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Fig. 25.5 Reconstruction of
a dorsomedial foot defect
using a neurotized free
fasciocutaneous ap from the
posterior calf (Medial Sural
Artery Perforator Flap)
E. Shiah et al.
Local aps for the medial ankle include the extensor hallicus longus, extensor digitorum longus, and peroneus tertius muscle aps [57]. Suitable options for defects of the
lateral ankle include the peroneus brevis, abductor digiti
minimi, and extensor digitorum brevis muscle aps, or the
supramalleolar and lateral calcaneus fasciocutaneous aps
[51, 56, 117–119]. Pedicled aps that can be used to recon-
struct either the medial or lateral ankle include the retrograde sural and the dorsalis pedis aps [60, 116, 120].
Similar to the dorsal foot for free-ap reconstruction, thinner aps such as the lateral arm, radial forearm, SCIP, and
parascapular and ALT free aps are frequently used. In
obese patients, fascial aps or muscle aps in combination
with skin grafts are more suitable.
25 Reconstruction oftheDiabetic Foot
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Fig. 25.6 Reconstruction of a large medial ankle defect after treatment
of a necrotizing soft tissue infection using a split thickness skin graft
471
Summary
Many reconstructive options exist for soft tissue defects
resulting from ulceration and deep-space infection, in the
diabetic foot. Prerequisites to successful reconstruction of
the diabetic foot include glycemic control, medical optimization, vascularization, nutrition, pressure ofoading, all in the
setting of a multidisciplinary limb preservation service.
From healing by secondary intention to free ap reconstruction, reconstructive options are numerous. Their choice
depends largely on patient factors, wherefore a custom,
patient-centric approach is preferred.
Acknowledgements The authors sincerely thank Dr. Natalie Pawlak,
Nimish Saxena, Frances R.Lara, and Shannon R.Garvey, who contributed to the research, writing, and revising of this chapter.
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The Charcot Foot inDiabetes
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LeeC.Rogers, StephanieN.Campbell,
andRobertG.Frykberg
26
Abstract
The Charcot Foot, although not exclusive to diabetes, is
indeed a major and life-changing lower extremity complication of the disease. A consequence of even subtle trauma
to those persons with peripheral neuropathy, this devastating complication all too often leads to signicant foot and
ankle deformities that place the foot at high risk for ulceration, infection, gangrene, and potential limb loss.
Fortunately, our understanding of the etiology and management of the Charcot foot has markedly improved since
its rst description in 1883. With improved recognition of
the underlying pathophysiology and inammatory underpinnings, our approaches to treatment have evolved as
well. While rest, ofoading, and immobilization remain
the mainstays of treatment in the early, active stages, specic pharmacological interventions have not been proven
effective in mitigating the course of the disease process.
Nonetheless, we now also recognize the importance
that surgical reconstruction plays in managing chronic
deformities or instability in preserving a functional foot
and limb.
Affecting literally hundreds of thousands of persons
with diabetes in the United States alone, the Charcot foot
is no longer considered to be a rare complication of the
disease. Indeed, the last several decades have seen a literal
explosion of reports of Charcot foot incidence and management strategies from every corner of the Globe. Most
importantly, with the improved understanding of this
entity, we now recognize that a high index of suspicion in
persons at risk is critical for making the diagnosis early—
and thereby preventing those limb-threatening deformities resulting from delayed diagnosis and management.
L. C. Rogers · S. N. Campbell
Department of Orthopaedics, University of Texas Health Science
Center at San Antonio, San Antonio, TX, USA
R. G. Frykberg (
College of Podiatric Medicine at Midwestern University,
Glendale, AZ, USA
*)
Introduction
The diabetic Charcot foot is a potentially limb-threatening
deformity associated with peripheral neuropathy and concomitant injury. Often, the precipitating injury is disproportionately minor and unrecognized due to the underlying
peripheral sensory neuropathy. Loss of protective sensation
by the neuropathic individual leads to repetitive trauma
with continued walking on the injured extremity causing
progressive inammation with varying degrees of bone and
joint injury. Severe deformity can ensue predisposing the
patient to ulceration, infection, and potential amputation.
