|Year : 2021 | Volume
| Issue : 1 | Page : 10-17
Charcot foot – current concepts
Gautam Kumar, Rajesh Simon, Dennis P Jose
Department of Orthopaedics, VPS Lakeshore Hospital, Kochi, Kerala, India
|Date of Submission||01-Jun-2021|
|Date of Acceptance||01-Jun-2021|
|Date of Web Publication||25-Jul-2021|
Department of Orthopaedics, VPS Lakeshore Hospital, Kochi - 682 040, Kerala
Source of Support: None, Conflict of Interest: None
Charcot neuropathic osteoarthropathy (CNO) is painless, progressive, noninfectious, degenerative arthropathy affecting single or multiple joints and soft tissues of foot and ankle caused by an underlying neurological deficit. The primary indication for surgical correction is a nonbraceble, nonplantigrade foot, instability, and impending or established ulceration. The goal of surgical management is to provide a stable, ulcer-free, plantigrade foot that can accommodate therapeutic footwear for self-ambulation. The choice of implants in midfoot CNO can be a combination of plate and screws well beyond the area of deformity to achieve rigid stability and good alignment following the principle of a super construct. The deformities involving the talus and ankle joint require a Total contact casting (TCC) arthrodesis, preferably with an intramedullary nail. The choices for soft tissue coverage as an additional procedure for ulcer management are guided by anatomic location, size, depth of ulcer, condition of surrounding soft tissue, and underlying deformity.
Keywords: Calcaneal pitch, Charcot foot, Charcot neuropathic osteoarthropathy, cuboid height, Meary's angle, rocker bottom-type deformity, super construct
|How to cite this article:|
Kumar G, Simon R, Jose DP. Charcot foot – current concepts. J Orthop Assoc South Indian States 2021;18:10-7
| Introduction|| |
Charcot neuropathic osteoarthropathy (CNO), more commonly referred to as Charcot's foot, was first described by Sir William Musgrave in 1703. In 1883 Jean-Martin Charcot described the neuropathic foot as the “pied tabatique,” now named Charcot's foot after him. CNO is defined as relatively painless, progressive, noninfectious, degenerative arthropathy affecting single or multiple joints and soft tissues of the foot and ankle caused by an underlying neurological deficit.
| Pathophysiology|| |
CNO is an infrequent but significant musculoskeletal sequela of diabetes that ends up in varying degree of destruction and deformity. The Charcot foot in the Diabetic population varies from 0.1% to 7.5%, but its estimated incidence sharply increases to 9.8%–16% in diabetic patients with peripheral neuropathy though no comprehensive epidemiological studies have been performed to date. Different theories have been advocated based on macroscopic or molecular levels, but there is still no consensus on the exact pathogenesis. The macroscopic theories include neuro-vascular theory, neuro-traumatic theory. The molecular pathways advocated include oxidative stress pathway, advanced glycation of end products (AGE)/Receptor of AGE (RAGE) pathway receptor activator of nuclear factor κβ ligand (RANKL)/Osteoprotegerin (OPG) pathway.
Charcot first advocated the neuro-vascular theory based on the hypothesis that a state of hyperemia generated from overactive vaso-autonomic neuropathy leading to increased capillary leakage culminating in high intercompartmental pressure and deep tissue ischemia. The increased blood flow is proposed to deliver osteoclast and monocyte at the site, leading to increased bone resorption. The relatively low incidence of CNO in diabetics suffering from peripheral artery disease supports this theory. Virchow proposed the neuro-traumatic theory based on the release of proinflammatory products posttrauma in the absence of a protective mechanism. But it does not explain other changes.
| Molecular Theories|| |
The oxidative stress and AGE pathway focus on the local dysregulation of the immune-inflammatory process, where oxidative stress leads to the subsequent production of reactive oxygen species (ROS) formation. The ROS further generate AGE via sequential oxidative reactions. The AGEs are formed by nonenzymatic reactions between glucose and glycating compounds with proteins. The elevated AGEs promote irreversible posttranslational modification of both intra and extracellular proteins. This modification renders these proteins ineffective. The increased AGEs then bind to RAGE, further accelerate ROS production. The accelerated ROS production activates NF-κβ activity and the generation of proinflammatory cytokines, including interleukin-1, tumor necrosis factor α (TNF-α), transforming growth factor. The (RANKL) is a member of the TNF superfamily. OPG) is a competitive protein of RANKL and antagonizes the pathway. This systemic is a key mediator of metabolism and has been used to evaluate the osteoclast and osteolytic activity. The increased levels of AGEs, ROS, and proinflammatory cytokines enhance the expression of RANKL. The increased activity of RANKL stimulates the synthesis of NF-κβ that stimulates the maturation of osteoclast from osteoclast precursor cells, leading to local osteolysis.
