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Surgical treatment for chronic Charcot neuroarthropathy
Accepted Manuscript Title: Surgical treatment for chronic Charcot Neuroarthropathy Author: Galli Marco Scavone Giuseppe Vitiello Raffaele Andrea Flex Caputo Salvatore Pitocco Dario PII: DOI: Reference:
S0958-2592(17)30134-7 https://doi.org/doi:10.1016/j.foot.2018.02.001 YFOOT 1527
To appear in:
The Foot
Received date: Revised date: Accepted date:
12-7-2017 27-1-2018 14-2-2018
Please cite this article as: Marco G, Flex A, Surgical treatment for chronic Charcot Neuroarthropathy, The Foot (2018), https://doi.org/10.1016/j.foot.2018.02.001 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Surgical treatment for chronic Charcot Neuroarthropathy
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• Charcot Neuro-arthropathy (CN) is a condition characterized by a progressive derangement of the joints, in individuals affected with sensitive and autonomic neuropathy. • CN is a well know dilemma in the management of the diabetic foot. In literature, there is no uniformity in the clinical and surgical care of this condition, and the treatment is often left to the surgeon’s experience. • There are several surgical procedures accepted in Charcot foot surgery. Their goal is to obtain a plantigrade foot and prevent recurrent ulcerations. • Exostectomy is a viable option provided the deformity is stable. • Arthrodesis is a well-known surgical procedure that addresses severe joint derangement through a surgically induced bony fusion. In Charcot foot, arthrodesis is usually indicated when there is significant skeletal instability. • Arthrodesis could concern midfoot or/and ankle. This procedure can be done by internal or external fixation. • Patients may eventually undergo a major amputation because of comorbidities, residual intractable deformity, infection, recurrent ulcers, failure obtaining a solid bony fusion and consequent recurrence of structural instability.
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Surgical treatment for chronic Charcot Neuroarthropathy Galli Marco, Scavone Giuseppe, Vitiello Raffaele, Andrea Flex, Caputo Salvatore, Pitocco Dario
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Galli Marco, Università Cattolica del Sacro Cuore, [email protected]
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Scavone Giuseppe, Università Cattolica del Sacro Cuore, [email protected]
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Vitiello Raffaele, Università Cattolica del Sacro Cuore, [email protected]
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Andrea Flex, Università Cattolica del Sacro Cuore, [email protected]
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Caputo Salvatore, Università Cattolica del Sacro Cuore, [email protected]
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Dario Pitocco, Università Cattolica del Sacro Cuore, [email protected]
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Corresponding author: Vitiello Raffaele, Università Cattolica del Sacro Cuore,
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[email protected], +393407723095
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Surgical treatment for chronic Charcot Neuroarthropathy
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[1] Charcot Neuro-arthropathy (CN) is a condition characterized by a progressive derangement of the joints (fig. 1), in individuals affected with sensitive and autonomic neuropathy [1]. Jean-Martin Charcot who related this pathology to the syphilis first described the disorder. In 1936 Jordan observed CN among diabetic patients, but it was later recognized that the condition could be found also in other diseases such as leprosy, HIV, spina bifida, amyloidosis, alcoholism and renal dialysis [2]. The pathogenesis of CN is undoubtedly multifactorial [2]. A central role is played by the loss of sensitivity, but it is sure that sensitivity impairment alone is not enough to trigger the pathology. About 5 out of a 100 patients with DM will develop peripheral neuropathy but among this latter population only 8.5 out of 1000 individuals will suffer with CN involving the joints of the foot [34]. Peripheral neuropathy leads to a loss of protective sensation and abnormal foot biomechanics with altered distribution of the load. These alterations help to developed dislocations, trauma and fracture. In this acute phase, an inflammatory cascade through increased expression of proinflammatory cytokines, like TNFα and interleukin 1β leads to increased expression of the nuclear transcription factor, NF-κB, which results in increased osteoclastogenesis [5]. Osteoclasts cause progressive impairment of the bones until fractures, dislocations and then ulcerations occur. For this reason, cytokines and their receptors are now day intensively investigated. Rizzo et al. studied the association between post-translational modifications of collagen I and II and the presence of related autoantibodies in CN population [6]. Another topic concerns the role of genetic predisposition as studied by Pitocco and coll. [7] that founded a significant genetic association of CN patients with a osteoprotegerin pleomorphic expression that leads to a defective osteoprotegerin-RANKL regulation. Another important chapter of pathophysiology of CN concern the dysregulation of Autonomic Nervous System. In fact, neuropathy may affect the peripheral autonomic nervous system with an impairing arterial perfusion and altered cellular turnover of foot and ankle bones [8]. The consequences of this changes are the formation of arteriovenous shunting and increased arterial perfusion [9] that causes during the acute inflammatory phase an intensification of bone osteolysis. When CN turn into its chronic stage those features that are characteristic of the acute inflammatory stage give way to other manifestations such as deformity, unstable joint dislocations, untreatable bony protrusions, ulceration with superficial or deep infection and osteomyelitis. Infection results in a high incidence of amputations, Saltzman et al. estimated that amputation affects 2.7 % of patients with CN [10]. CN almost exclusively affects the foot and ankle, being extremely rare other locations in DM patients. It commonly presents in the midfoot, but it may also occur in the forefoot and hindfoot. Today diabetes is the most common cause of CN in developed countries. CN is cause of significant increase of morbidity and mortality in the DM population (mortality rate is increased about 28% in patient affected by CN) [11]. CN is a well know dilemma in the management of the diabetic foot. In literature, there is no uniformity in the clinical and surgical care of this condition, and the treatment is often left to the surgeon’s experience [12].
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Intro
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Pre-op management The main indications for surgery in Charcot disease at the foot and ankle are fixation of potentially unstable bony structure derangements and correction of a severe stable deformity that compromises the functionality of the limb and is at high risk for ulceration and infection [12]. Careful pre-operative patient assessment should first consider patient’s general condition, comorbidities and compliance. Multidisciplinary teams should carry out appropriate preoperative renal and cardiovascular evaluations and provide an acceptable control of blood sugar levels. Good patient compliance is important for the outcome of complex surgical procedures and should not be overlooked altogether with a realistic analysis of the social and logistic set up. Vascularity is seldom a problem in CN patients, but should always be carefully investigated to avoid significant drawbacks. Preoperative transcutaneous oximetry is a widely-accepted procedure for patient selection. A pressure gradient of >50 mm Hg is the least acceptable preoperative threshold for a safe surgical treatment. Lower values require further investigations [13]. Doppler ultrasound and, if necessary, Angio-CT of the lower limbs are indicated. Patients susceptible of an effective revascularization should go for a Angio-PTA or other more invasive vascular procedures to recover distal tissues to an acceptable oxygen partial pressure. If transcutaneous oximetry levels persist below 40/35 mm Hg, an amputation should be considered. Local cutaneous conditions as well as the presence or absence of a deep infection or osteomyelitis profoundly influence the indication to surgery. Ulcers should be carefully assessed and classified. A clinical examination is generally sufficient to rule out deep and massive cutaneous losses with bone exposure and infection or osteomyelitis. In diabetic patients, deep infections and severe osteomyelitis are serious surgical and medical problems that overcome the presence of a CN disease. They should be promptly addressed and often conduct to mayor amputations. Superficial ulcers do not represent a contraindication for CN surgical procedures, but significantly impact on the selection of the surgical treatment. First, it should be ascertained whether the ulcer is infected or simply contaminated. Contaminated ulcers may be treated simultaneously with a CN disorder in a one staged surgical procedure. Infected ulcers with an undermining osteomyelitis are preferentially treated before a major surgery for CN. Osteomyelitis is a dreaded complication that affects up to 20% of all diabetic patients who experience a cutaneous lesion at the foot [14]. The detection of an infection to the bone underneath an ulcer and the correct appraisal of its extent and relevance are sometime very complicated. A final decision is a matter of clinical experience. There is a consensus on the liability of some clinical indicators of osteomyelitis occurrence. The most obvious is the presence of exposed bone at the bottom of the ulcer. Other less immediate clinical indicators are: the observation of signs of inflammation involving the cutis stretching around the ulcer’s boundaries for more than 2 cm; the other is named “probe to bone test” and suggests an undermining osteomyelitis if one can feel the sensation of touching the bone beneath the tip of a probe exploring deeply into the lesion. Once osteomyelitis is suspected many other examinations are commonly carried out in the attempt to refine the diagnosis and acquire a better understanding of the severity of the disease. Although there are a remarkable number of investigations that may be considered, either simple such as blood tests or more sophisticated such as WBS scintigraphy, MDP scintigraphy and MRI, it is not uncommon that a final reliable diagnosis is made upon the results of a bone biopsy with cultural examination. There are many confounding factors among diabetic patients with plenty of comorbidities and a massive normal anatomy derangement due to CN. Imaging modalities and diagnostic tests show ambiguous value of sensitivity and specificity and it is difficult to determine which examination is the most reliable. In table 1 we present the value of LR+ (Positive Likelihood Ratio), LR‐ (Negative Likelihood Ratio) and DOR (Diagnostic Odds Ratio) for those afore mentioned most credited clinical indicators of osteomyelitis confronted with the same values for blood tests and functional or morphological studies by means of different imaging modalities. LR+,
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LR‐ and DOR are determined using the values of sensitivity and specificity reported on two reviews published in 2015 [15, 16]. Table 1 highlights how MRI is the most credited diagnostic modality by displaying the highest overall diagnostic value (DOR=33.1). But, due to its low specificity, the liability of a MRI positive results remains below that of the mere clinical judgment (LR+ = 4.3 vs 5.5 respectively), let alone that of other clinical finding such as “Probe to bone test” (LR+ = 6.4), ulcers wider than 2 cm2 (LR+ = 7.2) and exposed bone (LR+ = 9.2). In addiction, if one considers that these values are drawn from studies broadly concerned with diabetic foot infections it is not unlikely that MRI performance might be even worse in CN patients. It is not a secret that it remains a challenge to discriminate active Charcot neuro-osteoarthropathy from acute osteomyelitis with MRI. This is simply the case because MR imaging features are quite similar. Both entities will show subchondral bone marrow edema, joint effusions, soft tissue inflammatory changes (high signal intensity on T2 fatsat or STIR, somewhat low signal intensity on T1) and enhancement of bone and soft tissue after contrast administration [17]. A possible overcome to the problem might come from a widespread diffusion of the new Hybrid PET/MRI scanners that combine the high sensitivity of MRI studies to the high specificity of FDG-PET investigations. Even though X-ray might be inconclusive for bone infections they are certainly fundamental for planning surgical treatment and identifying the pattern type of foot involvement. Sanders-Frykberg classification describes five patterns, according to the localization of bone and joint pathology. The acknowledgment of the pattern type provides valuable prognostic information. Forefoot CN is the least progressive and harmful pattern (pattern1 of Sanders-Frykberg classification). In forefoot CN, metatarsophalangeal (MTP) and interphalangeal joints are involved [18-19-20]. Disease progression is usually favorable and conservative treatment is generally sufficient. Surgery is rarely necessary, but is mandatory for correction of an intractable first metatarsophalangeal dislocation. Midfoot CN is far more likely to proceed to severe deformity and plantar ulcerations (patterns 2 and 3 of Sanders-Frykberg classification). Diabetic midfoot CN is characterized by the involvement of either the Lisfranc or the Chopart joints or both (patterns 2 and 3 of Sanders-Frykberg classification respectively). In these cases, the typical deformity that eventually develops is the so-called “rocker bottom deformity” which is characterized by a plantar collapse of the midfoot. The disease causes a weakening of the skeletal structure of the foot that collapses losing its normal “arch” configuration (fig. 1). The process takes place at different spots in the bony and ligamentous structure. If the process starts with a navicular and cuboid fragmentation it generally progresses with a talus and cuboid plantar dislocation and ulceration below the calcaneo-cuboid prominence (fig. 2). If the process begins with a naviculocuneiform dislocation, instead, it will continue with first metatarsal dorsal displacement and medial cuneiform or navicular plantar displacement causing plantar ulceration. In this case, the pull of the anterior tibialis muscle on the first metatarsal actively exacerbate the fragmentation and displacement, making conservative treatment ineffective even in non-weight bearing conditions. Both processes are equally common and unfortunately once fragmentation has intervened it is impossible to tell what was the type of onset and the eventual outcome. Midfoot CN usually respond to conservative treatment. Conservative treatment is based on foot unloading and immobilization into a Total Contact Cast or a dedicated orthotic boot. It is mandatory at the early stages of the disease. Cases irresponsive to conservative treatment are demanded to surgery. Ankle and subtalar joint CN patterns are the most intractable because they give rise to extremely unstable deformities (patterns 4 and 5 of Sanders-Frykberg classification respectively). Ankle and subtalar joint CN are rarely responsive to conservative treatment and surgery remains the only valid option. If multiple locations are concerned, a major below knee amputation should be considered.
