge of the bone prominence is
scored with an oscillating saw by about 5 mm
depth. A curved osteotome is used to excise the
exostosis completely within the marked zone.
The bone surface of the excised area is examined
for any areas of necrosis, discolouration, and
altered consistency, which may represent residual
area of infection and if present, this is thoroughly
explored and excised. The surface and the edge
of the excised area are carefully inspected and
palpated for any residual bone prominence and
excised if present. Local antibiotic eluting calcium preparation can be applied around the bone
or injected into bone channels drilled in the exostectomy area to eradicate any residual infection
[79, 80]. The choice of the antibiotic is based on
microbiological sensitivities of deep tissue or
bone biopsy specimen culture results. The open
wound is managed with either a local transposition ap or negative pressure wound therapy
(NPWT).
Surgical Management ofDiabetic
Foot Attack
Diabetic foot infection presentations can occasionally spread rapidly along the tissue planes
resulting in necrosis and systemic inammatory
response. This is often triggered by a blister or
skin break from minor trauma that leads to local
spreading of infection in different tissue planes
resulting in development of ulceration and
spreading cellulitis. Such presentation is labelled
as diabetic foot attack (DFA) and without a
timely and emergent intervention, it can be limb
and life threatening [83]. Vainieri etal. reported
the outcomes of 106 patients presented with diabetic foot attack, with a mean follow-up of
18.4 ± 3.6 months [84]. They noted a major
amputation free survival in 71% of patients during the rst 12 months from admission that
reduced to 55.4% by the end of the follow-up.
DFA presentation is best managed by a multidisciplinary diabetic foot team for optimal outcomes. It is critical that the diagnosis is reached
rapidly by performing appropriate clinical assessment and urgent investigations. The investigations should focus on assessing the extent of
infection and obtaining microbiological sensitivities. Plain radiographs often show soft tissue
changes, including the presence of gas shadow.
Deep tissue specimens are obtained for microbiological culture and sensitivities, before commencing empirical intravenous antibiotic therapy
[85]. In the absence of an open ulcer or wound,
ultrasound examination can be performed for
assessment of deep collection and aspiration for
microbiological studies. MRI is the most useful
imaging investigation as it provides the diagnosis
and information on the extent of infection spread
that can be useful for surgical planning. However,
it is critical that the appropriate investigations are
performed in a timely manner so that the surgery
is not delayed.
DFA often needs emergent surgical intervention. Aggressive surgical debridement, using the
principles described above, is performed soon
after diagnosis as delay can cause further tissue
necrosis and potential limb loss. Repeat surgical
debridement is often required if the systemic
inammatory response does not improve or any
further tissue necrosis is identied. Targeted
intravenous antibiotic therapy, based on microbiological sensitivities, is continued until the infection is completely cleared, as noted by the
improvement in the clinical ndings and normali-
210
V. Kavarthapu and J. A. Sánchez
sation of serological markers. The open surgical
wound is managed with NPWT followed by skin
grafting or a local tissue ap. Due to the degree
of soft tissue and bone loss from the spread of
infection and surgical debridement, the affected
feet often require expert treatment after the resolution of DFA presentation, including deformity
corrective procedures.
Conclusion
Diabetic foot infections, including osteomyelitis,
range from simple presentations to complex limb
and life threatening DFA.These require thorough
clinical assessment, often in a multidisciplinary
setup, and address the sequala of such infections,
including revascularisation and deformity correction, to provide optimal outcomes [86, 87].
Surgery is a critical component of treatment and
should be considered in the presence of tissue
necrosis.
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Charcot Foot Syndrome: Aetiology
andDiagnosis
WilliamJecoate andFranGame
17
The Bottom Line
Although the Charcot foot is not rare, it is thought
to be rare by many clinicians and few are aware
that any delay in diagnosis may lead to irreversible, and potentially life-threatening, damage. In
a recent survey of medical staff in a very large
teaching hospital in Michigan, some 68% respondents admitted that their knowledge of the condition was either rudimentary or non-existent [1]. A
similar survey in any other hospital—or in nonspecialist practice—in any country of the world
would conrm that such ignorance is common.