| Clinical Presentation|| |
The CNO has an active phase and resolution phase with or without deformity. Minor trauma may precede clinical events. The acute stage usually presents with unilateral erythema [Figure 1]a, edema, raised skin temperature (>2°C) compared to the contralateral foot. There is an absence of fever with normal or slightly raised erythrocyte sedimentation rate (ESR) and C reactive protein (CRP) levels. If there are ulcers or fever associated, we have to consider other possibilities like cellulitis or osteomyelitis, but these symptoms may also occur in CNO'.
|Figure 1: Active stage of Charcot – (a) Clinical Picture-warm erythematous swollen foot (b) Radiograph-Fragmentation and resorption of distal tibia, fibula, talus, and proximal part of calcaneum|
Click here to view
It commonly involves the midfoot but forefoot and hindfoot involvement is also prevalent. The diminished vibratory and proprioceptive sensation and dry skin are important clinical findings that need to be noted. It shows rapid progression, bone and joint destruction [Figure 1]b may happen within days or weeks.
The chronic CNO loses warmth and redness, while edema may persist. Joint deformity, including subluxation and dislocation, may lead to rocker bottom-type deformity [Figure 2]a. There is flattening of the arch with characteristic ulceration beneath the bony protuberance due to displacement of midtarsal bone [Figure 2]b. The neuropathic deformed foot is prone to abnormal pressure distribution, making them vulnerable to excessive callus formation, blisters, and ulcers. The ulceration further predisposes to secondary infections such as abscess, osteomyelitis, and cellulitis. The differential diagnosis includes infection (cellulitis, septic arthritis, osteomyelitis), inflammation (gout).
|Figure 2: Rocker bottom deformity in Chronic stage (a) clinical picture (b) radiological image role of investigations in diagnosis|
Click here to view
The plain radiograph of foot and ankle is the initial screening modality in suspected CNO. Radiographs provide useful information regarding the anatomy, which may be helpful for the interpretation of other modalities, differential diagnosis, and it may serve as a control for further follow-up. The classical radiographic description of CNO can be summarised as 6 D's: Preserved bone density, joint distention, bony debris, dislocation, disorganisation and destruction of joint. The bone density is usually normal except in the case of the elderly or type I diabetes mellitus. Most of the patients who have effusion will show distended joints in the radiograph. Those presenting in later stages will show debris localized or away from the site due to destruction. In disorganization of the joint, the destruction of cartilage precedes that of bone.
The radiograph views that help us in making a diagnosis include anteroposterior (AP), oblique and lateral views of the foot, and AP view of the ankle. The plain radiograph can be helpful to have a good view of calcaneal pitch [Figure 3], Tarsometatarsal joint, Meary's angle [Figure 4], cuboid height [Figure 5], and callus [Figure 6].
|Figure 3: (a) Calcaneal pitch – normal (b) reduced calcaneal pitch in Charcot neuropathic osteoarthropathy (c) correction of calcaneal pitch after midfoot arthrodesis|
Click here to view
|Figure 4: (a) Meary's angle – normal (b) increased Meary's angle in Charcot neuropathic osteoarthropathy (c) correction of Meary's angle after midfoot arthrodesis|
Click here to view
|Figure 5: (a) Cuboid height – (a) positive – normal (b) negative – rocker bottom Charcot neuropathic osteoarthropathy foot|
Click here to view
| Classifications|| |
The classifications used for CNO were based on a plain radiograph that includes Sanders and Frykberg, Brodsky, and Eichenholtz classification. The classification of Sanders-Frykberg and Brodsky et al. was based on the anatomic location of foot and ankle joints involved. The Eichholtz classification [Table 1] is based on the pathophysiological progression of disease that can be assessed on plain radiograph. The initial classification described in 1966 included 3 stages based on the stages of fragmentation, coalescence, and remodeling of the bone. Stage 0 was added in due course to include those cases with radiographic changes that were minimal or absent, but clinical features were suggestive. It was further modified by Mautone and Naidoo to include the clinical features in it. Eichholtz classification has some limitations even after modifications due to the use of radiographs as their base. They do not cover the whole spectrum of CNO, fail to diagnose bone edema, fracture in the early stages of the disease, and fail to diagnose between early active and healed inactive stage.