Complications of this lower extremity deformity can further contribute to systemic health and social issues such as
weakness, loss of function, foot ulceration, serious infections, depression, nancial burden, and extended periods of
disability or unemployment. It is therefore critical to diagnose this condition early to prevent progressive foot or
ankle deformity and instability. This chapter reviews the
etiology, diagnostic methods, and various treatment options
for both active and inactive diabetic Charcot arthropathy of
the foot and ankle.
The Charcot foot is a devastating, but oftentimes preventable, complication of diabetes with peripheral neuropathy. It
is named after Jean-Martin Charcot (1825–1893), a French
neurologist who rst described the joint disease associated
with tabes dorsalis and named it “arthropathy of locomotor
ataxia” [1]. In 1881, J.-M.Charcot presented his ndings at
the Seventh International Medical Congress in London
which was attended by many acclaimed physicians of the
era. During this meeting, the eponym “Charcot’s disease”
was designated by Sir James Paget describing degenerative
neuropathic changes in bones and joints [1–3]. Although
W.Musgrave in 1703 and later J.K.Mitchell in 1831 ostensibly described osteoarthropathy associated with venereal
disease and spinal cord lesions, respectively, Charcot’s name
remains synonymous with neuropathic arthropathies regardless of etiology [4]. Comprehensively, the pathology for
active disease requires an inammatory storm with
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A. Veves et al. (eds.), The Diabetic Foot, Contemporary Diabetes, https://doi.org/10.1007/978-3-031-55715-6_26
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L. C. Rogers et al.
neuropathy [3]. The condition has several synonyms including Charcot joint disease, Charcot arthropathy, Charcot syndrome, neuroarthropathy, osteoarthropathy, and derivations
or combinations thereof.
In 1936, W.R.Jordan was the rst to fully recognize and
report on the association of neuropathic arthropathy with
diabetes mellitus in the archives of internal medicine [5, 6].
In Jordan’s comprehensive review of the neuritic manifestations of diabetes, he presented on a case of a 56-year-old
woman with diabetes for approximately 14years who presented with “a rather typical, painless Charcot joint of the
ankle.” His description typies the classic presentation now
commonly recognized in patients with long-standing diabetes and neuropathy with fracture or dislocation deformity.
Subsequently, Bailey and Root in their 1947 series noted
that 1 in 1100 patients with diabetes mellitus developed
neurogenic osteoarthropathy [6]. In the classic 1972 Joslin
Clinic review of 68,000 patients by Sinha etal., 101 patients
were encountered with diabetic Charcot foot [7]. This ratio
of 1in 680 patients with diabetes and Charcot foot brought
greater attention to the disorder and characterized the
affected patients’ clinical and radiographic presentations. In
the subsequent decades, there has been a signicant increase
in the number of reports on diabetic neuroarthropathy and
its complications and management [5–10]. The reported
prevalence of this condition is highly variable, ranging from
0.15% of all diabetic patients to as high as 29% in a population of patients with diabetes and neuropathy [2, 7, 10, 11].
As such, neuropathy is considered a driving predictive factor for the development of Charcot arthropathy. A prospective study of a large group of patients with diabetes from the
University of Texas reported an annual incidence of 8.5 per
1000 people. Neuroarthropathy was signicantly more common in Caucasians than in Mexican Americans (11.7/1000
vs. 6.4/1000) [12]. While this study may give us better
insight into the true frequency of neuroarthropathy in diabetes, much of the data we currently rely upon is based upon
retrospective studies of small single center cohorts.
Nonetheless, the incidence of Charcot foot cases reported is
very likely an underestimation since many cases go undetected, especially in the early stages, patients newly or undiagnosed with diabetes, and minorities, and cases that receive
early appropriate treatment may never be formally diagnosed if the natural history is interrupted [2, 8, 11]. The frequency of diagnosis of Charcot foot appears to be increasing
as a result of increased awareness of its signs and symptoms
and increased screening tools by family medicine, endocrinology, and podiatric medicine [13]. Although the original
descriptions of neuropathic osteoarthropathy were attributed to patients with tertiary syphilis, diabetes mellitus has
now become the disease most often associated with this progressive foot disorder and deformity. Not only are patients
with Charcot foot deformities at greater risk of amputation
than those with neuropathic ulcers but without Charcot foot,
but a study from the UK has associated higher mortality
rates [14, 15]. While the power of this study did not allow
for signicant differences to emerge, it does conrm the
need for larger population- based study to fully elucidate the
epidemiology of this limb- threatening complication.