And while most doctors would be mortied if
they missed a common cancer in its early stages
and failed to arrange for early expert assessment,
few realise that the same approach is needed for
the best management of the Charcot foot. There
are observational data to suggest that delay in
diagnosis of active Charcot syndrome is associated with a far worse outcome [2–4]. It is for
these reasons that this review starts with its bottom line.
W. Jeffcoate
Nottingham University Hospitals NHS Trust,
Nottingham, UK
F. Game (*)
University Hospitals of Derby and Burton NHS
Foundation Trust, Derby, UK
e-mail: frances.game@nhs.net
The 1, 2, 3 of Diagnosis of the Charcot Foot:
The Bottom Line
Every clinician who is approached for
advice by a person with an inamed foot
which has no obvious cause should remember three simple points:
1. Has this person got diabetes?
2. Has this person got peripheral
neuropathy?
3. If yes to either of these, it should be
assumed that they have an active
Charcot foot until proved otherwise.
They should be advised to minimise
weight- bearing and should be referred
for urgent expert assessment.
Introduction
The condition is known variously as the Charcot
foot, Charcot neuropathic osteoarthropathy or
neuro-inammatory osteoarthropathy and is a
complex disorder which occurs in people with
some form of peripheral neuropathy. It is characterised by inammation and varying degrees of
structural damage to the bones and joints of the
foot. In some cases the damage is severe, disabling and potentially limb-threatening but in
other cases the changes are relatively minor.
© 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_17
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W. Jecoate and F. Game
The Charcot Foot Is aSyndrome: Not
aDisease
The Charcot foot should be considered as a syndrome rather than a disease. It can be recognised
but has no denition and no current dened diagnostic criteria.
History
The condition was rst described by Jean-Martin
Charcot (1825–1893) in the spine and upper part
of the leg in 1868 and by Herbert William Page
(1845–1926) in the foot in 1881 [5]. In these
reports, as well as in Charcot’s ve case series of
1883, the underlying cause was tertiary syphilis
with tabes dorsalis and ‘progressive locomotor
ataxia’. Charcot suggested that the problem was
in part the result of reduced pain sensation and in
part the result of inammation with increased
blood ow. Non-syphilitic Charcot disease was
rst described in people with diabetes in 1936. It
can also complicate leprosy [6], alcohol abuse,
chemotherapy and other causes of neuropathy.
There have been a number of major reviews in
recent years [7–9].
The Clinical Presentation
oftheCharcot Syndrome
The condition is most often seen in the foot but it
may occur further up the lower limb and even in
the spine. In this chapter, however, attention is
focused on the foot in diabetes—not least because
it is by far the most common site affected and
diabetes is by far the most common cause in most
parts of the world.
Active Phase
The active phase has been traditionally referred
to as ‘acute Charcot’ but the word ‘acute’ can be
misleading in that the active phase of the disease
can be anything but ‘acute’ and can last for days,
weeks or for up to 18months. The term ‘acute
Charcot’ is a misnomer and should be abandoned
in favour of ‘active Charcot’ [10].
The hallmark/principal feature of the active
phase is local inammation. If there is any associated deformity (from dislocation, fracture), it
may be apparent clinically and/or on imaging.
There may or may not be associated discomfort.
Any discomfort or pain is, however, rarely, if
ever, as severe as would be expected from any
changes seen on imaging. When the affected foot
is fully rested by immobilisation in a below knee
cast, the inammation reduces but it does not
settle completely until the underlying process
goes into remission.