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There are several surgical procedures accepted in Charcot foot surgery. Their goal is to obtain a plantigrade foot and prevent recurrent ulcerations. Achilles tendon lengthening, plantar bony prominence resection, osseous debridement, corrective or “in situ” bone fusion are the most widely used to achieve the desired result.
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Exostectomy
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Roker bottom deformities, either because of Lisfranc or Chopart joint complex breakdown, are frequently cause of intractable plantar ulcers (fig. 2). Problematic plantar bony prominences due to tarsal bones displacement into non-anatomic position may not be easily accommodated with orthotic and prosthetic measures. Exostectomy is then a viable option provided the deformity is stable. In fact, if the deformity is unstable surgery might worsen the plantar displacement of tarsal bones with recurrent ulcers due to intractable bony prominences [21-22-23]. When the deformity is stable the resection of plantar bony prominences improves plantar pressure distribution, promoting ulcers healing. Thus, exostectomy is used to restore a plantigrade foot and return the patient to full weight bearing without addressing the deformity. Exostectomy is performed through a direct or indirect surgical approach. Direct approach is carried out by means of a single surgical approach either for excision of the ulcer and for removal the underlying bony prominence. In order to prevent cross contamination, indirect approach requires two separate incisions: one for excision of the ulcer and another for removal of the bony prominence.. Unfortunately indirect approach is often unfeasible. Deep ulcers reaching down to the exostoses together with bone exposure often hamper a double approach. Exostectomy is a well-established surgical practice and its effectiveness in midfoot Charcot complication treatment had been confirmed by several studies [24]. Exostectomy may be performed alone or in combination with Achilles’ tendon lengthening or gastrocnemius recession. These adjunctive procedures are required when there is a severe contracture of the triceps surae that brings the rear and midfoot into an equinus position [25]. The aim is direct to decrease dynamic forefoot plantar pressure and improve rear-midfoot to forefoot alignment. A test used to determine whether the contracture is confined to the Gastrocnemius muscles is the “Silfverskiod Test” [26]. It consists of a clinical maneuver that assesses the variation of maximum foot and ankle dorsiflexion when the knee is brought from a full extension to a 90 degrees flexed position. The test is considered positive when there is a significant increase of foot and ankle dorsiflexion at knee flexion. Mueller and colleagues [27] carried out a randomized controlled trial to compare the recurrence rate of ulceration in patients with neuropathic plantar ulcers treated with Achilles-tendon lengthening plus PCC (test group), and PCC alone (control group). At seven months’ follow-up, 15% of patients in the test group had an ulcer recurrence, compared to the 59% of patients in the control group. Percutaneous Achilles tendon lengthening represents one of the most frequent surgical choices for triceps surae muscle contracture. Care should be taken to minimize the loss of overall muscular strength to avoid a ticeps surae muscle insufficiency that is the most fearful drawback of the procedure.
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Arthrodesis Arthrodesis is a well-known surgical procedure that addresses severe joint derangements through a surgically induced bony fusion. In diabetic foot, arthrodesis is usually indicated in some of type 2 and 3 CN midfoot skeletal collapses and almost always in type 4 and 5 CN structural failure.
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Midfoot In midfoot collapse, when there is significant skeletal instability a simple Exostectomy of a plantar bony prominence does not ensure long-term results. Arthrodesis instead can reach durable results by surgical fusion of midfoot joints. Functional impairment secondary to such a massive loss of motion segments is accepted because the primary goal of surgical treatment in CN is to return the patient to full weight bearing and free deambulation without supportive aids (canes, crutches etc.) and recurrent ulceration. Diabetic foot surgeries are preferentially limb salvage procedures that aim to acceptable functional and clinical results with sustainable medical costs. [28] Schon et al. observed that midfoot lateral column collapse has a worse prognosis either a plantar ulceration had already occurred or not [29]. Furthermore, Catanzariti et al. reported that lateral column collapse show a lower rate of plantar ulcer healing compared to medial column collapse after esostectomy alone [30]. It seems that lateral column collapse with plantar bony prominences should be treated more aggressively at once avoiding unsuccessful delays. In a broad view the main indications for arthrodesis in type 2 and 3 CN are the following: • Unstable midfoot skeletal derangement where conservative treatment has failed to prevent further evolution of the deformity • Lateral midfoot collapse with rocker bottom deformity that presents a plantar ulcer or is susceptible to produce ulceration • Recurrent ulceration after esostectomy for plantar bony prominence • Stable gross deformity with ulceration or pre-ulcerative lesion where esostectomy is not feasible or insufficient. Internal fixation has been for long the most widely accepted method for arthrodesis fixation in midfoot CN surgery. Arthrodesis is performed through large surgical approaches to remove prominent bone, reduce dislocated bony segments and grossly align the rearfoot to the forefoot. Internal fixation is then performed by means of screws, plates or staples to stabilize the site of arthrodesis and the neighbouring bones [31-32]. To maximize the probability of good results, it is accepted and advisable to spread the internal fixation beyond common limits as to form a so-called “super-construct”. In a super-construct, internal fixation prolongs well beyond the limits of the areas involved by the Charcot process. Its purpose is to increase stability and decrease the likelihood of fixation failure. Super-construct locking plates span the entire length of the medial column, providing rigid stability and good anatomic alignment [33-34]. Suggested criteria are the following [35]: • internal fixation should extend beyond the zone of skeletal collapse and include non-affected bone • bone resection should be performed to shorten the skeleton to achieve adequate reduction of the deformity without tension on the soft tissues • the hardware needed for fixation should not be so superficial or massive as to interfere with soft tissues healing. • hardware should be applied in a position that maximize its mechanical competence. Together with the above criteria there is another recommended principle to follow. Arthrodesis by internal fixation should be avoided in acute inflammatory Eichenholtz stage 1 CN in order to prevent poor outcomes due to disease progression. A massive surgical exposure triggers disease
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progression with fragmentation and bony destruction. Surgery by invasive internal fixation should be confined to Eichenholtz stage 2 or 3 CN. Ankle Patients suffering from Type 4 CN that caused either a remarkable derangement of the joints surrounding the talus or a massive talar bone loss are eligible for tibiocalcaneal arthrodesis. Tibiocalcaneal arthrodesis is performed by internal or external fixation. In diabetic patients, external fixation is mandatory in case of deep infection, osteomyelitis and poor soft tissue coverage [36]. Poor patient compliance, frequent pin tract medications, long duration of patient surveillance and medicalization often discourage the usage of external fixation. Several internal fixation systems have been put forward in the recent years. Retrograde intramedullary ankle nail fixation has gained popularity because of its many mechanical advantages [37]. It can provide the patient with such a stable fixation that adjunctive external immobilization devices such as plasters or braces are generally felt unnecessary. An enhancement of the overall stability through an external immobilization is necessary only when there is some concern that a solid internal fixation could not be obtained because of poor bone stock. Bone union rates vary among diabetic patients (fig. 3). Dalla Paola and others [38] achieved a solid bony union in 14 patients out 18 of their series, the remaining 4 patients showing findings of fibrous union (fig 4). Their rate of limb salvage was 100%. Caravaggi and others [39] reported only one case of unsuccessful result that required a below-knee amputation and obtained a 71% bony union rate, a fibrous union in the 21%. Recent incremental innovations in retrograde ankle nails design have furthermore refined the already sophisticated previous nails. There are new dedicated nails that allow correct hindfoot alignment and fixation by an adequate bending along their longitudinal axis and plenty availability of interlocking screws along the sagittal plane of the os calcis. Pinzur et al in 2005 reported on a consecutive series of nine diabetic patients with ankle Charcot arthropathy [40]. They used long retrograde femoral nails for internal fixation of their ankle arthrodesis to cover the whole length of the tibia with the surgical instrumentation to prevent the occurrence of mechanical stress concentration and stress fractures at the tip of the nails. Although tibia stress fractures at the tip of the nail do occur, they are not reported in recently published series of diabetic Charcot foot patients [39]. A recent study tried to evaluate the results of retrograde intramedullary nailing (IMN) for severe ankle/hindfoot pathology in a group of patients with diabetic neuropathy and compare them to a cohort of non-diabetic patients. Although a postoperative complication was experienced in a 59% of cases with DM compared to a 44% without DM, the difference did not reach statistical significance due to the small number of patients available [41]. In their statistical analysis, they calculated that a sample of at least 100 patients in each group would be necessary to achieve an adequate statistical power. Since large series from multicentric studies are yet to be investigated, no definitive agreement had been reached. At the moment tibio-calcaneal arthrodesis in diabetic CN is generally felt as a salvage procedure with high rates of post-operative complication whatever the internal fixation construct utilized. Other undesired drawbacks are: poor anatomic correction (i.e. shortening of the foot or incomplete deformity correction), occasional neurovascular problems, wound healing complications and infections.
