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4 NEGATIVE PRESSURE WOUND THERAPY JOURNAL, VOL. 5, NO. 1, 2018
Charcot foot (neuropathic arthropathy) in diabetes
as a "special needs foot". Case report of an efficient
negative pressure wound therapy use.
Bartosz Cybułka
CASE REPORT
Abstract—Diabetes is the most common endocrine disorder
of carbohydrate metabolism. If left untreated, or improperly
treated, diabetes leads to multiple organ complications. One
of the serious consequences of the disease is damage to the
peripheral and autonomic nerves known as diabetic neuropathy.
The most advanced form of neuropathy, leading to damage
to the structures of the forefoot, midfoot and hindfoot, is
the so-called Charcot foot, or neuropathic osteoarthropathy.
Irreversible damage to the structures of the foot affects between
0,1% and 7.5% of patients with diabetes.
The optimal care for that form of foot damage is still a subject
to debate. Available methods of caring for Charcot foot include
invasive orthopedic treatment and conservative treatment. The
use of negative pressure wound therapy may be an effective, as
well as transitional, way of managing Charcot foot.
Keywords—Charcot neuro - osteoarthropathy, Charcot foot,
diabetic foot, diabetic neuropathy, negative pressure wound
therapy (NPWT)
I. INTRODUCTION
DIABETES mellitus is the most common endocrine
disorder. Impaired metabolism of carbohydrates leads
to numerous organ complications. Epidemiologically, in 2011
there were 285 million patients with diagnosed diabetes.
This number constituted 6.6% of the population aged 20–79.
It is estimated that about one-third of cases still remain
undiagnosed. Among them, 2.5% will develop one of the
most dangerous complications of diabetic foot, which is the
Charcot arthropathy.1
Osteoarticular lesions that result from disturbances of
innervation, referred to as neuropathic arthropathy, were
described in 1868 by Jean-Martin Charcot.2
Complicated form of diabetes is the most common cause
of neuropathic arthropathy in developed countries. Any pe-
ripheral neuropathy may lead to articular lesions. Other
causes that may, consequently, lead to lesions in the joint
structure are: syringomyelia, poliomyelitis, injuries of the
spinal cord, leprosy, alcohol abuse, multiple sclerosis, heavy
metal poisoning and rheumatoid arthritis.3, 4
Manuscript received 17.07.2017; revised 28.03.2018. This work did not
receive any financial support. Author declares no conflict of interest.
Author affiliations: Oddział Chirurgiczny z Pododdziałem Gastroen-
terologicznym Samodzielny Publiczny Zakład Opieki Zdrowotnej 62-065
Grodzisk Wlkp. ul. Mossego 3. , (BC)
*Correspondence to: Bartosz Cybułka: b.cybulka@wp.pl
The clinical classification of Charcot foot distinguishes the
acute form of the disease, characterized by edema, redness,
increased blood circulation, and increased foot temperature.
Charcot arthropathy should be suspected in patients with
these symptoms, without characteristic ulceration. The skin
temperature of a diseased foot may be increased even by
2-6oC. Pain intensity depends on the stage of diabetic neu-
ropathy.5
Charcot arthropathy is often diagnosed during the inactive,
chronic stage when inflammatory symptoms are not present.
In this phase, bones, joints and ligamentous apparatus of the
foot are being continuously damaged. The use of imaging
diagnostic (plain x-ray of the foot or magnetic resonance)
confirms the clinical diagnosis. It is worth mentioning that
the initial stage of metatarsal deformation will not be visible
on a typical X-ray image in two projections. At the initial
stage of the disease, magnetic resonance is the most sensitive
imaging method.
In 1966, Sidney N. Eichenholtz described in his mono-
graph cases of various osteoarticular lesions on the basis of
68 available radiograms, and introduced the term "Charcot
joint".6(Tab. I)
II. CA SE R EP ORT
A 58-year-old patient was admitted to a surgical ward
for the treatment of a massive wound located between the
second and third toe of the right foot. Medical history
interview revealed a long-term insulin-dependent diabetes
with numerous organ complications. Previously, the patient
required amputation of the hallux of the right foot and the
second toe of the left foot. Before the admission, the patient
was provided with ambulatory care due to a non-healing
clavus located on the plantar surface. Repeated resections
of the clavus did not allow to eliminate this hyperkartotic
lesion and during one of the visits, after a surgical resection
of the clavus, an intervention to stop bleeding from blood
vessels of the plantar surface was necessary.
Advanced destructive changes of the right foot were visible
on an X-ray image (Fig. 1). The radiograms revealed the
loss of the foot arch, fixed, spontaneous dislocation of the
metatarsophalangeal joint, and foci of decreased mineraliza-
tion in the tarsal and metatarsal bones (Fig. 2). No changes
were observed at the level of the ankle joint and calcaneus.