Active disease is most commonly triggered by
minor trauma. Such trauma was recalled by 36%
of 288 cases managed in 76 centres in the UK and
Ireland between 2005 and 2007. Other triggers
were preceding foot ulceration (35%), local surgery (12%) and osteomyelitis (7%) [11]. The
observation that 7% cases in this series were triggered by osteomyelitis has also been reported by
Ndip etal. [12] and is of great importance—not so
much in the diagnosis of Charcot syndrome but in
the assessment of apparent lack of resolution in
cases of treated osteomyelitis. When a case of
pedal osteomyelitis shows signs of deterioration
(either on clinical grounds or on imaging) despite
appropriate treatment, it might be assumed that
the infection was still active. This may not, however, be the case if the original infection has triggered the onset of an active Charcot syndrome.
The possibility needs to be considered because it
has clear implications for management. A bone
biopsy for microbiological sampling could be
considered, although more discriminatory radiological imaging may also be considered such as
radiolabelled white blood cell (WBC) scans [13].
The activity of the Charcot foot syndrome will
eventually prove self-limiting in many and the
foot will stabilise once the inammation settles—
even though any skeletal damage or deformity
will be permanent. Expert teams manage the condition by minimising trauma by ensuring effective off-loading [11] as well as the management
of complications (including secondary deformity,
ulceration and infection). Currently, there is no
effective systemic therapy to either prevent or
17 Charcot Foot Syndrome: Aetiology andDiagnosis
217
reduce the causative processes [14]. The condition is associated with high levels of anxiety and
depression [3, 15].
Inactive Phase andRecurrence
The majority will eventually enter remission but
this may not be for a number of months. There is
some variation in the reported time to inactivity
following conservative management with mean
times varying from less than 6 months in
Denmark [16], to a median of 51.5weeks in one
centre in UK [17], and 10–12months in the 76
UK centres in one large study from UK and
Ireland [11]. Some of these differences will relate
to some people having their off-loading discontinued inappropriately early and hence will be
accompanied by a correspondingly high relapse
rate [18]. Some of the difference between
reported times to resolution will relate also to
inclusion of the time which elapses between a
decision being made that the condition has
entered remission and the availability of the
required footwear needed for full ambulation.
However, one of the main causes is that there is
no agreed denition for resolution of the active
stage as demonstrated in a recent systematic
review [19].
Once, however, the disease is truly inactive, it
is extremely rare for the disease to recur in the
same position in the index foot even though occasional cases have been described [20]. Some 20%
of affected people will, however, have disease
affecting the contralateral foot—either at the
same time or usually a short time later.
Aetiology: Predisposition
The Charcot syndrome results from the variable
interaction of three principal factors: neuropathy,
fragility of bones and joint capsules and retention
of the capacity to mount a local inammatory
response to injury. Additional factors may contribute when the neuropathy is the result of
diabetes.
Neuropathy
Neuropathy affects up to 50% people with diabetes [21, 22]. The type and extent of nerve damage
varies from person to person but it is typically
symmetrical and affects one or more of many
aspects of peripheral nerve function including
sensory, motor, cardiac and non-cardiac autonomic, neurovascular and skeletal (variously
involving bone, joints and bone marrow) innervation. In the people presenting with an active
Charcot foot, however, the manifestation of neuropathy which is most obvious clinically is loss
of protective sensation and this means that even
gross distortion of the foot is relatively pain-free.
The loss of signicant pain is common to cases
which complicate diabetes as well as to those
which complicate other conditions, such as the
tertiary syphilis in which the syndrome was rst
described. This is despite the neurological defects
being different in different diseases: loss of deep
pain sensation in tabes dorsalis is from dorsal
column disease of the spine, for example, whereas
in diabetes it is mainly from dysfunction of
peripheral sensory bres.
Eect ofNeuropathy onBone
Aetiology oftheCharcot Syndrome
The Charcot syndrome can be regarded as a distortion of the normal complex responses of the
body to injury or insult with these responses
being normally reliant on close intercellular signalling. The factors contributing to its occurrence
are considered under the following subheadings:
predisposition, permissive factors, precipitation,
presentation, perpetuation and resolution.