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Arthrodesis with external fixation
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External fixation in diabetic CN has gained increasing popularity [40-42]. It offers some significant advantages being less invasive and avoiding the presence of bulky internal hardware [43]. It is mandatory in the presence of osteomyelitis or deep ulceration and is recommended with poor soft tissue coverage, poor bone quality and morbid obesity [44]. Pinzur and colleagues [45-46] carried out the largest study concerned with a single-stage procedure for arthrodesis of midfoot CN with osteomyelitis. They adopted the following protocol of treatment: -Bacterial isolation obtained from resected bone samples during surgical bone debridement to guide antibiotic therapy. -Surgical correction to achieve a plantigrade foot with percutaneous pins for temporary fixation and 3-level prebuilt static circular external fixator for definitive fixation (fig 5). External fixator was maintained for a period of 8 weeks in patients with midfoot CN and a minimum of 12 weeks in those with hindfoot or ankle CN. Post-operative wounds care was a little hampered by the presence of the external fixation hardware, but the overall management was easier and more effective than that it would have been in the presence of a cast or an orthotic boot. -Removal of external fixator and short leg casting for 4 to 6 weeks. -Definitive therapeutic footwear consisting in commercially available depth-inlay shoes and custom accommodative foot orthoses, occasionally preceded by commercially available diabetic patients orthopedic boots. Using this protocol, the researchers could achieve 95.7 % limb salvage. In addition, Pinzur used the external fixator to restore a plantigrade foot among obese patients with Charcot metatarsal deformity and ulceration. 24 out of 26 feet were free of ulcer and able to walk with custom made diabetic shoes and orthoses at a minimum one-year follow-up. Recently external fixation has been applied to patients with acute Eichenholtz stage I CN. There is an increasing number of studies confirming the possibility of preventing the progression of bone destruction and deformity through an external surgical fixation at this stage [47]. As already mentioned arthrodesis by internal fixation is contraindicated in Acute Eichenholtz stage I for two main reasons. One is that bone is soft and hyperemic and offers a poor mechanical support to internal fixation. The other is that the extensive surgical exposures needed for setting an internal fixation promote the progression of the CN itself. An external fixation instead offers the advantage of requiring only minimally invasive procedures. Thus, is explained the use of external fixation in the acute phase until evidences of bony coalescence at x-ray examination together with edema and thermal gradient decrease at clinical examination are accomplished. Moreover, external fixation allows a gradual realignment of bony segments, which reduces the risk of neurovascular injury secondary to overstretching. Among the disadvantages of external fixation, the most discouraging is poor patient compliance (fig. 6) and pin tract infection. Refusal of medicalization and poor selfhygiene make often part of the peculiar trait of diabetic patients. Thus, intolerance to the presence of the metallic hardware and to the long duration of treatment come often together with refusal to undergo regular pin-tract hygiene in a devastating combination that leads to failure of treatment and major amputation [48-49]. Prevention of infection is largely based on strict patient education about regular pin tract hygiene and regular medical referral. As soon as there are obvious signs of infection, the surgeon should consider the need to remove them or abandon external fixation in favour of other treatments. External fixation can also be used for improving internal fixation. Combined internal and external fixation is often preferred for complex and gradual reconstruction in severely deformed foot. Paley proposed a staged method of correction [50]. The first stage aims at skeletal realignment and simultaneous soft tissue healing by gradual correction with an external fixator. The second step is committed to stabilization of the result through the achievement of a solid arthrodesis by means of a
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minimally invasive internal fixation. The external fixator is removed and arthrodesis is accomplished with percutaneous insertion of intramedullary, fully threaded, cannulated screws that are drilled through the head of the metatarsal bones. Three screws are generally needed: one for the medial column through the first metatarsal up to the talus another for lateral column through the fifth metatarsal up to the calcaneus and eventually a third screw connecting the talus to the calcaneus. They should cover the entire length of the metatarsals to the calcaneus and talus and stabilize the affected joints to the adjacent unaffected bone. In this way one should seek to provide a solid fixation into sound bone and prevent the spread of CN destruction to the adjacent bony segments.
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Amputation
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Even though the main goal of CN surgical treatment is limb salvage, amputation should be considered in selected cases. A major amputation may be a valid option in patients with comorbidities, residual intractable deformity, infection, recurrent ulcers and failure of previous treatment with consequent recurrence of structural instability. The rate of major amputation is reasonably low in CN population nowadays. Saltzman et al. reported a 2.7% rate [51], but a major amputation remains an undesirable end term event among fragile diabetic patients and it should be as far as possible avoided. Fragile diabetic patients presents many unsolved rehabilitation problems and may hardly recover even with the more advanced prosthetic limbs. Disability reduces the life expectancy significantly in diabetic patients. 5 years mortality rate after unilateral below-knee amputation is about 50% among the general population. Within the diabetic population the same rate of mortality after unilateral below-knee amputation is reached two years earlier [52] and the risk of developing a contralateral amputation is almost doubled within 2 years [53]. A condition that strongly recommends a major amputation is that of patients with intractable infections, especially in case of multi-drug-resistant organisms in individuals with PAD of the lower limbs. Another condition is that of patients whose outcome after several surgical procedures is a poor functional lower limb, incapable of bearing weight, despite any success in healing from osteomyelitis [54-55]. Amputation may be performed at various levels. Trans-tibial amputation is usually preferred, as prosthetic fitting is easier. Alternative procedures should be considered for patients with limited mobility and vision problems. Syme and Pirogoff amputations are designed to leave the patient with a lower limb stump that allows an acceptable walking autonomy. The aim is to obtain a functional stump (shortening of about 5 cm at the worst) that allows the patient to walk short distances without accommodative shoes.
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Biography
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1. Charcot JM. Sur quelaques arthropathies qui paraissent depender d’une lesion du cerveau ou de la moele epiniere. Arch De Physiol Norm et Path 1868; 1: 161–171. 2. Wukich DK and Sung W. Charcot arthropathy of the foot and ankle: modern concepts and management review. J Diabetes Complications 2009; 23: 409–429. 3. Young MJ, Boulton AJM, Macleod AF, Williams DRR, Sonksen PH. A multicentre study of the prevalence of diabetic peripheral neuropathy in the United Kingdom hospital clinic population. Diabetologia 36:150–154, 1993 4. Lavery LA, Armstrong DG, Wunderlich RP, Tredwell J, Boulton AJ. Diabetic foot syndrome: evaluating the prevalence and incidence of foot pathology in MexicanAmericans and non-Hispanic whites from a diabetes management cohort. Dia- betes Care 26:1435–1438, 2003. 5. Rogers LC, Frykberg RG, Armstrong DG, Boulton AJ, Edmonds M, Van GH, Hartemann A, Game F, Jeffcoate W, Jirkovska A, Jude E, Morbach S, Morrison WB, Pinzur M, Pitocco D, Sanders L, Wukich DK, Uccioli L. The Charcot Foot in Diabetes. Diabetes Care 34:2123–2129, 2011 6. Rizzo P, Pitocco D, Zaccardi F, Di Stasio E, Strollo R, Rizzi A, Scavone G, Costantini F, Galli M, Tinelli G, Flex A, Caputo S, Pozzilli P, Landolfi R, Ghirlanda G, Nissim A. Autoantibodies to Post-Translationally Modified Type I and II Collagen in Charcot Neuroarthropathy in Subjects With Type 2 Diabetes Mellitus. Diabetes Metab Res Rev 33 (2). 2016 Oct 05. 7. Pitocco D, Zelano G, Gioffrè G, Di Stasio E, Zaccardi F, Martini F, Musella T, Scavone G, Galli M, Caputo S, Mancini L, Ghirlanda G. Association between osteoprotegerin G1181C and T245G polymorphisms and diabetic charcot neuroarthropathy: a case-control study. Diabetes Care. 2009 Sep;32(9):1694-7 8. Gouveri E, Papanas N. Charcot osteoarthropathy in diabetes: a brief review with an emphasis on clinical practice. World J Diabetes. 2011;2:59–65 9. Gilbey SG, Walters H, Edmonds ME, Archer AG, Watkins PJ, Parsons V, et al. Vascular calcification, autonomic neuropathy, and peripheral blood flow in patients with diabetic nephropathy. Diabet Med. 1989;6:37–42 10. Saltzman CL. Et coll. How effective is intensive nonoperative initial treatment of patients with diabetes and Charcot arthropathy of the feet? Clin Orthop Relat Res. 2005 Jun;(435):185-90. 11. Sohn MW, Lee TA, Stuck RD, et al. Mortality risk of Charcot arthropathy compared with that of diabetic foot ulcer and diabetes alone. Diabetes Care 2009; 32(5): 816–821. 12. Schneekloth BJ, Lowery NJ, Wukich DK. Charcot Neuroarthropathy in Patients With Diabetes: An Updated Systematic Review of Surgical Management. The Journal of Foot & Ankle Surgery 55 (2016) 586–590 13. Sohn MW, Stuck RM, Pinzur M, et al. Lower-extremity amputation risk after Charcot arthropathy and diabetic foot ulcer. Diabetes Care 2010; 33(1): 98–100. 14. Kagna O, Srour S et al. 18F‐FDG PET/CT imaging in the diagnosis of the osteomyelitis in the diabetic foot Eur J Med Molecul Imaging 2012; 39: 1545‐50 15. Markanday A Diagnosing diabetic foot osteomyelitis: narrative review and a suggested 2‐step – score‐based diagnostic pathway for clinicians Open Forum Infect Dis 2015 Jul3; 2(3) ofv098 16. Khodaee M, Lombardo D et al Q/What’s the best test for underlying osteomyelitis in patients with diabetic foot ulcers? The Journal of Family Practice 2015; 64(5): 309‐21