Overall, the 4- or 5-year relative mortality rate is 28–45% in
those with diabetes-related Charcot foot [14, 15]. van Baal
etal. reported median life expectancy of someone diagnosed
with acute Charcot foot is 7.88years in the UK.Furthermore,
life expectancy was reduced by approximately 14years in
this studied cohort [16].
Etiology andPathogenesis
Charcot foot can be dened as a noninfectious and progressive condition of single or multiple joints characterized by
pathologic fractures, joint dislocation of the foot or ankle,
and severe destruction of the pedal architecture which is
closely associated with peripheral neuropathy [2, 8]. Almost
uniformly, trauma of some degree superimposed on the neuropathic extremity precipitates the cascade of events leading
to bone and joint destruction. Neuroarthropathy, therefore,
may result in debilitating deformity, subsequent ulceration,
and limb amputation [17, 18]. Peripheral neuropathy can be
attributed to various disorders, potentiating Charcot foot.
Nevertheless, inciting factors for Charcot neuroarthropathy
can be associated with direct trauma, crush injury,
medication- induced neuropathy, peripheral neuropathy secondary to chemotherapy, or idiopathic neuropathy.
There are several conditions producing radiographic
changes similar to Charcot joints. These include acute
arthritides, psoriatic arthritis, osteoarthritis, osteomyelitis,
osseous tumors, and gouty arthritis. These joint manifestations, in the presence of neuropathy, make the correct diagnosis even more difcult to ascertain [7]. Nonetheless, the
characteristics of the joint changes, site for predilection, and
clinical correlation assist in determining the true underlying
diagnosis. The primary risk factors for this potentially limbthreatening deformity are the presence of dense peripheral
neuropathy, normal circulation or augmented local blood
ow, chronic inammation, and a history of preceding
trauma, often minor in nature and potentially unnoticed [17,
19]. There is no apparent predilection for either sex [2].
Trauma is not necessarily limited to typical injuries such as
sprains, contusions, or fractures. Foot deformities, prior
amputations, and joint infections may result in sufcient
stress that can lead to arthropathy. Likewise, foot surgery in
a patient with neuropathy can result in enough trauma and
spark a Charcot event [20]. Renal and pancreatic transplantation have also been implicated as an inciting event leading
to the development of a Charcot foot [21, 22]. Although the
26 The Charcot Foot inDiabetes
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exact pathogenesis may vary from patient to patient, it is
undoubtedly multifactorial in nature [19, 23]. The neuro-
traumatic (German) theory of Charcot foot has traditionally
been proposed as the primary etiology of osteoarthropathy
in which neuropathy and repeated trauma produce eventual
joint destruction and subsequent pedal collapse. The loss or
diminution of protective sensation allows repetitive microor macrotrauma producing intracapsular effusions, ligamentous laxity, and therefore joint instability with subluxation
or dislocation of single but, more commonly, multiple joints.
With continued use of the injured extremity, further degeneration ensues and eventually results in a Charcot event—a
foot with bone and joint breakdown. Underlying sensory
neuropathy resulting from any disorder is therefore a prerequisite under this theory of pathogenesis. However, the
neuro- traumatic theory does not explain all accounts of
Charcot arthropathy, especially its occurrence in bedridden
patients [2, 8, 17].
