Mid-term walking ability after Charcot foot reconstruction using the Ilizarov ring fixator.

BACKGROUND: Failed conservative treatment and complications are indications for foot reconstruction in Charcot arthropathy. External fixation using the Ilizarov principles offers a one-stage procedure for deformity correction and resection of osteomyelitic bone. The aim of this study was to determine whether external fixation with an Ilizarov ring fixator leads reliably to walking ability. MATERIALS AND METHODS: 29 patients treated with an Ilizarov ring fixator for Charcot arthropathy were retrospectively analyzed. Radiologic fusion at final follow up was assessed separately on conventional X-rays by two authors. The association between walking ability and the presence of osteomyelitis at the time of reconstruction, and the presence of fusion at final follow up was investigated using Fisher's exact test. RESULTS: Mean follow up was 35 months (range 5.3-107) months; mean time of external fixation was 113 days. Ten patients (34.5%) reached fusion, but 19 did not (65.5%). Two patients needed below knee amputation. 26 of the remaining 27 patients maintained walking ability, 23 of those without assistive devices. Walking ability was independent from the presence of osteomyelitis at the time of reconstruction and from the presence of fusion. CONCLUSION: Foot reconstruction with an Ilizarov ring fixator led to limb salvage in 93%. The vast majority (96.3%) of patients with successful limb salvage was ambulatory, independent from radiologic fusion, and presence of osteomyelitis at the time of reconstruction. These findings encourage limb salvage and deformity correction in this difficult-to-treat disease, even with underlying osteomyelitis.

Charcot Foot: Clinical Clues, Diagnostic Strategies, and Treatment Principles.

Acute Charcot neuroarthropathy of the foot and ankle is often difficult to diagnose because of limited findings in the patient history, physical examination, imaging, and laboratory studies. Delay in treatment results in the development of rigid foot and ankle deformities, increasing the risk of ulceration, infection, and major lower extremity amputation. Acute Charcot neuroarthropathy should be suspected in any patient 40 years or older with obesity and peripheral neuropathy who presents with an acutely swollen foot following minimal or no recalled trauma and who reports minimal to no pain, particularly if radiography and laboratory markers of infection are normal. Magnetic resonance imaging or computed tomography should be performed in these cases. If changes consistent with acute Charcot neuroarthropathy are observed, prompt immobilization and/or referral to a foot and ankle subspecialist is needed to minimize sequelae. Immobilization should continue until lower extremity edema and warmth resolve, and serial radiography shows evidence of osseous consolidation. Intranasal calcitonin salmon may have a role as adjunctive therapy. Although controversial, surgery may be indicated if there is severe dislocation or instability, concern for skin breakdown, or failure of conservative treatment to obtain a stable, plantigrade foot.

Osteomyelitis of the lower extremity: pathophysiology, imaging, and classification, with an emphasis on diabetic foot infection.

Osteomyelitis is inflammation of the bone caused by an infectious organism, and is a difficult clinical problem. The pathophysiology, imaging, and classification of osteomyelitis are challenging, varying with the age of the patient (child versus adult), the chronicity of the infection (acute versus chronic), and the route of spread (hematogenous versus contiguous focus), as well as the immune and vascular status of the patient and affected region. The two most common classification schemes are those of Lew and Waldvogel, and Cierny and Mader. Brodie's abscess is seen in subacute osteomyelitis, while sequestrum, involucrum, and cloaca are inter-related entities of chronic osteomyelitis. Imaging workup of suspected osteomyelitis should begin with radiographs, although MRI is the most accurate imaging test. Three patterns of T1 signal change have been described in the setting of suspected osteomyelitis including confluent intramedullary, hazy reticular, and subcortical. The confluent intramedullary pattern is most associated with osteomyelitis, while hazy reticular is rarely associated with hematogenous osteomyelitis, and subcortical is not associated with osteomyelitis. It can be challenging to differentiate neuropathic arthropathy from osteomyelitis. Osteomyelitis tends to involve a single bone subjacent to an ulcer or sinus tract. In contrast, neuropathic arthropathy tends to involve multiple bones of the midfoot. Subchondral cystic change, thin rim enhancement of a joint effusion, and the presence of intra-articular bodies are more indicative of a neuropathic joint without infection. Biopsy can play an important role in diagnosis and treatment of osteomyelitis.