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17. Ergen FB, Sanverdi SE, Oznur A. Charcot foot in diabetes and an update on imaging. Diabet Foot Ankle. 2013;4:21884. 18. Varma V, Varma AK, Mangalandan TS, Bal A, Kumar H. Use of polymethyl methacrylate as prosthetic replacement of destroyed foot bonesdcase series. J Diabetic Foot Complications 4:71–82, 2012. 19. Shibata T, Tada K, Hashizume C. The results of arthrodesis of the ankle for leprotic neuroarthropathy. J Bone Joint Surg Am 72:749–756, 1990. 20. Brodsky JW. The diabetic foot. In: Surgery of the Foot and Ankle, ed 6, pp. 278–283, edited by RA Mann, MJ Coughlin, Mosby, St. Louis, 1993. 21. Sanders LJ, Frykberg RG. The Charcot Foot. In: The High Risk Foot in Diabetes Mellitus, pp. 325–335, edited by RG Frykberg, Churchill Livingstone, New York, 1991. 22. Laurinaviciene R, Kirketerp-Moeller K and Holstein PE. Exostectomy for chronic midfoot plantar ulcer in Charcot deformity. J Wound Care 2008; 17: 53–59. 23. Brodsky JW and Rouse AM. Exostectomy for symptomatic bony prominences in diabetic Charcot feet. Clin Orthop Relat Res 1993; 296: 21−26. 24. Catanzariti AR, Mendicino R, Haverstock B. Ostectomy for diabetic neuro- arthropathy involving the midfoot. J Foot Ankle Surg 39:291–300, 2000. 25. Armstrong DG, Lavery LA. Elevated peak plantar pressures in patients who have Charcot arthropathy. J Bone Joint Surg Am 80:365–369, 1998. 26. Hastings MK, Mueller MJ, Sinacore DR, Salsich GB, Engsberg JR, Johnson JE. Effects of a tendo-Achilles lengthening procedure on muscle function and gait characteristics in a patient with diabetes mellitus. J Orthop Sports Phys Ther 30:85–90, 2000. 27. Symeonidis P.The Silfverskiöld Test. Foot Ankle Int. 2014 Aug;35(8):838. Epub 2014 Jul 28. Mueller MJ et Al. Effect of Achilles tendon lengthening on neuropathic plantar ulcers. A randomized clinical trial. J Bone Joint Surg Am. 2003 Aug;85-A(8):1436-45. 29. Dhawan V, Spratt KF, Pinzur MS, Baumhauer J, Rudicel S, Saltzman CL. Reliability of AOFAS diabetic foot questionnaire in Charcot arthropathy: stability, internal consistency, and measurable difference. Foot Ankle Int 26:717–731, 2005. 30. Schon LC. Charcot neuroarthropathy of the foot and ankle. Clin Orthop Relat Res. 1998 Apr;(349):116-31. 31. Catanzariti AR. Ostectomy for diabetic neuroarthropathy involving the midfoot. J Foot Ankle Surg. 2000 Sep-Oct;39(5):291-300. 32. Wukich DK, Joseph A, Ryan M, Ramirez C, Irrgang JJ. Outcomes of ankle fractures in patients with uncomplicated versus complicated diabetes. Foot Ankle Int 32:120–130, 2011. 33. Ayoub MA. Ankle fractures in diabetic neuropathic arthropathy: can tibiotalar arthrodesis salvage the limb? J Bone Joint Surg Br 90:906–914, 2008. 34. Crim B, Lowery N, Wukich D. Internal fixation techniques for midfoot Charcot neuroarthropathy in patients with diabetes. Clin Podiatric Med Surg 28:673–685, 2011. 35. Sammarco VJ. Superconstructs in the treatment of Charcot foot deformity: plantar plating, locked plating and axial screw fixation. Foot Ankle Clin 14:393– 407, 2009. 36. Moeckel BH, Patterson BM, Inglis AE, Sculco TP. Ankle arthrodesis. A comparison of internal and external fixation. Clin Orthop Relat Res. 1991 Jul;(268):78-83. 37. Millett PJ, O'Malley MJ, Tolo ET, Gallina J, Fealy S, Helfet D. Tibiotalocalcaneal fusion with a retrograde intramedullary nail: clinical and functional outcomes. Am J Orthop (Belle Mead NJ). 2002 Sep;31(9):531-6 38. Dalla Paola L, Brocco E, Ceccacci T, Ninkovic S, Sorgentone S, Marinescu MG, Volpe A. Limb salvage in Charcot foot and ankle osteomyelitis: combined use single stage/double stage of arthrodesis and external fixation. Foot Ankle Int 2009; 30(11): 1065–1070. 39. Carlo Caravaggi, MD, Marzio Cimmino, MD, Sebastiano Caruso, MD, and Sergio Dalla Noce, MD. Intramedullary Compressive Nail Fixation for the Treatment of Severe Charcot
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Deformity of the Ankle and Rear Foot. The Journal of Foot & Ankle Surgery 45(1):20–24, 2006. 40. Michael S. Pinzur, Timothy Noonan. Ankle Arthrodesis with a Retrograde Femoral Nail for Charcot Ankle Arthropathy. Foot & Ankle International/Vol. 26, No. 7/July 2005. 41. Dane K. Wukich, James Y.C. Shen, Claudia P. Ramirez, James J. Irrgang. Retrograde Ankle Arthrodesis Using an Intramedullary Nail: A Comparison of Patients with and without Diabetes Mellitus. The Journal of Foot & Ankle Surgery 50 (2011) 299–306 42. Zarutsky E, Rush SM and Schuberth JM. The use of circu- lar wire external fixation in the treatment of salvage ankle arthrodesis. J Foot Ankle Surg 2005; 44: 22–31. 43. Farber DC, Juliano PJ, Cavanagh PR, Ulbrecht J, Caputo G. Single stage cor- rection with external fixation of the ulcerated foot in individuals with Char- cot neuroarthropathy. Foot Ankle Int 2002; 23: 130–134. 44. Cooper PS. Application of external fixators for management of Charcot deformities of the foot and ankle. Foot Ankle Int 2002; 7(1): 207–254. 45. Pinzur MS, Sammarco VJ, Wukich DK. Charcot Foot: A Surgical Algorithm. Instructional Course Lectures of the American Academy of Orthopaedic Surgeons. 61: 423–440. 2012. PMID: 22301251. 46. Pinzur MS, Gil J, Belmares J.Treatment of osteomyelitis in Charcot foot with sin- gle stage resection of infection, correc- tion of deformity and maintenance with ring fixation. Foot Ankle Int 2012; 33: 1069-1074. PMID: 23199855. 47. Paul Dayton, Mindi Feilmeier, Mitchell Thompson, Paul Whitehouse, Rachel A. Reimer. Comparison of Complications for Internal and External Fixation for Charcot Reconstruction: A Systematic Review. The Journal of Foot & Ankle Surgery 54 (2015) 1072–1075 48. Caravaggi C, Cimmino M, Caruso S, Dalla Noce S. Intramedullary compressive nail fixation for the treatment of severe Charcot deformity of the ankle and rear foot. J Foot Ankle Surg 45:20–24, 2006. 49. Fleming B, Paley D, Kristiansen T, Pope M. A biomechanical analysis of the Ilizarov external fixator. Clin Orthop 241:95–105, 1989. 104. Bevilacqua N, Rogers L. Surgical management of Charcot midfoot deformities. Clin Podiatr Med Surg 25:81–94, 2008. 50. Lamm BM, Gottlieb HD, Paley D. A two-stage percutaneous approach to Charcot diabetic foot reconstruction. J Foot Ankle Surg 49:517–522, 2010. 51. Saltzman CL, Hagy ML, Zimmerman B, et al. How effec- tive is intensive nonoperative initial treatment of patients with diabetes and Charcot arthropathy of the feet? Clin Orthop Relat Res 2005; 435: 185–190. 52. Armstrong DG, Wrobel J, Robbins JM. Guest editorial: are diabetes-related wounds and amputations worse than cancer? Int Wound J 4:286–287, 2007. 53. Goldner MG. The fate of the second leg in the diabetic amputee. Diabetes 9:100–103, 1960. 54. Papa J, Myerson M and Girard P. Salvage, with arthrodesis, in intractable diabetic neuropathic arthropathy of the foot and ankle. J Bone Joint Surg Am 1993; 75(7): 1056– 1066. 55. Stone NC and Daniels TR. Midfoot and hindfoot arthrode- ses in diabetic Charcot arthropathy. Can J Surg 2000; 43: 449–455.
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634 Severe skeletal derangement after ankle and subtalar Charcot arthropathy
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636 637 Loss of plantar longitudinal arch after skeletal collapse secondary to Charcot disease is often cause of intractable ulcers.
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646 647 Patient with Type 4 CN who had been performed a talo-calcaneal arthrodesis by means of a retrograde ankle nail through a trans-fibular lateral approach. Soft tissues and vascular supply attached to the external portion of the distal fibula were preserved and, after the osteotomy, a longitudinal splitting of the lateral malleolus was performed. The external portion of the malleolus was then fixed by two spare screws to the tibia and calcaneus providing a sort of vascularized bone graft bridging the lateral side of the site of arthrodesis. At four months follow-up the patient presented with a radiographic appearance of a solid bone union. Full weight bearing was allowed and canes abandoned.
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Fig 3
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651 652 653 654 655 656 657 658 Patient with Type 4 CN who underwent a talo-calcaneal arthrodesis by means of a retrograde ankle nail through an anterior approach. Four weight bearing lateral views of the ankle show the evolution observed in a 6 years follow-up. A – 6 months follow-up. The patient had fully recovered with complete weight bearing and prompt return to its normal daily activity. Radiographs showed the presence of a fibrous union and it was decided to remove one of the proximal locking screws to stimulate bone formation. B - 11 months follow-up. 5 months after removal of the proximal screw (notice the empty hole in the nail profile – arrow) no bone formation at the site of arthrodesis. The patient asked the removal of the distal locking screw because of discomfort at prolonged walking. The distal locking screw had been deliberately inserted into the midfoot to restrain the Chopart joint movement and span into an unaffected motion segment according to the “superconstruct” criteria. C – 2 years follow-up. 13 months after removal of the distal screw, the patient was attaining its normal daily activities without discomfort and radiographs showed what appeared as a stable fibrous union. D – 6 years follow-up. Radiographs showed finally the achievement of a complete bony union
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Fig 4
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667 Surgical correction of a severe deformity through a lateral trans-fibular approach in a patient affected with Type 4 CN. A - After a wide excision of a deep ulcer at the tip of the lateral malleolus, bacterial isolation and debridement were completed by removal of the lateral malleolus itself. B - The correction of the deformity was achieved and it was held in place by a couple of percutaneous K-wire (black arrow). C - Temporary fixation with percutaneous pins (black arrow) in order to achieve a plantigrade foot. D - Three-level prebuilt static circular external fixator for definitive fixation. Percutaneous pins are removed at the end of the surgical procedure (black arrow).
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Patient with Type 4 CN who underwent talo-calcaneal arthrodesis through an anterio Osteosynthesis was performed by means of external fixation (a circular frame with tw tibia by fiches and K-wires connected to a composite frame fixed to the rear and midf spite of the pre-operative acceptance of the planned treatment, at follow-up the patien complained for the presence of external hardware. After a short period of poor genera scarce attendance to scheduled outpatient care and pin-tract medications, the patient w
669 670
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670 DOR 10.2 15 13.1 16.4
11* 5** 2.8**
0.34* 0.18** 0.27**
32.4 27.8 10.4
1.7** 4.3**
0.68** 0.13**
2.5 33.1
1.1**
0.68**
2.3*
0.38*
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LR– 0.54* 0.48* 0.7* 0.39 *
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Table 1 lists the values LR+ and LR- reported in two recent literature reviews: * Markanday A, 2015 [15] ** Khodaee M et al, 2015 [16]. Diagnostic Odd Ratio (DOR=LR+/LR-) was calculated to provide the overall diagnostic value of each diverse modality. ***with no other plausible explanation.