The plain radiograph has been useful to diagnose, but often they fail to diagnose the disease at earlier stages, so magnetic resonance imaging (MRI) and nuclear scans have been tried to overcome this limitation. MRI has been known for its ability to describe anatomical and pathological details of soft tissue, bone marrow, and ligaments in greater detail compared to other investigational modalities. The MRI protocols may be optimized for the case-to-case basis that usually involves a small field of view of 16–18 cm with thin sections of 3 mm to optimize spatial resolution. The sagittal views have been found better to evaluate the midfoot and posterior calcaneum, while axial and coronal views are found more suitable for evaluating ankle and surrounding tendons.
In the acute CNO, a conventional radiograph may appear normal, but in the early phase, MRI shows subchondral bone edema that may or may not be associated with microfractures, while in the advanced stage, MRI shows soft-tissue edema along with bone marrow edema along with joint effusion. An MRI-based classification [Table 2] has been advocated by Chantelau and Grützner. The main limitation of MRI to be used for diagnosis of CNO is difficulty in discriminating it from acute osteomyelitis, which has quite similar features.
Nuclear scans have been advocated to overcome the lacunae of the MRI for diagnosis of CNO in the early stages. Technetium 99-methylene diphosphate is highly sensitive, approaching 100% but suffers from poor specificity of around 40% compared to MRI. Indium 111 scans and F-18 FDG scans have also been advocated, but their superiority over MRI has not been confirmed yet. Nuclear scans are a promising investigation whose role in differential diagnosis and CNO management will be clearer in the near future.
| Differential Diagnosis|| |
It is difficult to differentiate based on MRI or radiograph. The clinical picture and the blood parameters such as ESR, CRP, and total white blood cell (WBC) count can serve as guidance. If an ulcer is present, those with a pink base, less or no pain, and with a warm foot with good pulse suggest more towards CNO, while painful ulcers having a grey/yellow base with reduced pulsation and cool foot are more likely to be infective in origin. The indium (In-111) scan is positive in the case of CNO and negative in infections, while the technetium (Tc-99) is inconclusive [Table 3].
|Table 3: Description of different modalities of treatment for Charcot neuropathic osteoarthropathy (CNO)|
Click here to view
Constitutional symptoms such as fever, malaise with markedly raised ESR, CRP, WBC count with warm, tender, and swollen foot are suggestive of cellulitis. We can differentiate it with the help of bedside clinical examination. When we keep the limb elevated for few minutes, there is reduced erythema in cellulitis while it remains unchanged in the case of C CNO. Although this test is not very specific, in our clinical practice, we found this bedside test to be quite helpful (check for the literature).
| Management|| |
The studies conducted with bisphosphonates show mixed bag results,, with some supporting the early resolution of disease and symptoms while others were disapproving of any additional benefits. Intranasal calcitonin has been found to reduce the bone turnover in CNO, but long-term overall benefits are still not clear. Denosumab has been one of the promising agents, and the study has reported early fracture healing with the use of a single dose of 60 mg.
Orthosis and cast
Total contact casting (TCC) is currently the mainstay of treatment for CNO. It reduces plantar pressures along with the redistribution of weight-bearing forces over a wider surface area. The compliance also increases, but some patients may not like it because of multiple applications needed till the period of developmental stage (Eichholtz Stage I) is complete and radiographic evidence of Stage II is visible.
The Charcot restraint orthotic walker (CROW) is a customized AFO prescribed for distal sensory neuropathy. The CROW [Figure 7] is a bivalve orthosis lined with perforated Plastazote® to assist in ventilation. It can be applied in Stage I as an alternate to TCC. It is highly useful in those where frequent wound dressing is needed and post arthrodesis ambulation.