Diabetic Driving Studies-Part 1: Brake Response Time in Diabetic Drivers With Lower Extremity Neuropathy.

Although the effect of lower extremity pathology and surgical intervention on automobile driving function has been a topic of contemporary interest, we are unaware of any analysis of the effect of lower extremity diabetic sensorimotor neuropathy on driving performance. The objective of the present case-control investigation was to assess the mean brake response time in diabetic drivers with lower extremity neuropathy compared with that of a control group and a brake response safety threshold. The driving performances of participants were evaluated using a computerized driving simulator with specific measurement of the mean brake response time and frequency of abnormally delayed brake responses. We analyzed a control group of 25 active drivers with neither diabetes nor lower extremity neuropathy and an experimental group of 25 active drivers with type 2 diabetes and lower extremity neuropathy. The experimental group demonstrated a 37.89% slower mean brake response time (0.757 ± 0.180 versus 0.549 ± 0.076 second; p < .001), with abnormally delayed responses occurring at a greater frequency (57.5% versus 3.5%; p < .001). Independent of a comparative statistical analysis, the observed mean brake response time in the experimental group was slower than the reported safety brake response threshold of 0.70 second. The results of the present investigation provide original data with respect to abnormally delayed brake responses in diabetic patients with lower extremity neuropathy and might raise the potential for impaired driving function in this population.

Acute Charcot neuro-osteoarthropathy.

Charcot neuro-osteoarthropathy (CN) is one of the most challenging foot complications in diabetes. Common predisposing and precipitating factors include neuropathy and increased mechanical forces, fracture and bone resorption, trauma and inflammation. In the last 15 years, considerable progress has been made in the early recognition of the acute Charcot foot when the X ray is still negative (stage 0 or incipient Charcot foot). Recent advances in imaging modalities have enabled the detection of initial signs of inflammation and underlying bone damage before overt bone and joint destruction has occurred. Casting therapy remains the mainstay of medical therapy of acute CN. If timely instituted, offloading can arrest disease activity and prevent foot deformity. In cases with severe deformity, modern surgical techniques can correct the unstable deformity for improved functional outcome and limb survival. Emerging new studies into the cellular mechanisms of severe bone destruction have furthered our understanding of the mechanisms of pathological bone and joint destruction in CN. It is hoped that these studies may provide a scientific basis for new interventions with biological agents.

Spinal Neuroarthropathy: Pathophysiology, Clinical and Imaging Features, and Differential Diagnosis.

Spinal neuroarthropathy (SNA), or Charcot spine, is a progressive destructive arthropathy occurring after loss of neuroprotective sensation and proprioceptive reflexes. Clinical diagnosis is difficult because of the variable length to presentation after initial neurologic damage and the limited symptoms given preexisting neurologic deficits. SNA is also a diagnostic challenge because its imaging features are similar to those of spinal conditions such as discitis-osteomyelitis, osseous tuberculosis, hemodialysis-related spondyloarthropathy, and pseudarthrosis. The most important imaging clues for diagnosis of SNA are involvement of both anterior and posterior elements at the thoracolumbar and lumbosacral junctions. Additional imaging clues include vacuum phenomenon within the disk (indicating excessive motion), malalignment, and paraspinal soft-tissue masses or fluid collections containing bone debris. Despite these imaging signs, findings may overlap in some cases with those of infection, or SNA can be superinfected, and biopsy may be necessary. Development of SNA requires a preexisting neurologic condition, most commonly traumatic spinal cord injury. Areas of greatest mobility and weight bearing within the desensate spine experience repetitive microtrauma and unregulated hyperemia, leading to destruction of the intervertebral articulations. The progressive and destructive nature of SNA causes substantial deformity, loss of function, and often further neurologic deficits. Patients present with deformity, back pain, audible noises during movement, or new neurologic symptoms. The mainstay of treatment is surgical débridement, reduction, and fusion. The radiologist can help initiate early intervention by using key imaging features to distinguish SNA from imaging mimics and prevent further neurologic deterioration. (©)RSNA, 2016.

Charcot arthropathy of the spine in spinal cord injured individuals with sacral deafferentation and anterior root stimulator implantation.