The RANK/RANKL-NFkappaB andWnt/β- catenin Pathways
One key pathway in bone modelling is the
RANKL/RANK signalling pathway. RANKL is
derived from monocyte derivatives and is the
polypeptide ligand for the RANK receptor,
so-called because it is the receptor for the activation of the nuclear transcription factor,
NFkappaB.NFkappaB has a number of functions
but one of these is the activation of osteoclasts,
with resultant bone breakdown. Osteoprotegerin
218
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W. Jecoate and F. Game
(OPG) acts as a decoy receptor for RANKL and
thereby helps to limit its action. RANKL and
OPG are both released at the same time, even
though their actions are essentially opposite. The
ratio of the two at any one time could, however,
be of importance in the relative effects of RANKL
vs. OPG on bone quality.
Another pathway which also affects both bone
quality is the Wnt/β-catenin pathway. High levels
of Wnt ligand prevent the breakdown of β-catenin,
which in turn promotes osteoblast maturation and
therefore bone formation. Low levels, therefore,
would be consistent with bone breakdown.
Sclerostin and Dickkopf-1 are inhibitors of Wnt
and have been found to be signicantly higher in
a small series of post-menopausal women with
type-2 diabetes than in sex and age-matched controls [23].
Neuropathy is associated with osteolysis and
increased bone fragility. The integrity of bones is
normally maintained by a variety of nervederived neurotransmitters which encourage the
synthesis of OPG in preference to activation of
RANK receptor and NFkappaB. These are
derived from both autonomic and somatic neurones and include calcitonin gene related peptide
(CGRP), substance P (SP), vasoactive intestinal
polypeptide (VIP), tyrosine hydroxylase (TH),
norepinephrine (NE), neuropeptide Y (NPY),
glutamate and leptin [24, 25]. All are associated
with the release of anti-inammatory factors,
including IL-4 and Il-10 [26]. In contrast, a further nerve-derived transmitter nitric oxide (NO)
favours the proliferation of osteoclasts.
In one very small study of bone samples from
eight people with diabetes, four samples from
those with neuropathy were found to have lower
levels of NO compared with the four nonneuropathic diabetic control samples, as well as a
trend towards an increase in CGRP [27], although
the ndings were not conclusive due to the small
size of the study.
Eect ofNeuropathy ontheJoint Capsule
Dislocation is a common feature of the active
Charcot foot and may occur even in joints which
are not otherwise prone to dislocation, including
the tarso-metatarsal (Lisfranc) and talonavicular
(Chopart) joints. Such dislocation may be caused
by partial avulsion of the joint capsule as a result
of weakened attachment or, potentially from
changes to the integrity of the capsule and other
soft tissues which are normally richly innervated
with nerves secreting SP, CRGP and NPY [28].
While the loss of innervation is known to have
major effects on bone structure and fragility, it is
also possible that it may compromise the integrity of the capsule in people with Charcot foot.
Eect ofNeuropathy
ontheVasculature
It is well established that there is an association
between calcication of the cells of the arterial
walls and osteoporosis, including osteopenia
associated with neuropathies and it is thought to
result from the contrasting effects of the RANKL/
OPG signalling system in the two tissues [29,
30]. Both are also associated with neuropathy.
Neuropathy is particularly closely associated
with calcication of the tunica media of the
medium to small arteries of the periphery (medial
arterial sclerosis, MAC; Mönckeberg’s sclerosis)
[31, 32] where it has been shown to have the histological features of bone [33].
Additional Predisposing Factors
Associated withDiabetes
Eects ofNeuropathy ontheVasculature
There is a very extensive literature on the relationships between low grade, metabolic inammation and disease of the heart and larger arteries
in diabetes. In this context, the ‘inammation’ is
not clinically apparent but refers to the effects
which result from the pro-inammatory effects
of glucose, oxidised lipids and advanced glycation end-products (AGEs) linked to reduced
expression of the AGE receptor (RAGE) [34].
The broad subject has been well-reviewed elsewhere [35].
In the Charcot foot syndrome, however, it is
the distal vasculature which is just as important
and any predisposition in a person with diabetes
will include the combined effects of both. Indeed,
the ndings of one controlled observational study
suggested that overt clinical signs of more proxi-
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