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LR+ 5.5* 7.2* 9.2* 6.4 *
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Table 1 Clinical Judgment Ulc. > 2 cm2 Exposed Bone PTB (probe to bone) test ESR >70/1h *** CRP >14 mg/L Procalcitonin> 0.3 ng/ml Standard X-Rays Magnetic Resonance (MR) MDP Bone Scintigraphy Radiolabeled WBC Scintigraphy
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Surgical treatment for chronic Charcot Neuroarthropathy
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No one of the authors have any Conflict of Interest
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S0958-2592(17)30134-7 https://doi.org/doi:10.1016/j.foot.2018.02.001 YFOOT 1527
To appear in:
The Foot
Received date: Revised date: Accepted date:
12-7-2017 27-1-2018 14-2-2018
Please cite this article as: Marco G, Flex A, Surgical treatment for chronic Charcot Neuroarthropathy, The Foot (2018), https://doi.org/10.1016/j.foot.2018.02.001 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Surgical treatment for chronic Charcot Neuroarthropathy
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• Charcot Neuro-arthropathy (CN) is a condition characterized by a progressive derangement of the joints, in individuals affected with sensitive and autonomic neuropathy. • CN is a well know dilemma in the management of the diabetic foot. In literature, there is no uniformity in the clinical and surgical care of this condition, and the treatment is often left to the surgeon’s experience. • There are several surgical procedures accepted in Charcot foot surgery. Their goal is to obtain a plantigrade foot and prevent recurrent ulcerations. • Exostectomy is a viable option provided the deformity is stable. • Arthrodesis is a well-known surgical procedure that addresses severe joint derangement through a surgically induced bony fusion. In Charcot foot, arthrodesis is usually indicated when there is significant skeletal instability. • Arthrodesis could concern midfoot or/and ankle. This procedure can be done by internal or external fixation. • Patients may eventually undergo a major amputation because of comorbidities, residual intractable deformity, infection, recurrent ulcers, failure obtaining a solid bony fusion and consequent recurrence of structural instability.
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Surgical treatment for chronic Charcot Neuroarthropathy Galli Marco, Scavone Giuseppe, Vitiello Raffaele, Andrea Flex, Caputo Salvatore, Pitocco Dario
52 Authors
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Galli Marco, Università Cattolica del Sacro Cuore, [email protected]
55
Scavone Giuseppe, Università Cattolica del Sacro Cuore, [email protected]
56
Vitiello Raffaele, Università Cattolica del Sacro Cuore, [email protected]
57
Andrea Flex, Università Cattolica del Sacro Cuore, [email protected]
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Caputo Salvatore, Università Cattolica del Sacro Cuore, [email protected]
59
Dario Pitocco, Università Cattolica del Sacro Cuore, [email protected]
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Corresponding author: Vitiello Raffaele, Università Cattolica del Sacro Cuore,
64
[email protected], +393407723095
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Surgical treatment for chronic Charcot Neuroarthropathy
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[1] Charcot Neuro-arthropathy (CN) is a condition characterized by a progressive derangement of the joints (fig. 1), in individuals affected with sensitive and autonomic neuropathy [1]. Jean-Martin Charcot who related this pathology to the syphilis first described the disorder. In 1936 Jordan observed CN among diabetic patients, but it was later recognized that the condition could be found also in other diseases such as leprosy, HIV, spina bifida, amyloidosis, alcoholism and renal dialysis [2]. The pathogenesis of CN is undoubtedly multifactorial [2]. A central role is played by the loss of sensitivity, but it is sure that sensitivity impairment alone is not enough to trigger the pathology. About 5 out of a 100 patients with DM will develop peripheral neuropathy but among this latter population only 8.5 out of 1000 individuals will suffer with CN involving the joints of the foot [34]. Peripheral neuropathy leads to a loss of protective sensation and abnormal foot biomechanics with altered distribution of the load. These alterations help to developed dislocations, trauma and fracture. In this acute phase, an inflammatory cascade through increased expression of proinflammatory cytokines, like TNFα and interleukin 1β leads to increased expression of the nuclear transcription factor, NF-κB, which results in increased osteoclastogenesis [5]. Osteoclasts cause progressive impairment of the bones until fractures, dislocations and then ulcerations occur. For this reason, cytokines and their receptors are now day intensively investigated. Rizzo et al. studied the association between post-translational modifications of collagen I and II and the presence of related autoantibodies in CN population [6]. Another topic concerns the role of genetic predisposition as studied by Pitocco and coll. [7] that founded a significant genetic association of CN patients with a osteoprotegerin pleomorphic expression that leads to a defective osteoprotegerin-RANKL regulation. Another important chapter of pathophysiology of CN concern the dysregulation of Autonomic Nervous System. In fact, neuropathy may affect the peripheral autonomic nervous system with an impairing arterial perfusion and altered cellular turnover of foot and ankle bones [8]. The consequences of this changes are the formation of arteriovenous shunting and increased arterial perfusion [9] that causes during the acute inflammatory phase an intensification of bone osteolysis. When CN turn into its chronic stage those features that are characteristic of the acute inflammatory stage give way to other manifestations such as deformity, unstable joint dislocations, untreatable bony protrusions, ulceration with superficial or deep infection and osteomyelitis. Infection results in a high incidence of amputations, Saltzman et al. estimated that amputation affects 2.7 % of patients with CN [10]. CN almost exclusively affects the foot and ankle, being extremely rare other locations in DM patients. It commonly presents in the midfoot, but it may also occur in the forefoot and hindfoot. Today diabetes is the most common cause of CN in developed countries. CN is cause of significant increase of morbidity and mortality in the DM population (mortality rate is increased about 28% in patient affected by CN) [11]. CN is a well know dilemma in the management of the diabetic foot. In literature, there is no uniformity in the clinical and surgical care of this condition, and the treatment is often left to the surgeon’s experience [12].
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Pre-op management The main indications for surgery in Charcot disease at the foot and ankle are fixation of potentially unstable bony structure derangements and correction of a severe stable deformity that compromises the functionality of the limb and is at high risk for ulceration and infection [12]. Careful pre-operative patient assessment should first consider patient’s general condition, comorbidities and compliance. Multidisciplinary teams should carry out appropriate preoperative renal and cardiovascular evaluations and provide an acceptable control of blood sugar levels. Good patient compliance is important for the outcome of complex surgical procedures and should not be overlooked altogether with a realistic analysis of the social and logistic set up. Vascularity is seldom a problem in CN patients, but should always be carefully investigated to avoid significant drawbacks. Preoperative transcutaneous oximetry is a widely-accepted procedure for patient selection. A pressure gradient of >50 mm Hg is the least acceptable preoperative threshold for a safe surgical treatment. Lower values require further investigations [13]. Doppler ultrasound and, if necessary, Angio-CT of the lower limbs are indicated. Patients susceptible of an effective revascularization should go for a Angio-PTA or other more invasive vascular procedures to recover distal tissues to an acceptable oxygen partial pressure. If transcutaneous oximetry levels persist below 40/35 mm Hg, an amputation should be considered. Local cutaneous conditions as well as the presence or absence of a deep infection or osteomyelitis profoundly influence the indication to surgery. Ulcers should be carefully assessed and classified. A clinical examination is generally sufficient to rule out deep and massive cutaneous losses with bone exposure and infection or osteomyelitis. In diabetic patients, deep infections and severe osteomyelitis are serious surgical and medical problems that overcome the presence of a CN disease. They should be promptly addressed and often conduct to mayor amputations. Superficial ulcers do not represent a contraindication for CN surgical procedures, but significantly impact on the selection of the surgical treatment. First, it should be ascertained whether the ulcer is infected or simply contaminated. Contaminated ulcers may be treated simultaneously with a CN disorder in a one staged surgical procedure. Infected ulcers with an undermining osteomyelitis are preferentially treated before a major surgery for CN. Osteomyelitis is a dreaded complication that affects up to 20% of all diabetic patients who experience a cutaneous lesion at the foot [14]. The detection of an infection to the bone underneath an ulcer and the correct appraisal of its extent and relevance are sometime very complicated. A final decision is a matter of clinical experience. There is a consensus on the liability of some clinical indicators of osteomyelitis occurrence. The most obvious is the presence of exposed bone at the bottom of the ulcer. Other less immediate clinical indicators are: the observation of signs of inflammation involving the cutis stretching around the ulcer’s boundaries for more than 2 cm; the other is named “probe to bone test” and suggests an undermining osteomyelitis if one can feel the sensation of touching the bone beneath the tip of a probe exploring deeply into the lesion. Once osteomyelitis is suspected many other examinations are commonly carried out in the attempt to refine the diagnosis and acquire a better understanding of the severity of the disease. Although there are a remarkable number of investigations that may be considered, either simple such as blood tests or more sophisticated such as WBS scintigraphy, MDP scintigraphy and MRI, it is not uncommon that a final reliable diagnosis is made upon the results of a bone biopsy with cultural examination. There are many confounding factors among diabetic patients with plenty of comorbidities and a massive normal anatomy derangement due to CN. Imaging modalities and diagnostic tests show ambiguous value of sensitivity and specificity and it is difficult to determine which examination is the most reliable. In table 1 we present the value of LR+ (Positive Likelihood Ratio), LR‐ (Negative Likelihood Ratio) and DOR (Diagnostic Odds Ratio) for those afore mentioned most credited clinical indicators of osteomyelitis confronted with the same values for blood tests and functional or morphological studies by means of different imaging modalities. LR+,
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LR‐ and DOR are determined using the values of sensitivity and specificity reported on two reviews published in 2015 [15, 16]. Table 1 highlights how MRI is the most credited diagnostic modality by displaying the highest overall diagnostic value (DOR=33.1). But, due to its low specificity, the liability of a MRI positive results remains below that of the mere clinical judgment (LR+ = 4.3 vs 5.5 respectively), let alone that of other clinical finding such as “Probe to bone test” (LR+ = 6.4), ulcers wider than 2 cm2 (LR+ = 7.2) and exposed bone (LR+ = 9.2). In addiction, if one considers that these values are drawn from studies broadly concerned with diabetic foot infections it is not unlikely that MRI performance might be even worse in CN patients. It is not a secret that it remains a challenge to discriminate active Charcot neuro-osteoarthropathy from acute osteomyelitis with MRI. This is simply the case because MR imaging features are quite similar. Both entities will show subchondral bone marrow edema, joint effusions, soft tissue inflammatory changes (high signal intensity on T2 fatsat or STIR, somewhat low signal intensity on T1) and enhancement of bone and soft tissue after contrast administration [17]. A possible overcome to the problem might come from a widespread diffusion of the new Hybrid PET/MRI scanners that combine the high sensitivity of MRI studies to the high specificity of FDG-PET investigations. Even though X-ray might be inconclusive for bone infections they are certainly fundamental for planning surgical treatment and identifying the pattern type of foot involvement. Sanders-Frykberg classification describes five patterns, according to the localization of bone and joint pathology. The acknowledgment of the pattern type provides valuable prognostic information. Forefoot CN is the least progressive and harmful pattern (pattern1 of Sanders-Frykberg classification). In forefoot CN, metatarsophalangeal (MTP) and interphalangeal joints are involved [18-19-20]. Disease progression is usually favorable and conservative treatment is generally sufficient. Surgery is rarely necessary, but is mandatory for correction of an intractable first metatarsophalangeal dislocation. Midfoot CN is far more likely to proceed to severe deformity and plantar ulcerations (patterns 2 and 3 of Sanders-Frykberg classification). Diabetic midfoot CN is characterized by the involvement of either the Lisfranc or the Chopart joints or both (patterns 2 and 3 of Sanders-Frykberg classification respectively). In these cases, the typical deformity that eventually develops is the so-called “rocker bottom deformity” which is characterized by a plantar collapse of the midfoot. The disease causes a weakening of the skeletal structure of the foot that collapses losing its normal “arch” configuration (fig. 1). The process takes place at different spots in the bony and ligamentous structure. If the process starts with a navicular and cuboid fragmentation it generally progresses with a talus and cuboid plantar dislocation and ulceration below the calcaneo-cuboid prominence (fig. 2). If the process begins with a naviculocuneiform dislocation, instead, it will continue with first metatarsal dorsal displacement and medial cuneiform or navicular plantar displacement causing plantar ulceration. In this case, the pull of the anterior tibialis muscle on the first metatarsal actively exacerbate the fragmentation and displacement, making conservative treatment ineffective even in non-weight bearing conditions. Both processes are equally common and unfortunately once fragmentation has intervened it is impossible to tell what was the type of onset and the eventual outcome. Midfoot CN usually respond to conservative treatment. Conservative treatment is based on foot unloading and immobilization into a Total Contact Cast or a dedicated orthotic boot. It is mandatory at the early stages of the disease. Cases irresponsive to conservative treatment are demanded to surgery. Ankle and subtalar joint CN patterns are the most intractable because they give rise to extremely unstable deformities (patterns 4 and 5 of Sanders-Frykberg classification respectively). Ankle and subtalar joint CN are rarely responsive to conservative treatment and surgery remains the only valid option. If multiple locations are concerned, a major below knee amputation should be considered.