Patellar tendon bearing braces (PTBB) is used to redistribute the weight-bearing forces from foot and ankle to patellar tendon. The PTBB reduces the peak force by around 32%–90%, especially more from hindfoot compared to forefoot and midfoot.
The surgical management has evolved with the better understanding of biomechanics and the pathophysiology of the disease. Debridement, osteotomies, ostectomies, and corrective arthrodesis help in salvaging the CNO which otherwise would have ended in amputation.
The simplest method of ulcer management involves ulcer excision with or without exostectomy with primary closure of the wound, but most of the time, it is inadequate. In the case of a patient with Charcot neuropathy, the presence of osteomyelitis and deformity adds an extra layer of difficulty in management. The goal of ulcer management is to manage the etiology rather than the presentation.
The plantar bony prominences due to tarsal bones displacement into nonanatomic position lead to bony exostosis may end up as nonhealing ulcer. Nonanatomical position of displaced lead to difficult accommodation in orthotics and modified footwear. If the deformity is stable, exostectomy is an acceptable surgical practice. The exostectomy can be performed either using the direct or indirect surgical method. In the case of the direct method, the bony prominence excision with soft tissue management is done with a single incision directly over the exostosis. In the indirect method, we use two separate incisions, the first one for the ulcer removal and a separate incision for the exostosis removal to prevent contamination. In most cases, ulcers reach down to the exostosis, so the direct method is the preferred one.
Dead space management
The management of potential dead space created due to bone destruction and removal of infected or devascularized tissue is still evolving. Allografts had poor outcome as compared to autografts in CNO. It is preferrable not to use bone substitutes such as G bone® or bone cement as fillers for the dead space.
Soft tissue procedures
Wound debridement allows the full inspection of the wound, removes the nonviable soft tissue, and stimulates the wound healing. The choices for soft tissue coverage as an additional procedure for ulcer management are guided by anatomic location, size, depth of ulcer, condition of surrounding soft tissue, and underlying deformity. The prerequisite for any additional procedure is to make sure that infection has been adequately addressed before the additional procedure is planned. The choices available based on the modified reconstructive soft tissue pyramid include primary or delayed closure, ortho biologics, negative pressure wound therapy (NPWT), autologous skin grafting, local flaps, muscle flaps, pedicle flaps, perforator flaps, and free flaps. NPWT is beneficial to those wounds with adequate perfusion. The NPWT [Figure 8] reduces the requirement of frequent dressing change and supports healthy granulation and preparation of the wound for skin grafting.
|Figure 8: Negative pressure wound therapy applied on the wound over the dorsum aspect of Charcot neuropathic osteoarthropathy foot|
Click here to view
Role of the external fixators
The multiplanar external fixators most commonly employed with 3 level static ring fixators for deformity correction, correcting the leg length discrepancy, and wound management in case of infected ulcers. Once the deformity is corrected, the pins are still kept in position to maintain the correction. The fine wires are rarely replaced, even in pin tract infection, as the infection regresses once the implants are removed.
Deformity correction and stabilization surgeries
The goal of surgical management is to provide a stable, ulcer-free, plantigrade foot that can accommodate therapeutic footwear and help in the self-ambulation of the patient. Indications for arthrodesis include nonplantigrade foot, instability, impending or established ulceration, a deformity that cannot accommodate the footwear. Contraindications for arthrodesis include active infection or osteomyelitis and the acute phase of the disease.
The axial loading leads to flattening of medial and lateral longitudinal arches in CNO foot, leading to the multiplanar deformity. The associated neuropathy and metabolic bone diseases in the case of CNO foot, we need a robust construct to counter the severe stress encountered as a result. The choice of implants has been surgeons' preference based on the deformity and experience with no ideal implants established till now. The commonly used implants have been 6 or 6.5 mm screws of various length, 3.5 mm locking plates, 2.7 mm variable angle plates, or a combination of the above. The solid intramedullary (IM) 6.5 mm bolts or beam screws [Figure 9] were designed to withstand higher load demands during the weight-bearing in the CNO patients.