The neurovascular reex (French) theory, in contrast, pro-
poses that autonomic neuropathy directly increases peripheral blood ow leading to hyperemic bone resorption with
the washing away of bone minerals and contribution to
Charcot neuroarthropathy [24]. This theory might more
closely correspond to Charcot’s original hypothesis of a central “nutritional” defect, although we now recognize this process as a peripheral nerve disorder. Autonomic neuropathy
and endothelial dysfunction results in an impairment of vascular smooth muscle tone and consequently produces a vasodilatory condition in the small arteries of the distal extremities
[25, 26]. Impairment of neurogenic vascular responses in
patients with diabetic neuropathy supports one study that
consequently also showed preserved maximal hyperemic
responses to cutaneous heating in patients with Charcot
arthropathy [25, 27]. In concert with associated arteriovenous shunting, there is a demonstrable increase in bone vascularity in the neuropathic limb. The resultant osteolysis,
demineralization, and weakening of the bone factor in the
development of Charcot foot [2, 24, 27–30]. Several studies
have demonstrated that reduced bone mineral density primes
an apparent imbalance between the normally linked bone
resorption and bone production in patients with osteoarthropathy [30–32]. Specically, greater osteoclastic activity
has been noted in acute stage neuroarthropathy, suggesting
an explanation for the excessive bone resorption by the comparably downregulated osteoblastic activity [25, 30].
The modern understanding of the actual pathogenesis of
Charcot arthropathy is a combined effect of both the neurotraumatic and neurovascular theories [19, 29, 33]. It is gener-
ally accepted that trauma superimposed on a well-perfused
but densely neuropathic extremity can precipitate the development of an active Charcot joint. Approximately 50% of
those with Charcot foot recall some incipient trauma [34].
But the presence of sensory neuropathy can render the patient
unaware of the initial trauma, and often profound osseous
destruction takes place during continued ambulation, a process that can occur in a few days to weeks. The concomitant
autonomic neuropathy with its associated osteopenia and
relative weakness of the bone predisposes it to fracture [25,
31]. A vicious cycle then ensues where the insensate patient
continues to walk on the injured foot, causing further damage [9]. With added trauma and fractures in the face of an
abundant hyperemic response to injury, marked inammation and edema soon follow. Subsequently, capsular and ligamentous distension or rupture leads to the typical joint
subluxations and loss of normal pedal architecture culminating in the classic rocker-bottom foot deformity. The degree
of joint destruction and resultant deformity is highly dependent upon the time at which the proper diagnosis is made and
when ofoading and immobilization begin [9]. A simplied
cycle of the pathogenesis of Charcot foot development is
illustrated in Fig.26.1.
Tightening of the posterior leg muscle group and equinus
contracture may play a special role in the development of the
Charcot midfoot deformity. The Achilles tendon in Charcot
foot patients is morphologically different than diseasematched controls [35, 36]. The pull of the tendon on the calcaneus directly increases the forces resulting in subluxation
or dislocation at the midfoot joints (Fig.26.2).
Often it is a fracture, either intra-articular or extraarticular, which initiates the destructive process. This had not
been fully appreciated until Johnson presented a series of
cases in which diabetic patients developed typical Charcot
joints after sustaining neuropathic fractures [37].
Additionally, amputation of the great toe or rst ray, often a
consequence of infection or gangrene in the diabetic patient,
may lead to neuropathic joint changes in the lesser metatarsophalangeal (MTP) joints and tarsometatarsal (TMT) joints.
Presumably, this is a stress-related factor secondary to an
acquired biomechanical imbalance. Intra-articular infection
can also be implicated as an inciting event leading to this
endpoint. In effect, almost any inammatory or destructive
process introduced to a neuropathic joint has the potential for
creating inciting the Charcot process. Herbst etal. reported
their ndings concerning the type of presentation as related
to patients’ bone mineral density (BMD) [38]. They found
that patients with normal BMD had typical changes in the
midfoot primarily consisting of joint dislocations. However,
in those patients with reduced BMD, fracture patterns predominated in the ankle and forefoot [38].
Several authors have noted the similarities between the
acute destructive phase in Charcot arthropathy and complex
regional pain syndrome (CRPS), known previously as reex
sympathetic dystrophy [25, 26, 39]. Both conditions are
associated with an exaggerated vascular response and the
development of osteopenia. Both can also be related to previous acute trauma. While the underlying pathophysiological
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Fig. 26.1 Pathogenic cycle
of diabetic neuroarthropathy
L. C. Rogers et al.
Fig. 26.2 The contribution of
the Achilles tendon and
Charcot foot equinus
deformity
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