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There are several surgical procedures accepted in Charcot foot surgery. Their goal is to obtain a plantigrade foot and prevent recurrent ulcerations. Achilles tendon lengthening, plantar bony prominence resection, osseous debridement, corrective or “in situ” bone fusion are the most widely used to achieve the desired result.
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Exostectomy
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Roker bottom deformities, either because of Lisfranc or Chopart joint complex breakdown, are frequently cause of intractable plantar ulcers (fig. 2). Problematic plantar bony prominences due to tarsal bones displacement into non-anatomic position may not be easily accommodated with orthotic and prosthetic measures. Exostectomy is then a viable option provided the deformity is stable. In fact, if the deformity is unstable surgery might worsen the plantar displacement of tarsal bones with recurrent ulcers due to intractable bony prominences [21-22-23]. When the deformity is stable the resection of plantar bony prominences improves plantar pressure distribution, promoting ulcers healing. Thus, exostectomy is used to restore a plantigrade foot and return the patient to full weight bearing without addressing the deformity. Exostectomy is performed through a direct or indirect surgical approach. Direct approach is carried out by means of a single surgical approach either for excision of the ulcer and for removal the underlying bony prominence. In order to prevent cross contamination, indirect approach requires two separate incisions: one for excision of the ulcer and another for removal of the bony prominence.. Unfortunately indirect approach is often unfeasible. Deep ulcers reaching down to the exostoses together with bone exposure often hamper a double approach. Exostectomy is a well-established surgical practice and its effectiveness in midfoot Charcot complication treatment had been confirmed by several studies [24]. Exostectomy may be performed alone or in combination with Achilles’ tendon lengthening or gastrocnemius recession. These adjunctive procedures are required when there is a severe contracture of the triceps surae that brings the rear and midfoot into an equinus position [25]. The aim is direct to decrease dynamic forefoot plantar pressure and improve rear-midfoot to forefoot alignment. A test used to determine whether the contracture is confined to the Gastrocnemius muscles is the “Silfverskiod Test” [26]. It consists of a clinical maneuver that assesses the variation of maximum foot and ankle dorsiflexion when the knee is brought from a full extension to a 90 degrees flexed position. The test is considered positive when there is a significant increase of foot and ankle dorsiflexion at knee flexion. Mueller and colleagues [27] carried out a randomized controlled trial to compare the recurrence rate of ulceration in patients with neuropathic plantar ulcers treated with Achilles-tendon lengthening plus PCC (test group), and PCC alone (control group). At seven months’ follow-up, 15% of patients in the test group had an ulcer recurrence, compared to the 59% of patients in the control group. Percutaneous Achilles tendon lengthening represents one of the most frequent surgical choices for triceps surae muscle contracture. Care should be taken to minimize the loss of overall muscular strength to avoid a ticeps surae muscle insufficiency that is the most fearful drawback of the procedure.
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Arthrodesis Arthrodesis is a well-known surgical procedure that addresses severe joint derangements through a surgically induced bony fusion. In diabetic foot, arthrodesis is usually indicated in some of type 2 and 3 CN midfoot skeletal collapses and almost always in type 4 and 5 CN structural failure.
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Midfoot In midfoot collapse, when there is significant skeletal instability a simple Exostectomy of a plantar bony prominence does not ensure long-term results. Arthrodesis instead can reach durable results by surgical fusion of midfoot joints. Functional impairment secondary to such a massive loss of motion segments is accepted because the primary goal of surgical treatment in CN is to return the patient to full weight bearing and free deambulation without supportive aids (canes, crutches etc.) and recurrent ulceration. Diabetic foot surgeries are preferentially limb salvage procedures that aim to acceptable functional and clinical results with sustainable medical costs. [28] Schon et al. observed that midfoot lateral column collapse has a worse prognosis either a plantar ulceration had already occurred or not [29]. Furthermore, Catanzariti et al. reported that lateral column collapse show a lower rate of plantar ulcer healing compared to medial column collapse after esostectomy alone [30]. It seems that lateral column collapse with plantar bony prominences should be treated more aggressively at once avoiding unsuccessful delays. In a broad view the main indications for arthrodesis in type 2 and 3 CN are the following: • Unstable midfoot skeletal derangement where conservative treatment has failed to prevent further evolution of the deformity • Lateral midfoot collapse with rocker bottom deformity that presents a plantar ulcer or is susceptible to produce ulceration • Recurrent ulceration after esostectomy for plantar bony prominence • Stable gross deformity with ulceration or pre-ulcerative lesion where esostectomy is not feasible or insufficient. Internal fixation has been for long the most widely accepted method for arthrodesis fixation in midfoot CN surgery. Arthrodesis is performed through large surgical approaches to remove prominent bone, reduce dislocated bony segments and grossly align the rearfoot to the forefoot. Internal fixation is then performed by means of screws, plates or staples to stabilize the site of arthrodesis and the neighbouring bones [31-32]. To maximize the probability of good results, it is accepted and advisable to spread the internal fixation beyond common limits as to form a so-called “super-construct”. In a super-construct, internal fixation prolongs well beyond the limits of the areas involved by the Charcot process. Its purpose is to increase stability and decrease the likelihood of fixation failure. Super-construct locking plates span the entire length of the medial column, providing rigid stability and good anatomic alignment [33-34]. Suggested criteria are the following [35]: • internal fixation should extend beyond the zone of skeletal collapse and include non-affected bone • bone resection should be performed to shorten the skeleton to achieve adequate reduction of the deformity without tension on the soft tissues • the hardware needed for fixation should not be so superficial or massive as to interfere with soft tissues healing. • hardware should be applied in a position that maximize its mechanical competence. Together with the above criteria there is another recommended principle to follow. Arthrodesis by internal fixation should be avoided in acute inflammatory Eichenholtz stage 1 CN in order to prevent poor outcomes due to disease progression. A massive surgical exposure triggers disease
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progression with fragmentation and bony destruction. Surgery by invasive internal fixation should be confined to Eichenholtz stage 2 or 3 CN. Ankle Patients suffering from Type 4 CN that caused either a remarkable derangement of the joints surrounding the talus or a massive talar bone loss are eligible for tibiocalcaneal arthrodesis. Tibiocalcaneal arthrodesis is performed by internal or external fixation. In diabetic patients, external fixation is mandatory in case of deep infection, osteomyelitis and poor soft tissue coverage [36]. Poor patient compliance, frequent pin tract medications, long duration of patient surveillance and medicalization often discourage the usage of external fixation. Several internal fixation systems have been put forward in the recent years. Retrograde intramedullary ankle nail fixation has gained popularity because of its many mechanical advantages [37]. It can provide the patient with such a stable fixation that adjunctive external immobilization devices such as plasters or braces are generally felt unnecessary. An enhancement of the overall stability through an external immobilization is necessary only when there is some concern that a solid internal fixation could not be obtained because of poor bone stock. Bone union rates vary among diabetic patients (fig. 3). Dalla Paola and others [38] achieved a solid bony union in 14 patients out 18 of their series, the remaining 4 patients showing findings of fibrous union (fig 4). Their rate of limb salvage was 100%. Caravaggi and others [39] reported only one case of unsuccessful result that required a below-knee amputation and obtained a 71% bony union rate, a fibrous union in the 21%. Recent incremental innovations in retrograde ankle nails design have furthermore refined the already sophisticated previous nails. There are new dedicated nails that allow correct hindfoot alignment and fixation by an adequate bending along their longitudinal axis and plenty availability of interlocking screws along the sagittal plane of the os calcis. Pinzur et al in 2005 reported on a consecutive series of nine diabetic patients with ankle Charcot arthropathy [40]. They used long retrograde femoral nails for internal fixation of their ankle arthrodesis to cover the whole length of the tibia with the surgical instrumentation to prevent the occurrence of mechanical stress concentration and stress fractures at the tip of the nails. Although tibia stress fractures at the tip of the nail do occur, they are not reported in recently published series of diabetic Charcot foot patients [39]. A recent study tried to evaluate the results of retrograde intramedullary nailing (IMN) for severe ankle/hindfoot pathology in a group of patients with diabetic neuropathy and compare them to a cohort of non-diabetic patients. Although a postoperative complication was experienced in a 59% of cases with DM compared to a 44% without DM, the difference did not reach statistical significance due to the small number of patients available [41]. In their statistical analysis, they calculated that a sample of at least 100 patients in each group would be necessary to achieve an adequate statistical power. Since large series from multicentric studies are yet to be investigated, no definitive agreement had been reached. At the moment tibio-calcaneal arthrodesis in diabetic CN is generally felt as a salvage procedure with high rates of post-operative complication whatever the internal fixation construct utilized. Other undesired drawbacks are: poor anatomic correction (i.e. shortening of the foot or incomplete deformity correction), occasional neurovascular problems, wound healing complications and infections.