AIMS: To investigate the occurrence of Charcot spinal arthropathy (CSA) after sacral deafferentation (SDAF) and sacral anterior root stimulation (SARS) of the bladder in patients suffering from neurogenic lower urinary tract dysfunction (NLUTD) as a result of spinal cord injury (SCI). METHODS: Retrospective evaluation of patients who had undergone SDAF/SARS at a single SCI rehabilitation centre. The occurrence rate of stimulation dysfunction was determined, and the medical records and radiological images of the included patients were examined for CSA. The diagnosis of CSA was based on radiological criteria. The occurrence rate of CSA was estimated for all SARS patients and for those with SARS dysfunction, and the odds ratios (OR) for the occurrence of CSA were calculated. RESULTS: In 11/130 SARS patients (8%), CSA was observed a median 8 years (95% CI 5-16 years) after SDAF/SARS or a median 21 years (95% CI 9-41 years) after SCI had occurred. The median follow-up time was 14 years (range 6-25 years). The proportion of patients with CSA was significantly (P = 0.036) greater in patients with SARS dysfunction (7/41) than in patients without SARS dysfunction (4/89). The odds of CSA were four times greater (OR 4.3, 95% CI 1.0-21.5) in patients with SARS dysfunction compared to those without. Furthermore, the odds of CSA were 20 times greater (OR 20.2, 95% CI 8.4-47.0) in patients with SARS compared to those without. CONCLUSIONS: Charcot spinal arthropathy should be considered a potential long-term complication of SDAF/SARS, and spinal instability is a possible reason for SARS dysfunction.

Total knee arthroplasty in patients with Charcot joints.

PURPOSE: Although total knee arthroplasty (TKA) entails diverse operative techniques and achieves varying results in patients with different knee pathologies, few studies have discussed TKA for Charcot joints. This study aimed to investigate the efficacy of TKA in patients with Charcot knees. METHODS: From 2009 to 2013, seven patients with eight Charcot knees were admitted to our institution. They were confirmed by pre-operative examination and subsequently underwent TKAs. The pre-operative clinical and imaging characteristics of their knees indicated that all were in the Charcot stages of reconstruction or coalescence. Rotating hinge prostheses were selected for three knees with severe bone deficiency and soft tissue imbalance, whereas long stem condylar-constrained prostheses were implanted in the remaining five cases. Autogenous bone grafts were used in three patients to repair residual defects after osteotomy. Clinical data, including Hospital for Special Surgery (HSS) knee scores, range of motion (ROM), complications, and radiographic data, were used to assess surgical efficacy. RESULTS: The mean HSS score increased from 45.8 ± 14.2 (24-60) points pre-operatively to 84.6 ± 4.8 (75-90) points at final follow-up (P < 0.01). ROM was 65° ± 25° (30°-100°) pre-operatively and 92° ± 11° (75°-110°) after arthroplasty (P < 0.05), indicating satisfactory outcomes. Radiographic findings, including assessment for prosthetic loosening and alignment changes, suggested favourable outcomes. CONCLUSIONS: TKA using constrained condylar or rotating hinge prostheses and autografts for massive bone defects is effective for Charcot knees in the reconstruction or coalescence stage. LEVEL OF EVIDENCE: IV.

[A DESTRUCTIVE SHOULDER ARTHROPATHY]. / Une arthropathie destructrice de l'épaule.

Charcot arthropathy is a progressive, chronic and degenerative destruction of one or several joints caused by a central or peripheral neurological disorder. Approximately 25 % of the patients with syringomyelia develop this arthropathy located in the upper limb in 80 % of the cases. An early etiological diagnosis is essential to begin the treatment of the underlying neurological disorder. Afterwards, a conservative treatment of the arthropathy is preferred. We report the story of a patient with an arthropathy of the left shoulder due to Arnold-Chiari's malformation of type I with syringomyelia.

Inflammatory and bone turnover markers in a cross-sectional and prospective study of acute Charcot osteoarthropathy.