Medigent.org cb DOI: 10.18487/npwtj.v5i1.24
CYBUŁKA et al. : CHARCOT FOOT IN DIABETES AS A "SPECIAL NEEDS FOOT". EFFICIENT USE OF NPWT. 5
Table I
CLA SSI FIC ATION O F TH E CHAR COT N EUR O-ART HRO PATHY (E ICHENHOLTZ 1966)
Stage Clinical characteristics X-ray features
Stage I (development or fragmen-
tation)
Edema of diabetic foot. Inflammatory stage: - ode-
matous, - erythematous, - hot and hyperemic foot.
Luxation, subluxation, dislocation of joint. Peri-articular frac-
tures. Foot deformity. Decrease of diabetic foot stability.
Stage II (coalescence) Gradual remission of the inflamatory skin signs.
Reduction of edema.
Osteoporosis, resorption, bone debris. Increase of diabetic
foot stability.
Stage III (consolidation or repara-
tion)
Absence of inflamatory signs, Absence edema of
diabetic foot.
Consolidated remodeling and deformation of the foot bones
and joints.
Figure 1. Displacement of the matatarsophalangeal joint (MTP). Sanders
and Frykberg’s classification - pattern I
Figure 2. Previous amputation of the hallux
On the day of admission, after initial preparation of the bed
and edge of the wound, a negative pressure dressing Vivano
Tec produced by Hartmann was used. A 10 cm x 7.5 cm x
3.3 cm sponge had been modeled to the elliptic shape of the
wound. Due to the fact that the wound was located between
toes, it required special attention to maintain the seal of the
dressing (Fig. 3).
Continuous mode of negative pressure (-125 mmHg) was
applied. For better protection, the skin near the wound was
covered with a stripe of silicon drape. The first dressing
remained on the wound for 48 hours. During the first change
of dressing, normal formation of granulation tissue and
early signs of epithelialization of the wound edges were
observed (Fig. 4). Negative pressure therapy was continued.
The second negative pressure dressing remained intact for 72
hours. The third dressing set remained on the wound for 9
Figure 3. Management of the bleeding after initial debridement
Figure 4. 1st wound dressing change after 48 hours of NPWT.
days due to full impermeability (Fig. 5). After the last 216-
hours course the negative pressure therapy was finished and
a reduction of the total wound surface was observed, as well
as a proliferation of the vital, healthy granulation tissue. The
tendency of spontaneous wound edges approximation was
also observed (Fig. 6).
Finally, the upper pole of the wound, between the second
and third toe, was approximated with the use of an interrupted
dermal suture (Dafilon 2.0). The defect, dressed in such a
way, healed properly by further approximation of the wound
edges (Fig. 7). No foci of necrosis, abnormal exudate, or
clinical symptoms of infection were observed during the
treatment of the wound. In this case, the course of healing
of the wound in a deformed diabetic foot was finished
successfully.
6 NEGATIVE PRESSURE WOUND THERAPY JOURNAL, VOL. 5, NO. 1, 2018
Figure 5. Granulation tissue and maceration of the epidermis
Figure 6. Evident reduction of tissue loss after 216 hours of continuous
NPWT
III. DISCUSSION
Peripheral neuropathy relates to 29% of patients with
diabetes mellitus.7Charcot foot is a specific form of pe-
ripheral neuropathy in diabetes. Continuous destruction of
nerve fibers leads to an autonomic neuropathy. Apart from
hyposesthesia, blood circulation disorders and intensification
of bone destruction are common this situation. The latter
are due to the prevalence of osteolytic activity of osteoclasts
on osteoblasts. The pathogenesis of Charcot foot is chronic,
multifactorial, and progressive.
The chronic form of the disease is characterized by
the reduction of edema, reduction of redness, reduction of
Figure 7. Postponed skin sutures in the diabetic foot
increased temperature and leads to permanent anatomical
changes at the level metatarsal level. A diabetic foot de-
formed in this process becomes more prone to repetitive
minor unnoticed injuries that can further ulcerate. Disruption
of the skin continuity opens the door for infection. Infectious
complications in cases of diabetic foot are the most common
cause of amputations in diabetes mellitus.