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Arthrodesis with external fixation
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External fixation in diabetic CN has gained increasing popularity [40-42]. It offers some significant advantages being less invasive and avoiding the presence of bulky internal hardware [43]. It is mandatory in the presence of osteomyelitis or deep ulceration and is recommended with poor soft tissue coverage, poor bone quality and morbid obesity [44]. Pinzur and colleagues [45-46] carried out the largest study concerned with a single-stage procedure for arthrodesis of midfoot CN with osteomyelitis. They adopted the following protocol of treatment: -Bacterial isolation obtained from resected bone samples during surgical bone debridement to guide antibiotic therapy. -Surgical correction to achieve a plantigrade foot with percutaneous pins for temporary fixation and 3-level prebuilt static circular external fixator for definitive fixation (fig 5). External fixator was maintained for a period of 8 weeks in patients with midfoot CN and a minimum of 12 weeks in those with hindfoot or ankle CN. Post-operative wounds care was a little hampered by the presence of the external fixation hardware, but the overall management was easier and more effective than that it would have been in the presence of a cast or an orthotic boot. -Removal of external fixator and short leg casting for 4 to 6 weeks. -Definitive therapeutic footwear consisting in commercially available depth-inlay shoes and custom accommodative foot orthoses, occasionally preceded by commercially available diabetic patients orthopedic boots. Using this protocol, the researchers could achieve 95.7 % limb salvage. In addition, Pinzur used the external fixator to restore a plantigrade foot among obese patients with Charcot metatarsal deformity and ulceration. 24 out of 26 feet were free of ulcer and able to walk with custom made diabetic shoes and orthoses at a minimum one-year follow-up. Recently external fixation has been applied to patients with acute Eichenholtz stage I CN. There is an increasing number of studies confirming the possibility of preventing the progression of bone destruction and deformity through an external surgical fixation at this stage [47]. As already mentioned arthrodesis by internal fixation is contraindicated in Acute Eichenholtz stage I for two main reasons. One is that bone is soft and hyperemic and offers a poor mechanical support to internal fixation. The other is that the extensive surgical exposures needed for setting an internal fixation promote the progression of the CN itself. An external fixation instead offers the advantage of requiring only minimally invasive procedures. Thus, is explained the use of external fixation in the acute phase until evidences of bony coalescence at x-ray examination together with edema and thermal gradient decrease at clinical examination are accomplished. Moreover, external fixation allows a gradual realignment of bony segments, which reduces the risk of neurovascular injury secondary to overstretching. Among the disadvantages of external fixation, the most discouraging is poor patient compliance (fig. 6) and pin tract infection. Refusal of medicalization and poor selfhygiene make often part of the peculiar trait of diabetic patients. Thus, intolerance to the presence of the metallic hardware and to the long duration of treatment come often together with refusal to undergo regular pin-tract hygiene in a devastating combination that leads to failure of treatment and major amputation [48-49]. Prevention of infection is largely based on strict patient education about regular pin tract hygiene and regular medical referral. As soon as there are obvious signs of infection, the surgeon should consider the need to remove them or abandon external fixation in favour of other treatments. External fixation can also be used for improving internal fixation. Combined internal and external fixation is often preferred for complex and gradual reconstruction in severely deformed foot. Paley proposed a staged method of correction [50]. The first stage aims at skeletal realignment and simultaneous soft tissue healing by gradual correction with an external fixator. The second step is committed to stabilization of the result through the achievement of a solid arthrodesis by means of a
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minimally invasive internal fixation. The external fixator is removed and arthrodesis is accomplished with percutaneous insertion of intramedullary, fully threaded, cannulated screws that are drilled through the head of the metatarsal bones. Three screws are generally needed: one for the medial column through the first metatarsal up to the talus another for lateral column through the fifth metatarsal up to the calcaneus and eventually a third screw connecting the talus to the calcaneus. They should cover the entire length of the metatarsals to the calcaneus and talus and stabilize the affected joints to the adjacent unaffected bone. In this way one should seek to provide a solid fixation into sound bone and prevent the spread of CN destruction to the adjacent bony segments.
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Amputation
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Even though the main goal of CN surgical treatment is limb salvage, amputation should be considered in selected cases. A major amputation may be a valid option in patients with comorbidities, residual intractable deformity, infection, recurrent ulcers and failure of previous treatment with consequent recurrence of structural instability. The rate of major amputation is reasonably low in CN population nowadays. Saltzman et al. reported a 2.7% rate [51], but a major amputation remains an undesirable end term event among fragile diabetic patients and it should be as far as possible avoided. Fragile diabetic patients presents many unsolved rehabilitation problems and may hardly recover even with the more advanced prosthetic limbs. Disability reduces the life expectancy significantly in diabetic patients. 5 years mortality rate after unilateral below-knee amputation is about 50% among the general population. Within the diabetic population the same rate of mortality after unilateral below-knee amputation is reached two years earlier [52] and the risk of developing a contralateral amputation is almost doubled within 2 years [53]. A condition that strongly recommends a major amputation is that of patients with intractable infections, especially in case of multi-drug-resistant organisms in individuals with PAD of the lower limbs. Another condition is that of patients whose outcome after several surgical procedures is a poor functional lower limb, incapable of bearing weight, despite any success in healing from osteomyelitis [54-55]. Amputation may be performed at various levels. Trans-tibial amputation is usually preferred, as prosthetic fitting is easier. Alternative procedures should be considered for patients with limited mobility and vision problems. Syme and Pirogoff amputations are designed to leave the patient with a lower limb stump that allows an acceptable walking autonomy. The aim is to obtain a functional stump (shortening of about 5 cm at the worst) that allows the patient to walk short distances without accommodative shoes.
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Biography
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1. Charcot JM. Sur quelaques arthropathies qui paraissent depender d’une lesion du cerveau ou de la moele epiniere. Arch De Physiol Norm et Path 1868; 1: 161–171. 2. Wukich DK and Sung W. Charcot arthropathy of the foot and ankle: modern concepts and management review. J Diabetes Complications 2009; 23: 409–429. 3. Young MJ, Boulton AJM, Macleod AF, Williams DRR, Sonksen PH. A multicentre study of the prevalence of diabetic peripheral neuropathy in the United Kingdom hospital clinic population. Diabetologia 36:150–154, 1993 4. Lavery LA, Armstrong DG, Wunderlich RP, Tredwell J, Boulton AJ. Diabetic foot syndrome: evaluating the prevalence and incidence of foot pathology in MexicanAmericans and non-Hispanic whites from a diabetes management cohort. Dia- betes Care 26:1435–1438, 2003. 5. Rogers LC, Frykberg RG, Armstrong DG, Boulton AJ, Edmonds M, Van GH, Hartemann A, Game F, Jeffcoate W, Jirkovska A, Jude E, Morbach S, Morrison WB, Pinzur M, Pitocco D, Sanders L, Wukich DK, Uccioli L. The Charcot Foot in Diabetes. Diabetes Care 34:2123–2129, 2011 6. Rizzo P, Pitocco D, Zaccardi F, Di Stasio E, Strollo R, Rizzi A, Scavone G, Costantini F, Galli M, Tinelli G, Flex A, Caputo S, Pozzilli P, Landolfi R, Ghirlanda G, Nissim A. Autoantibodies to Post-Translationally Modified Type I and II Collagen in Charcot Neuroarthropathy in Subjects With Type 2 Diabetes Mellitus. Diabetes Metab Res Rev 33 (2). 2016 Oct 05. 7. Pitocco D, Zelano G, Gioffrè G, Di Stasio E, Zaccardi F, Martini F, Musella T, Scavone G, Galli M, Caputo S, Mancini L, Ghirlanda G. Association between osteoprotegerin G1181C and T245G polymorphisms and diabetic charcot neuroarthropathy: a case-control study. Diabetes Care. 2009 Sep;32(9):1694-7 8. Gouveri E, Papanas N. Charcot osteoarthropathy in diabetes: a brief review with an emphasis on clinical practice. World J Diabetes. 2011;2:59–65 9. Gilbey SG, Walters H, Edmonds ME, Archer AG, Watkins PJ, Parsons V, et al. Vascular calcification, autonomic neuropathy, and peripheral blood flow in patients with diabetic nephropathy. Diabet Med. 1989;6:37–42 10. Saltzman CL. Et coll. How effective is intensive nonoperative initial treatment of patients with diabetes and Charcot arthropathy of the feet? Clin Orthop Relat Res. 2005 Jun;(435):185-90. 11. Sohn MW, Lee TA, Stuck RD, et al. Mortality risk of Charcot arthropathy compared with that of diabetic foot ulcer and diabetes alone. Diabetes Care 2009; 32(5): 816–821. 12. Schneekloth BJ, Lowery NJ, Wukich DK. Charcot Neuroarthropathy in Patients With Diabetes: An Updated Systematic Review of Surgical Management. The Journal of Foot & Ankle Surgery 55 (2016) 586–590 13. Sohn MW, Stuck RM, Pinzur M, et al. Lower-extremity amputation risk after Charcot arthropathy and diabetic foot ulcer. Diabetes Care 2010; 33(1): 98–100. 14. Kagna O, Srour S et al. 18F‐FDG PET/CT imaging in the diagnosis of the osteomyelitis in the diabetic foot Eur J Med Molecul Imaging 2012; 39: 1545‐50 15. Markanday A Diagnosing diabetic foot osteomyelitis: narrative review and a suggested 2‐step – score‐based diagnostic pathway for clinicians Open Forum Infect Dis 2015 Jul3; 2(3) ofv098 16. Khodaee M, Lombardo D et al Q/What’s the best test for underlying osteomyelitis in patients with diabetic foot ulcers? The Journal of Family Practice 2015; 64(5): 309‐21
