Neuropathic changes in the foot are common with a prevalence of approximately 1%. The diagnosis of neuropathic arthropathy is often delayed in diabetic patients with harmful consequences including amputation. The appropriate diagnosis and treatment can avoid an extensive programme of treatment with significant morbidity for the patient, high costs and delayed surgery. The pathogenesis of a Charcot foot involves repetitive micro-trauma in a foot with impaired sensation and neurovascular changes caused by pathological innervation of the blood vessels. In most cases, changes are due to a combination of both pathophysiological factors. The Charcot foot is triggered by a combination of mechanical, vascular and biological factors which can lead to late diagnosis and incorrect treatment and eventually to destruction of the foot. This review aims to raise awareness of the diagnosis of the Charcot foot (diabetic neuropathic osteoarthropathy and the differential diagnosis, erysipelas, peripheral arterial occlusive disease) and describe the ways in which the diagnosis may be made. The clinical diagnostic pathways based on different classifications are presented. Cite this article: Bone Joint J 2016;98-B:1155–9

Background. Charcot neuropathic osteoarthropathy is a rare, destructive process affecting the bones and joints of feet in patients with diabetic peripheral neuropathy. The aetiology of Charcot remains unknown, although it has been suggested that it is triggered by the occurrence of inflammation in the foot of a susceptible individual, and that the inflammation results in increased osteoclastic activity. Hypothesis. The increased bone turnover in acute Charcot is associated with increased concentrations of pro-inflammatory cytokines, related signalling peptides and bone turnover markers. Methods. 17 patients newly presenting with acute Charcot in diabetes and 16 non-diabetic patients without neuropathy undergoing elective forefoot surgery provided informed consented to participate. Samples of bone were taken by needle biopsy, and were stained with H&E to determine bone architecture and bone remodelling. Serum ALP, CTX, OPG and sRANKL TNF, IL1-beta, IL6 and CRP were measured by immunoassay. Blood was taken from the dorsal foot vein of both the affected and the unaffected foot, as well as an antecubital vein. Results. Classic histopathology features of fracture and bone remodelling were evident in Charcot bone biopsies. Systemic circulating concentrations in the Charcot group antecubital vein for both IL6 and OPG were significantly greater than in controls (p<0.05). There were no significant differences between the dorsal vein concentrations of any analyte when the affected and unaffected feet were compared. However, in patients with an acute Charcot foot the concentration of OPG, ALP and CTX was higher in sera from the dorsal vein of affected foot when compared to controls (p<0.05), this difference was highly significant for IL6 (p<0.001). Conclusion. The elevation in CTX observed in the affected foot in patients with an acute Charcot foot reflects the bone breakdown and remodelling which is present. The higher circulating concentration of IL-6 in the Charcot patient group, reflects the inflammation which is present and which is thought to be central to the development of the condition. Although OPG values were significantly greater in Charcot than control group, circulating concentrations of OPG are known to be higher in diabetes

It is difficult to determine the safe timing of weight-bearing or reconstructive surgery in patients with Charcot arthropathy of the foot and ankle. In this study the Doppler spectrum of the first dorsal metatarsal artery was used to monitor the activity of the disease activity and served as a guideline for management. A total of 15 patients (seven men and eight women) with acute diabetic Charcot arthropathy of the foot and ankle were immobilised in a non-weight-bearing cast. They were followed at two-week intervals and bilateral Doppler spectra of the first dorsal metatarsal arteries were obtained using a 10 MHz linear ultrasound probe. The patients were allowed to start weight-bearing or undergo surgery after the Doppler spectrum had returned to normal pattern. The Doppler spectra in the unaffected limbs were triphasic in pattern, whereas those in limbs with active Charcot arthropathy showed monophasic forward flow. They returned to normal after a mean of 13.6 weeks (6 to 20) of immobilisation. Three patients underwent pan-talar arthrodesis to correct gross instability and deformity.

Doppler spectrum analysis of the foot may reflect the activity of the disease in patients with Charcot arthropathy, and may be used as a guide to begin weight-bearing or undergo reconstructive surgery.

Charcot osteoarthropathy of the foot is a chronic and progressive disease of bone and joint associated with a risk of amputation. The main problems encountered in this process are osteopenia, fragmentation of the bones of the foot and ankle, joint subluxation or even dislocation, ulceration of the skin and the development of deep sepsis. We report our experience of a series of 20 patients with Charcot osteoarthropathy of the foot and ankle treated with an Ilizarov external fixator. The mean age of the group was 30 years (21 to 50). Diabetes mellitus was the underlying cause in 18 patients. Five had chronic ulcers involving the foot and ankle. Each patient had an open lengthening of the tendo Achillis with excision of all necrotic and loose bone from the ankle, subtalar and midtarsal joints when needed. The resulting defect was packed with corticocancellous bone graft harvested from the iliac crest and an Ilizarov external fixator was applied. Arthrodesis was achieved after a mean of 18 weeks (15 to 20), with healing of the skin ulcers. Pin track infection was not uncommon, but no frame had to be removed before the arthrodesis was sound.

Every patient was able to resume wearing regular shoes after a mean of 26.5 weeks (20 to 45).

Introduction: Rapidly destructive arthrosis of the hip (RDHD) is a rare and incompletely understood disorder with scarce literature about variations in natural history within a population. A series of cases from North Wales with rapid progressive joint destruction and extensive subchondral bone loss in the femoral head and acetabulum are presented. Methods: A retrospective review of patients with a clinical profile and serial radiographs suggestive of a rapidly progressive hip disease was undertaken. This revealed 15 patients who met our criteria for RDHD. A retrospective analysis of clinical and radiographic records was performed. Radiographic findings mimicked those of other disorders such as septic arthritis, rheumatoid and seronegative arthritis, primary osteonecrosis with secondary osteoarthritis, or neuropathic osteoarthropathy, but none of the patients had clinical, pathologic, or laboratory evidence of these entities. Results: Rapid progression of hip pain and disability was a consistent clinical feature. The average duration of symptoms was 1.4 years. Radiographs obtained at various intervals before surgery (average 14 months) in 15 patients documented rapid hip destruction, involvement being unilateral in 10 cases. All patients underwent total hip arthroplasty, and osteoarthritis was confirmed at pathologic examination. Histology of femoral heads failed to show the findings typical of primary osteonecrosis & no evidence of sepsis. Discussion: The authors postulate that these cases represent an uncommon subset of osteoarthritis and regular review, both clinically and radiologically, are required to assess speed of progression and prevent rapid loss of bone stock without the surgeon being aware. These cases are unsuitable for being placed on long waiting list due to technical difficulties in delayed surgery and compromised outcome following surgery. The decisions about the need for surgery and the selection of cases should be made purely on clinical grounds and not on their rank in the waiting lists.(295)