AIMS: To assess markers of inflammation and bone turnover at presentation and at resolution of Charcot osteoarthropathy. METHODS: We measured serum inflammatory and bone turnover markers in a cross-sectional study of 35 people with Charcot osteoarthropathy, together with 34 people with diabetes and 12 people without diabetes. In addition, a prospective study of the subjects with Charcot osteoarthropathy was conducted until clinical resolution. RESULTS: At presentation, C-reactive protein (P = 0.007), tumour necrosis factor-α (P = 0.010) and interleukin-6 (P = 0.002), but not interleukin-1ß, (P = 0.254) were significantly higher in people with Charcot osteoarthropathy than in people with and without diabetes. Serum C-terminal telopeptide (P = 0.004), bone alkaline phosphatase (P = 0.006) and osteoprotegerin (P < 0.001), but not tartrate-resistant acid phosphatase (P = 0.126) and soluble receptor activator of nuclear factor-κß ligand (P = 0.915), were significantly higher in people with Charcot osteoarthropathy than in people with and without diabetes. At follow-up it was found that tumour necrosis factor-α (P = 0.012) and interleukin-6 (P = 0.003), but not C-reactive protein (P = 0.101), interleukin-1ß (P = 0.457), C-terminal telopeptide (P = 0.743), bone alkaline phosphatase (P = 0.193), tartrate-resistant acid phosphatase (P = 0.856), osteoprotegerin (P = 0.372) or soluble receptor activator of nuclear factor-kß ligand (P = 0.889), had significantly decreased between presentation and the 3 months of casting therapy time point, and all analytes remained unchanged from 3 months of casting therapy until resolution. In people with Charcot osteoarthropathy, there was a positive correlation between interleukin-6 and C-terminal telopeptide (P = 0.028) and tumour necrosis factor-α and C-terminal telopeptide (P = 0.013) only at presentation. CONCLUSIONS: At the onset of acute Charcot foot, serum concentrations of tumour necrosis factor-α and interleukin-6 were elevated; however, there was a significant reduction in these markers at resolution and these markers may be useful in the assessment of disease activity.

Role of Wnt/ß-catenin and RANKL/OPG in bone healing of diabetic Charcot arthropathy patients.

BACKGROUND AND PURPOSE: Charcot neuropathy is characterized by bone destruction in a foot leading to deformity, instability, and risk of amputation. Little is known about the pathogenic mechanisms. We hypothesized that the bone-regulating Wnt/ß-catenin and RANKL/OPG pathways have a role in Charcot arthropathy. PATIENTS AND METHODS: 24 consecutive Charcot patients were treated by off-loading, and monitored for 2 years by repeated foot radiography, MRI, and circulating levels of sclerostin, dickkopf-1, Wnt inhibitory factor-1, Wnt ligand-1, OPG, and RANKL. 20 neuropathic diabetic controls and 20 healthy controls served as the reference. RESULTS: Levels of sclerostin, Dkk-1 and Wnt-1, but not of Wif-1, were significantly lower in Charcot patients than in the diabetic controls at inclusion. Dkk-1 and Wnt-1 levels responded to off-loading by increasing. Sclerostin levels were significantly higher in the diabetic controls than in the other groups whereas Wif-1 levels were significantly higher in the healthy controls than in the other groups. OPG and RANKL levels were significantly higher in the Charcot patients than in the other groups at inclusion, but decreased to the levels in healthy controls at 2 years. OPG/RANKL ratio was balanced in all groups at inclusion, and it remained balanced in Charcot patients on repeated measurement throughout the study. INTERPRETATION: High plasma RANKL and OPG levels at diagnosis of Charcot suggest that there is high bone remodeling activity before gradually normalizing after off-loading treatment. The consistently balanced OPG/RANKL ratio in Charcot patients suggests that there is low-key net bone building activity by this pathway following diagnosis and treatment. Inter-group differences at diagnosis and changes in Wnt signaling following off-loading treatment were sufficiently large to be reflected by systemic levels, indicating that this pathway has a role in bone remodeling and bone repair activity in Charcot patients. This is of particular clinical relevance considering the recent emergence of promising drugs that target this system.

Neuropathy and the vascular-bone axis in diabetes: lessons from Charcot osteoarthropathy.

Emerging evidence from the last two decades has shown that vascular calcification (VC) is a regulated, cell-mediated process orchestrated by vascular smooth muscle cells (VSMCs) and that this process bears many similarities to bone mineralization. While many of the mechanisms driving VSMC calcification have been well established, it remains unclear what factors in specific disease states act to promote vascular calcification and in parallel, bone loss. Diabetes is a condition most commonly associated with VC and bone abnormalities. In this review, we describe how factors associated with the diabetic milieu impact on VSMCs, focusing on the role of oxidative stress, inflammation, impairment of the advanced glycation end product (AGE)/receptor for AGE system and, importantly, diabetic neuropathy. We also explore the link between bone and VC in diabetes with a specific emphasis on the receptor activator of nuclear factor κß ligand/osteoprotegerin system. Finally, we describe what insights can be gleaned from studying Charcot osteoarthropathy, a rare complication of diabetic neuropathy, in which the occurrence of VC is frequent and where bone lysis is extreme.