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17. Ergen FB, Sanverdi SE, Oznur A. Charcot foot in diabetes and an update on imaging. Diabet Foot Ankle. 2013;4:21884. 18. Varma V, Varma AK, Mangalandan TS, Bal A, Kumar H. Use of polymethyl methacrylate as prosthetic replacement of destroyed foot bonesdcase series. J Diabetic Foot Complications 4:71–82, 2012. 19. Shibata T, Tada K, Hashizume C. The results of arthrodesis of the ankle for leprotic neuroarthropathy. J Bone Joint Surg Am 72:749–756, 1990. 20. Brodsky JW. The diabetic foot. In: Surgery of the Foot and Ankle, ed 6, pp. 278–283, edited by RA Mann, MJ Coughlin, Mosby, St. Louis, 1993. 21. Sanders LJ, Frykberg RG. The Charcot Foot. In: The High Risk Foot in Diabetes Mellitus, pp. 325–335, edited by RG Frykberg, Churchill Livingstone, New York, 1991. 22. Laurinaviciene R, Kirketerp-Moeller K and Holstein PE. Exostectomy for chronic midfoot plantar ulcer in Charcot deformity. J Wound Care 2008; 17: 53–59. 23. Brodsky JW and Rouse AM. Exostectomy for symptomatic bony prominences in diabetic Charcot feet. Clin Orthop Relat Res 1993; 296: 21−26. 24. Catanzariti AR, Mendicino R, Haverstock B. Ostectomy for diabetic neuro- arthropathy involving the midfoot. J Foot Ankle Surg 39:291–300, 2000. 25. Armstrong DG, Lavery LA. Elevated peak plantar pressures in patients who have Charcot arthropathy. J Bone Joint Surg Am 80:365–369, 1998. 26. Hastings MK, Mueller MJ, Sinacore DR, Salsich GB, Engsberg JR, Johnson JE. Effects of a tendo-Achilles lengthening procedure on muscle function and gait characteristics in a patient with diabetes mellitus. J Orthop Sports Phys Ther 30:85–90, 2000. 27. Symeonidis P.The Silfverskiöld Test. Foot Ankle Int. 2014 Aug;35(8):838. Epub 2014 Jul 28. Mueller MJ et Al. Effect of Achilles tendon lengthening on neuropathic plantar ulcers. A randomized clinical trial. J Bone Joint Surg Am. 2003 Aug;85-A(8):1436-45. 29. Dhawan V, Spratt KF, Pinzur MS, Baumhauer J, Rudicel S, Saltzman CL. Reliability of AOFAS diabetic foot questionnaire in Charcot arthropathy: stability, internal consistency, and measurable difference. Foot Ankle Int 26:717–731, 2005. 30. Schon LC. Charcot neuroarthropathy of the foot and ankle. Clin Orthop Relat Res. 1998 Apr;(349):116-31. 31. Catanzariti AR. Ostectomy for diabetic neuroarthropathy involving the midfoot. J Foot Ankle Surg. 2000 Sep-Oct;39(5):291-300. 32. Wukich DK, Joseph A, Ryan M, Ramirez C, Irrgang JJ. Outcomes of ankle fractures in patients with uncomplicated versus complicated diabetes. Foot Ankle Int 32:120–130, 2011. 33. Ayoub MA. Ankle fractures in diabetic neuropathic arthropathy: can tibiotalar arthrodesis salvage the limb? J Bone Joint Surg Br 90:906–914, 2008. 34. Crim B, Lowery N, Wukich D. Internal fixation techniques for midfoot Charcot neuroarthropathy in patients with diabetes. Clin Podiatric Med Surg 28:673–685, 2011. 35. Sammarco VJ. Superconstructs in the treatment of Charcot foot deformity: plantar plating, locked plating and axial screw fixation. Foot Ankle Clin 14:393– 407, 2009. 36. Moeckel BH, Patterson BM, Inglis AE, Sculco TP. Ankle arthrodesis. A comparison of internal and external fixation. Clin Orthop Relat Res. 1991 Jul;(268):78-83. 37. Millett PJ, O'Malley MJ, Tolo ET, Gallina J, Fealy S, Helfet D. Tibiotalocalcaneal fusion with a retrograde intramedullary nail: clinical and functional outcomes. Am J Orthop (Belle Mead NJ). 2002 Sep;31(9):531-6 38. Dalla Paola L, Brocco E, Ceccacci T, Ninkovic S, Sorgentone S, Marinescu MG, Volpe A. Limb salvage in Charcot foot and ankle osteomyelitis: combined use single stage/double stage of arthrodesis and external fixation. Foot Ankle Int 2009; 30(11): 1065–1070. 39. Carlo Caravaggi, MD, Marzio Cimmino, MD, Sebastiano Caruso, MD, and Sergio Dalla Noce, MD. Intramedullary Compressive Nail Fixation for the Treatment of Severe Charcot
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Deformity of the Ankle and Rear Foot. The Journal of Foot & Ankle Surgery 45(1):20–24, 2006. 40. Michael S. Pinzur, Timothy Noonan. Ankle Arthrodesis with a Retrograde Femoral Nail for Charcot Ankle Arthropathy. Foot & Ankle International/Vol. 26, No. 7/July 2005. 41. Dane K. Wukich, James Y.C. Shen, Claudia P. Ramirez, James J. Irrgang. Retrograde Ankle Arthrodesis Using an Intramedullary Nail: A Comparison of Patients with and without Diabetes Mellitus. The Journal of Foot & Ankle Surgery 50 (2011) 299–306 42. Zarutsky E, Rush SM and Schuberth JM. The use of circu- lar wire external fixation in the treatment of salvage ankle arthrodesis. J Foot Ankle Surg 2005; 44: 22–31. 43. Farber DC, Juliano PJ, Cavanagh PR, Ulbrecht J, Caputo G. Single stage cor- rection with external fixation of the ulcerated foot in individuals with Char- cot neuroarthropathy. Foot Ankle Int 2002; 23: 130–134. 44. Cooper PS. Application of external fixators for management of Charcot deformities of the foot and ankle. Foot Ankle Int 2002; 7(1): 207–254. 45. Pinzur MS, Sammarco VJ, Wukich DK. Charcot Foot: A Surgical Algorithm. Instructional Course Lectures of the American Academy of Orthopaedic Surgeons. 61: 423–440. 2012. PMID: 22301251. 46. Pinzur MS, Gil J, Belmares J.Treatment of osteomyelitis in Charcot foot with sin- gle stage resection of infection, correc- tion of deformity and maintenance with ring fixation. Foot Ankle Int 2012; 33: 1069-1074. PMID: 23199855. 47. Paul Dayton, Mindi Feilmeier, Mitchell Thompson, Paul Whitehouse, Rachel A. Reimer. Comparison of Complications for Internal and External Fixation for Charcot Reconstruction: A Systematic Review. The Journal of Foot & Ankle Surgery 54 (2015) 1072–1075 48. Caravaggi C, Cimmino M, Caruso S, Dalla Noce S. Intramedullary compressive nail fixation for the treatment of severe Charcot deformity of the ankle and rear foot. J Foot Ankle Surg 45:20–24, 2006. 49. Fleming B, Paley D, Kristiansen T, Pope M. A biomechanical analysis of the Ilizarov external fixator. Clin Orthop 241:95–105, 1989. 104. Bevilacqua N, Rogers L. Surgical management of Charcot midfoot deformities. Clin Podiatr Med Surg 25:81–94, 2008. 50. Lamm BM, Gottlieb HD, Paley D. A two-stage percutaneous approach to Charcot diabetic foot reconstruction. J Foot Ankle Surg 49:517–522, 2010. 51. Saltzman CL, Hagy ML, Zimmerman B, et al. How effec- tive is intensive nonoperative initial treatment of patients with diabetes and Charcot arthropathy of the feet? Clin Orthop Relat Res 2005; 435: 185–190. 52. Armstrong DG, Wrobel J, Robbins JM. Guest editorial: are diabetes-related wounds and amputations worse than cancer? Int Wound J 4:286–287, 2007. 53. Goldner MG. The fate of the second leg in the diabetic amputee. Diabetes 9:100–103, 1960. 54. Papa J, Myerson M and Girard P. Salvage, with arthrodesis, in intractable diabetic neuropathic arthropathy of the foot and ankle. J Bone Joint Surg Am 1993; 75(7): 1056– 1066. 55. Stone NC and Daniels TR. Midfoot and hindfoot arthrode- ses in diabetic Charcot arthropathy. Can J Surg 2000; 43: 449–455.
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634 Severe skeletal derangement after ankle and subtalar Charcot arthropathy
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636 637 Loss of plantar longitudinal arch after skeletal collapse secondary to Charcot disease is often cause of intractable ulcers.
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Fig 2
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646 647 Patient with Type 4 CN who had been performed a talo-calcaneal arthrodesis by means of a retrograde ankle nail through a trans-fibular lateral approach. Soft tissues and vascular supply attached to the external portion of the distal fibula were preserved and, after the osteotomy, a longitudinal splitting of the lateral malleolus was performed. The external portion of the malleolus was then fixed by two spare screws to the tibia and calcaneus providing a sort of vascularized bone graft bridging the lateral side of the site of arthrodesis. At four months follow-up the patient presented with a radiographic appearance of a solid bone union. Full weight bearing was allowed and canes abandoned.
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Fig 3
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651 652 653 654 655 656 657 658 Patient with Type 4 CN who underwent a talo-calcaneal arthrodesis by means of a retrograde ankle nail through an anterior approach. Four weight bearing lateral views of the ankle show the evolution observed in a 6 years follow-up. A – 6 months follow-up. The patient had fully recovered with complete weight bearing and prompt return to its normal daily activity. Radiographs showed the presence of a fibrous union and it was decided to remove one of the proximal locking screws to stimulate bone formation. B - 11 months follow-up. 5 months after removal of the proximal screw (notice the empty hole in the nail profile – arrow) no bone formation at the site of arthrodesis. The patient asked the removal of the distal locking screw because of discomfort at prolonged walking. The distal locking screw had been deliberately inserted into the midfoot to restrain the Chopart joint movement and span into an unaffected motion segment according to the “superconstruct” criteria. C – 2 years follow-up. 13 months after removal of the distal screw, the patient was attaining its normal daily activities without discomfort and radiographs showed what appeared as a stable fibrous union. D – 6 years follow-up. Radiographs showed finally the achievement of a complete bony union
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Fig 4
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667 Surgical correction of a severe deformity through a lateral trans-fibular approach in a patient affected with Type 4 CN. A - After a wide excision of a deep ulcer at the tip of the lateral malleolus, bacterial isolation and debridement were completed by removal of the lateral malleolus itself. B - The correction of the deformity was achieved and it was held in place by a couple of percutaneous K-wire (black arrow). C - Temporary fixation with percutaneous pins (black arrow) in order to achieve a plantigrade foot. D - Three-level prebuilt static circular external fixator for definitive fixation. Percutaneous pins are removed at the end of the surgical procedure (black arrow).
668
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668
Patient with Type 4 CN who underwent talo-calcaneal arthrodesis through an anterio Osteosynthesis was performed by means of external fixation (a circular frame with tw tibia by fiches and K-wires connected to a composite frame fixed to the rear and midf spite of the pre-operative acceptance of the planned treatment, at follow-up the patien complained for the presence of external hardware. After a short period of poor genera scarce attendance to scheduled outpatient care and pin-tract medications, the patient w
669 670
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670 DOR 10.2 15 13.1 16.4
11* 5** 2.8**
0.34* 0.18** 0.27**
32.4 27.8 10.4
1.7** 4.3**
0.68** 0.13**
2.5 33.1
1.1**
0.68**
2.3*
0.38*
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LR– 0.54* 0.48* 0.7* 0.39 *
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Table 1 lists the values LR+ and LR- reported in two recent literature reviews: * Markanday A, 2015 [15] ** Khodaee M et al, 2015 [16]. Diagnostic Odd Ratio (DOR=LR+/LR-) was calculated to provide the overall diagnostic value of each diverse modality. ***with no other plausible explanation.
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671 672 673 674 675 676 677 678 679 680 681 682 683 684 685 686 687 688 689 690 691 692 693 694 695 696 697 698 699 700 701 702 703
LR+ 5.5* 7.2* 9.2* 6.4 *
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Table 1 Clinical Judgment Ulc. > 2 cm2 Exposed Bone PTB (probe to bone) test ESR >70/1h *** CRP >14 mg/L Procalcitonin> 0.3 ng/ml Standard X-Rays Magnetic Resonance (MR) MDP Bone Scintigraphy Radiolabeled WBC Scintigraphy
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Surgical treatment for chronic Charcot Neuroarthropathy
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No one of the authors have any Conflict of Interest
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