The study done by Richter et al. reported that the use of standalone beam screws for midfoot arthrodesis has shown to have high union rates of around 98%, with delayed wound healing (21%) and recurrent ulceration (13%) being the most common complication. The studies, have shown that the use of locking or variable angle plates with locking screws for arthrodesis have shown union rates of 97%–100%. The complications associated include more extensive soft tissue dissection. The concept of super construct was mooted as the idea to use a combination of plate and screws [Figure 10] well beyond the area of deformity, providing rigid stability and good anatomic alignment. The medial column arthrodesis is done with locking plates on the medial aspect, usually reinforced with an additional plate on the plantar aspect to provide a more robust fixation.
|Figure 10: An example of super construct to stabilize the midfoot (a) – Anteroposterior (b) – Oblique (c) – Lateral view. Medial column fused with 6 hole 3.5 mm locking plate and supported by 5 hole 2.7 mm variable angle plate from the plantar aspect. Lateral column stabilized with 6 hole 3.5 mm locking plate. Subtalar joint fused with 6 mm cannulated cancellous screw|
Click here to view
If the surgeon prefers to use IM screws for arthrodesis, the maximum diameter accommodated by the particular bone should be used. The deformity is corrected and stabilized with large bore IM screws. The screws are introduced in a retrograde manner to build the column and correct the deformity in the sagittal and axial plane. The standalone fixation of the medial column had unacceptable revision rates, so arthrodesis should include both medial and lateral column of the foot. The subtalar arthrodesis is recommended along with midfoot stabilization. theoretically. It is postulated that the subtalar fusion eliminates the frontal plane motion, thus reducing the effect of supinator and pronator lever arms across the newly stabilized medial column.
The deformities of CNO neuropathy may include varus/valgus, rotation deformities, and various degrees of associated shortening due to collapse of talus or calcaneum secondary to avascular necrosis or neuropathic fracture. Traditionally surgery in CNO is delayed till the inactive (consolidation) stage of CNO in neuropathy is reached, but in ankle joints with nonbraceble deformity, instability, and high risk of ulcer predisposition, early surgical intervention is warranted. If there is only isolated involvement of subtalar or transverse talar joints (calcaneonavicular, calcaneocuboid), then triple arthrodesis should suffice. The deformities involving the talus and ankle joint require a talotibiocalcaneal (TTC) arthrodesis. IM nails [Figure 11] being the load-sharing device with less soft tissue stripping, are preferred for TTC arthrodesis.
|Figure 11: Tibiotalocalcaneal arthrodesis done using intramedullary nail|
Click here to view
The infected CNO foot especially those with ulcers carry a higher risk for amputation. The data with regards to anatomic location of surgically treated CNO in relation to amputation and mortality rates is limited. The better understanding of the pathophysiology and better management infection with surgical correction of the deformity has led to improvement in the major amputation rates over the years.
The patient should be put on a short leg cast with nonweight bearing till radiological healing of bone is observed. Once satisfactory healing is achieved, we can start with protected weight-bearing in CROW. Once the lymphedema and swelling subside, patients can be prescribed customised shoes and footwear.
| Conclusion|| |
CNO is painless, progressive, noninfectious, degenerative arthropathy affecting single or multiple joints and soft tissues of foot and ankle caused by an underlying neurological deficit. The goal of surgical management is to provide a stable, ulcer-free, plantigrade foot that can accommodate therapeutic footwear for self-ambulation. The choice of implants in midfoot CNO can be a combination of plate and screws well beyond the area of deformity to achieve rigid stability and good alignment following the principle of a super construct, while deformities involving the talus and ankle joint require a tibiotalocalcaneal (TCC) arthrodesis, preferably with an IM nail.
The study was performed in accordance with the highest ethical standards.
Informed consent: The informed consent was obtained from the patient for using their clinical data and pictures for publication.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Charcot JM, Fe ´re ´ C. Affections osseuses et articulaires du pied chez les tabe ´tiques (pied tabe ´tique). Arch Neurol 1883;6:305-19.
Rogers LC, Frykberg RG, Armstrong DG, Boulton AJ, Edmonds M, Van GH, et al.
The Charcot foot in diabetes. J Am Podiatr Med Assoc 2011;101:437-46.
Schoots IG, Slim FJ, Busch-Westbroek TE, Maas M. Neuro-osteoarthropathy of the foot-radiologist: Friend or foe? Semin Musculoskelet Radiol 2010;14:365-76.
Salini D, Harish K, Minnie P, Sundaram KR, Arun B, Sandya CJ, et al.