Neuropathy can relate to peripheral nerves that are re-
sponsible for transferring pain stimuli, as well as auto-
nomic nerves determining the cellular equilibrium of the
bones. In the advanced form of the diabetic foot, there
is a prevalence of destructive activity of osteoclasts at the
expense of osteogenic activity of the osteoblasts. Autonomic
neuropathy leads to an increased arterial blood inflow by
impairing arteriovenous capillary connections.8, 9 Clinically,
increased temperature, redness of foot skin and hypervolemia
occur.10–12 Increased blood flow also influences the bone
tissue, leading to its increased resorption with bone mineral
density loss.13, 14
Peripheral neuropathy, referred to as the distal sensorimo-
tor polyneuropathy is responsible for the loss of the protective
pain, temperature, and touch sensation. A foot that is devoid
of innervation is exposed to various kinds of damage that
also disturb proper anatomy of the foot.
Another cause of foot damage is an increase of
non-enzymatic glycation of collagen. Impaired collagen
metabolism leads to the weakening of tendons, ligaments,
therefore, leading to the change of foot biomechanics.15
In the case of Charcot foot, there is an increased pressure
impacting the plantar surface.
Characteristic clinical symptoms of Charcot
neuroarthropathy are described using the 5D acronym
according to Rajbhandari:16
•joint distension
•dislocation
•debris
•disorganization
•increased density
If observed, any symptoms from foot fully oblige to
prepare X-ray image of parts of the metatarsus. Visible
changes characteristic for osteoarthropathy are dislocations
and subluxations of foot joints, periarticular osteoporosis,
bone tissue resorption, the presence of debris, loss of the
foot arch, traces of previous surgical interventions.
Anatomical classification by Sanders and Frykberg differ-
entiates five areas of foot damage:17
I (15%) lesions at the level of the forefoot, affecting
the metatarsophalangeal (MTP) and interphalangeal (IP)
joints.
II (40%) affecting the tarsometatarsal joint (TMT). Lis-
franc joint.
III (30%) affecting the cuneonavicular, talonavicular, and
calcaneocuboid joints. Chopart joint.
IV 10%) affecting the ankle joint.
V (5%) affecting th ecalcaneus.
According to the American Orthopedic Foot and Ankle
Society, an optimal manner of treating various lesions re-
ferred to as Charcot neuroarthropathy still evokes therapeutic
CYBUŁKA et al. : CHARCOT FOOT IN DIABETES AS A "SPECIAL NEEDS FOOT". EFFICIENT USE OF NPWT. 7
controversies. It is one of the two most often discussed
problems in this profession.18
The most common cause of Charcot osteoarthropathy is
diabetes mellitus. The most common location of lesions is
the foot. Unfortunately, in most cases, accurate diagnosis is
significantly delayed. In Pakarinen’s observation, the time
to accurate diagnosis was 29 weeks after emergence of first
symptoms [19]. In another study, the delay in diagnosis was
10 weeks.19
Appropriate treatment in advanced Charcot neuropathic
osteoarthropathy is still a great therapeutic challenge. One of
the available ways of Charcot foot treatment is an orthopedic
operation. During an open surgery, any possible dislocation
or subluxation of foot joints can be corrected. After reposi-
tioning of the joints, internal or external stabilization is used.
Inserting an implant into foot bones is considered by many
to be an unjustified practice.
In most cases, diabetic foot is treated conservatively. After
initial termination of the inflammatory process, necrotic and
ischaemic tissues are removed. Unfortunately, most cases of
complicated diabetic foot require more radical procedures. In
many patients, limbs need to be amputated below the level
of talocrural joint. Such surgeries are referred to as minor
amputations. Radical procedures at the level of the thigh or
shin are called major amputations.
An optimal management in cases of Charcot neuropathic
osteoarthropathy still evokes therapeutic controversies. Some
patients require an orthopedic intervention with the use of
bone connecting materials. A significant group of patients is
treated conservatively due to an increased risk of infectious
complications and coexistence of systemic complications of
diabetes. Any form of diabetic foot is a real threat to lower
limb amputation. A special case of diabetic neuropathy is
Charcot arthropathy. Deformation of the anatomy of the foot
and impairment of its functioning increase the risk of various
complications. Therefore, it is important to take early and
appropriate multidisciplinary care of a foot with ’special
needs’. In the above example, the immediate use of negative
pressure treatment protected the structure of the foot from
infection in Charcot arthropathy, as well as allowed for an
effective healing of the wound.
IV. CONCLUSIONS
As shown in the example above, the use of efficient
methods of negative pressure therapy can be a recommended
[2] J.-M. Charcot, “Sur quelques arthropathies qui paraissent dependre
d’une lesion du cerveau ou de la moelle epiniere,” Arch Physiol
Normale Pathol., vol. 1, pp. 161–178, 1868.
compromise between radical surgical treatment and conser-
vative, expectant management. In many cases, negative pres-
sure therapy inhibits further foot damage. Negative pressure
therapy does not, in any way, supersede other available
therapeutic possibilities but it remains the only effective
method of treatment for many patients.
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