Surgical reconstruction of charcot foot neuroarthropathy, a case based review.

Our case-based review focuses on limb salvage through operative management of Charcot neuroarthropathy of the diabetic foot. We describe a case, when a below-knee amputation was considered in a patient with chronic Charcot foot with a rocker-bottom deformity and chronic plantar ulceration. Conservative treatment failed. Targeted antibiotic therapy and operative management (Tendo-Achilles lengthening, resectional arthrodesis of Lisfranc and midtarsal joints, fixation with large-diameter axial screws, and plaster cast) were performed. On the basis of this case, we discuss options and drawbacks of surgical management. Our approach led to healing of the ulcer and correction of the deformity. Two years after surgery, we observed a significant improvement in patient's quality of life. Advanced diagnostic and imaging techniques, a better understanding of the biomechanics and biology of Charcot neuroarthropathy, and suitable osteosynthetic material enables diabetic limb salvage.

Polymethylmethacrylate (PMMA) Augmentation Enhances the Mechanical Characteristics of Midfoot Beam Constructs in Charcot Neuroarthropathy Cadaver Model.

BACKGROUND: Even with the best conservative care, patients with Charcot neuroarthropathy (CN) of the foot and ankle often ulcerate, increasing their risk of infection, amputation, and death. Surgical fixation has been associated with risk of recurrent ulceration, potentially due to poor bone quality prone to recurrent deformity and ulceration. We propose midfoot beam reconstruction with PMMA augmentation as a novel means of improving fixation. METHODS: A protocol was developed to create characteristic CN midfoot fragmentation both visually and fluoroscopically in each of 12 matched-pair cadaveric feet. Afterward, the pairs were divided into 2 groups: (1) midfoot beam fusion surgery alone, and (2) midfoot beam fusion surgery augmented with PMMA. A solid 7.0-mm beam was placed into the medial column and a solid 5.5-mm beam was placed across the lateral column. In the PMMA group, 8 to 10 mL of PMMA was inserted into the medial column. The hindfoot of each specimen was potted and the metatarsal heads were cyclically loaded for 1800 cycles, followed by load to failure while load and displacement were continually recorded. RESULTS: One specimen in the beam alone group failed before reaching the 1800th cycle and was not included in the failure analysis. The midfoot beam only group demonstrated greater mean displacement during cycle testing compared with the PMMA group, P < .05. The maximum force (N), stiffness (N/mm), and toughness (Nmm) were all significantly greater in the group augmented with PMMA, P < .05. CONCLUSION: In a CN cadaveric model, PMMA augmentation significantly decreased gapping during cyclic loading and nearly doubled the load to failure compared with midfoot beams alone. CLINICAL RELEVANCE: The results of this biomechanical study demonstrate that augmentation of midfoot beams with PMMA increases the strength and stiffness of the fusion construct. This increased mechanical toughness may help reduce the risk of nonunion and infection in patients with neuropathic midfoot collapse.

Role of body mass index in acute charcot neuroarthropathy.

Obesity has been posited as a predictor for the development of Charcot neuroarthropathy, a severe form of degenerative joint disease associated with peripheral neuropathy and diabetes mellitus. The present case-control study investigated the relationship between elevated (overweight and obese) body mass index and acute Charcot neuroarthropathy in a diabetic population. The final data set consisted of 49 patients, 20 (40.82%) of whom had Charcot foot and 29 (59.18%) who served as controls. In the present investigation, no statistically significant association was found between an elevated body mass index and the development of acute Charcot neuroarthropathy involving the foot.

Charcot neuroarthropathy of the foot and ankle: a review.