Prevalence of charcot arthropathy in type 2 diabetes patients aged over 50 years with severe peripheral neuropathy: A retrospective study in a tertiary care south Indian hospital. Indian J Endocrinol Metab 2018;22:107-11.
Strotman PK, Reif TJ, Pinzur MS. Charcot arthropathy of the foot and ankle. Foot Ankle Int 2016;37:1255-63.
Chisholm KA, Gilchrist JM. The Charcot joint: A modern neurologic perspective. J Clin Neuromuscul Dis 2011;13:1-3.
Chantelau E, Onvlee GJ. Charcot foot in diabetes: Farewell to the neurotrophic theory. Horm Metab Res 2006;38:361-7.
Paul RG, Bailey AJ. Glycation of collagen: The basis of its central role in the late complications of ageing and diabetes. Int J Biochem Cell Biol 1996;28:1297-310.
Katayama Y, Akatsu T, Yamamoto M, Kugai N, Nagata N. Role of nonenzymatic glycosylation of type I collagen in diabetic osteopenia. J Bone Miner Res 1996;11:931-7.
Ndip A, Williams A, Jude EB, Serracino-Inglott F, Richardson S, Smyth JV, et al.
The RANKL/RANK/OPG signaling pathway mediates medial arterial calcification in diabetic Charcot neuroarthropathy. Diabetes 2011;60:2187-96.
Mabilleau G, Petrova NL, Edmonds ME, Sabokbar A. Increased osteoclastic activity in acute Charcot's osteoarthropathy: The role of receptor activator of nuclear factor-kappaB ligand. Diabetologia 2008;51:1035-40.
Petrova NL, Moniz C, Elias DA, Buxton-Thomas M, Bates M, Edmonds ME. Is there a systemic inflammatory response in the acute charcot foot? Diabetes Care 2007;30:997-8.
Ledbetter LN, Salzman KL, Sanders RK, Shah LM. Spinal neuroarthropathy: Pathophysiology, clinical and imaging features, and differential diagnosis. Radiographics 2016;36:783-99.
Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR. The natural history of acute Charcot's arthropathy in a diabetic foot specialty clinic. Diabet Med 1997;14:357-63.
Sanders L, Frykberg R. Diabetic neuropathic osteoarthropathy: The Charcot foot. In: Frykberg R, editor. The High Risk Foot in Diabetes Mellitus. New York: Churchill Livingstone; 1991. p. 297-338.
Brodsky JW. The diabetic foot. In: Coughlin MJ, Mann RA, Saltzman CL, editors. Surgery of the Foot and Ankle. 8th
ed. St Louis, MO, USA: Mosby; 2007. p. 1281-368.
Eichenholtz SN. Charcot Joints. Springfield, Illinois: Thomas CC; 1966. p. 111.
Shibata T, Tada K, Hashizume C. The results of arthrodesis of the ankle for leprotic neuroarthropathy. J Bone Joint Surg Am 1990;72:749-56.
Mautone M, Naidoo P. What the radiologist needs to know about C harcot foot. J Med Imaging Radiat Oncol 2015;59:395-402.
Siriwanarangsun P, Bae WC, Statum S, Chung CB. Advanced MRI Techniques for the Ankle. AJR Am J Roentgenol 2017;209:511-24.
Rosskopf AB, Loupatatzis C, Pfirrmann CW, Böni T, Berli MC. The Charcot foot: A pictorial review. Insights Imaging 2019;10:1-3.
Chantelau EA, Grützner G. Is the Eichenholtz classification still valid for the diabetic Charcot foot? Swiss Med Wkly 2014;144:w13948.
Petrova NL, Edmonds ME. Charcot neuro-osteoarthrop- athy – Current standards. Diabetes Metab Res Rev 2008;24 Suppl 1:S58-61.
Baglioni P, Malik M, Okosieme OE. Acute Charcot foot. BMJ 2012;344:e1397.
Jude EB, Selby PL, Burgess J, Lilleystone P, Mawer EB, Page SR, et al.
Bisphosphonates in the treatment of Charcot neuroarthropathy: A double-blind randomised controlled trial. Diabetologia 2001;44:2032-7.
Pakarinen TK, Laine HJ, Mäenpää H, Mattila P, Lahtela J. The effect of zoledronic acid on the clinical resolution of Charcot neuroarthropathy: A pilot randomised controlled trial. Diabetes Care 2011;34:1514-6.
Bem R, Jirkovská A, Fejfarová V, Skibová J, Jude EB. Intranasal calcitonin in the treatment of acute Charcot neuroosteoarthropathy: A randomised controlled trial. Diabetes Care 2006;29:1392-4.
Armstrong DG, Lavery LA, Wu S, Boulton AJ. Evaluation of removable and irremovable cast walkers in the healing of diabetic foot wounds: A randomized controlled trial. Diabetes Care 2005;28:551-4.
Pollo FE, Brodsky JW, Crenshaw SJ, Kirksey C. Plantar pressures in fiberglass total contact casts vs. a new diabetic walking boot. Foot Ankle Int 2003;24:45-9.
Morgan JM, Biehl WC 3rd, Wagner FW Jr. Management of neuropathic arthropathy with the Charcot Restraint Orthotic Walker. Clin Orthop. 1993;296:58-63.
Kummen I, Phyo P, Kavarthapu V. Charcot foot reconstruction – How do hardware failure and non-union affect the clinical outcomes?. Ann Joint 2020;5:25.
Busch-Westbroek TE, Delpeut K, Balm R, Bus SA, Schepers T, Peters EJ, et al.
Effect of single dose of RANKL antibody treatment on acute charcot neuro-osteoarthropathy of the foot. Diabetes Care 2018;41:e21-2.
Capobianco CM, Zgonis T. Soft tissue reconstruction pyramid for the diabetic charcot foot. Clin Podiatr Med Surg 2017;34:69-76.
Saltzman CL, Johnson KA, Goldstein RH, Donnelly RE. The patellar tendon-bearing brace as treatment for neurotrophic arthropathy: A dynamic force monitoring study. Foot Ankle 1992;13:14-21.
Richter M, Mittlmeier T, Rammelt S, Agren PH, Hahn S, Eschler A. Intramedullary fixation in severe Charcot osteo-neuroarthropathy with foot deformity results in adequate correction without loss of correction – Results from a multi-centre study. Foot Ankle Surg 2015;21:269-76.
Nasser EM, LaPorta GA, Trott K. Medial column arthrodesis using an anatomic distal fibular locking plate. J Foot Ankle Surg 2015;54:671-6.
De Moraes Barros Fucs PM, Svartman C, de Assumpção RM, Yamada HH, Simis SD. Medial column arthrodesis in rigid spastic planovalgus feet. Clin Orthop Relat Res 2012;470:1334-43.
Galli M, Scavone G, Vitiello R, Flex A, Caputo S, Pitocco D. Surgical treatment for chronic Charcot neuroarthropathy. Foot (Edinb) 2018;36:59-66.
Pinzur MS, Gil J, Belmares J. Treatment of osteomyelitis in charcot foot with single-stage resection of infection, correction of deformity, and maintenance with ring fixation. Foot Ankle Int 2012;33:1069-74.
Eschler A, Wussow A, Ulmar B, Mittlmeier T, Gradl G. Intramedullary medial column support with the Midfoot Fusion Bolt (MFB) is not sufficient for osseous healing of arthrodesis in neuroosteoarthropathic feet. Injury 2014;45 Suppl 1:S38-43.
Wukich DK, Raspovic KM, Hobizal KB, Sadoskas D. Surgical management of Charcot neuroarthropathy of the ankle and hindfoot in patients with diabetes. Diabetes Metab Res Rev 2016;32 Suppl 1:292-6.
Lowery NJ, Woods JB, Armstrong DG, Wukich DK. Surgical management of Charcot neuroarthropathy of the foot and ankle: A systematic review. Foot Ankle Int 2012;33:113-21.
Ramanujam CL, Han D, Zgonis T. Lower extremity amputation and mortality rates in the reconstructed diabetic charcot foot and ankle with external fixation: Data analysis of 116 patients. Foot Ankle Spec 2016;9:113-26.
Frykberg RG, Attinger C, Smeets L, Koller A, Bal A, Kavarthapu V. Surgical strategies for prevention of amputation of the diabetic foot. J Clin Orthop Trauma 2021;17:99-105.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11]
[Table 1], [Table 2], [Table 3]