Charcot neuroarthropathy is a limb-threatening, destructive process that occurs in patients with neuropathy associated with medical diseases such as diabetes mellitus. Clinicians' treating diabetic patients should be vigilant in recognizing the early signs of acute Charcot neuroarthropathy, such as pain, warmth, edema, or pathologic fracture in a neuropathic foot. Early detection and prompt treatment can prevent joint and bone destruction, which, if untreated, can lead to morbidity and high-level amputation. A high degree of suspicion is necessary. Once the early signs have been detected, prompt immobilization and offloading are important. Treatment should be determined on an individual basis, and it must be determined whether a patient can be treated conservatively or will require surgical intervention when entering the chronic phase. If diagnosed early, medical and conservative measures only will be required. Surgery is indicated for patients with severe or unstable deformities that, if untreated, will result in major amputations. A team approach that includes a foot and ankle surgeon, a diabetologist, a physiotherapist, a medical social councilor, and, most importantly, the patient and immediate family members is vital for successful management of this serious condition.

A Surgeon's guide to advances in the pharmacological management of acute Charcot neuroarthropathy.

Acute Charcot neuroarthropathy is a devastating condition and, its incidence is increasing. Currently, treatment consists of immobilisation and off-loading of the involved extremity. Outcomes are frequently poor and novel treatments are being sought urgently. This review aims to outline advances in the pharmacological treatment of this, condition. PubMed and the Cochrane Database of systematic reviews were searched. Relevant papers were cross referenced. Eleven original studies were identified. The limited data available suggest pamidronate, alendronate and calcitonin provide some clinical and biochemical improvements while zoledronic acid is deleterious and, increases off-loading times. However, the data is not robust enough to convincingly demonstrate clinically meaningful effects. The studies were predominantly low quality and heterogeneous. They differed markedly in study type, pharmacological agent used, dosing regimen, disease, aetiology/stage/location, concurrent off-loading regimen, outcomes and, follow-up. Few were rigorous in controlling for associated confounding variables and none investigated long term outcomes. The routine use of pharmacological treatment modalities for this condition is not recommended in the United States by the Food and Drug Administration or in the United Kingdom by the National Institute for Health and Clinical Excellence. Given the evidence available this is justified and further higher quality research is required.

Recurrence of the acute Charcot foot in diabetes.

BACKGROUND: The acute Charcot foot is thought to occur in people who have a number of predisposing factors, of which distal neuropathy is the most important. But while occurrence in the contralateral foot is not infrequent, recurrence in the same foot seems to be very rare. CASE REPORT: A case is described in which discrete episodes of inflammation of the midfoot occurred in the same foot over a period of 14 years, and were attributed to acute Charcot neuroarthropathy (Charcot foot). There was coincidental evidence of osteomyelitis of the 4(th) toe but there was no suspicion that the inflammatory episodes of the midfoot were the result of bone infection and they settled without treatment with antibiotics. CONCLUSION: This case had clinically diagnosed recurrences of inflammation and destruction typical of the acute Charcot foot over an extended period, and this is most unusual. The implications of the rarity of such recurrences are discussed.

Pressure pain thresholds at the diabetic Charcot-foot: an exploratory study.

OBJECTIVE: Painless mechanical trauma is believed to induce neuroosteoarthropathy at the neuropathic foot in diabetes (diabetic Charcot-foot). To investigate pressure nociception at the diabetic foot, we measured the pain perception thresholds for deep pressure (DPPPT, using Algometer II®) and cutaneous pressure (CPPPT, using calibrated monofilaments). METHODS: In 24 diabetic patients with painless neuropathy (11 with a chronic, inactive Charcot-foot and a history of foot ulcer, and 13 control patients who never had an ulcer), and in 20 healthy subjects, CPPPT (at palmar and plantar digital skinfolds) and DPPPT (over musculus abductor pollicis, musculus hallucis longus, and over metacarpophalangeal and metatarsophalangeal joints) was measured. RESULTS: At the hands, DPPPT and CPPPT were similar in patients and healthy subjects. At the feet, CPPPT was above the upper safety limit of measurement (512 mN) in 2/20 healthy subjects, and in 11/11 Charcot patients compared to 6/13 neuropathic controls (p=0.005). At the feet, median DPPPT was similar in all groups. In Charcot patients only, DPPPT was higher over metatarsophalangeal joint than over m. hallucis longus (p=0.048). CONCLUSION: Perception thresholds for cutaneous pressure pain, but not for deep pressure pain, may be extremely elevated at the diabetic neuropathic foot, and particularly at the Charcot-foot.