Aims. In our unit, we adopt a two-stage surgical reconstruction approach using internal fixation for the management of infected Charcot foot deformity. We evaluate our experience with this functional limb salvage method. Methods. We conducted a retrospective analysis of prospectively collected data of all patients with infected Charcot foot deformity who underwent two-stage reconstruction with internal fixation between July 2011 and November 2019, with a minimum of 12 months’ follow-up. Results. We identified 23 feet in 22 patients with a mean age of 56.7 years (33 to 70). The mean postoperative follow-up period was 44.7 months (14 to 99). Limb salvage was achieved in all patients. At one-year follow-up, all ulcers have healed and independent full weightbearing mobilization was achieved in all but one patient. Seven patients developed new mechanical skin breakdown; all went on to heal following further interventions. Fusion of the hindfoot was achieved in 15 of 18 feet (83.3%). Midfoot fusion was achieved in nine of 15 patients (60%) and six had stable and painless fibrous nonunion. Hardware failure occurred in five feet, all with broken dorsomedial locking plate. Six patients required further surgery, two underwent revision surgery for infected nonunion, two for removal of metalwork and exostectomy, and two for dynamization of the hindfoot nail. Conclusion. Two-stage reconstruction of the infected and deformed Charcot foot using internal fixation and following the principle of ‘long-segment, rigid and durable internal fixation, with optimal bone opposition and
Aim. We describe a case series using adjuvant calcium sulphate bio composites with antibiotics in treating infected metalwork in the foot and ankle. Method. 11 patients aged 22–81 (9 males, 2 females) were treated with clinical evidence of infected limb metal work from previous orthopaedic surgery. Metal work removal with intra osseous application of either cerement in 8 cases (10–20ml including 175mg–350mg gentamycin) or stimulan in 3 cases (5–12ml including 1g vancomycin) into the site was performed. Supplemental systemic antibiotic therapy (oral/intravenous) was instituted based on intraoperative tissue culture and sensitivity. Results. 7 patients had infected ankle metalwork, 2 had infected foot metalwork and 2 had infected external fixators. Metal work was removed in all cases. Mean pre operative CRP was 25.4 mg/l (range 1–137mg/l). Mean postoperative CRP at 1 week was 15.4mg/l (range 2–36mg/l) and at 1 month was 16.1mg/l (range 2–63mg/l). Mean pre op WCC was 8.5×10. 9. (range 6.2–10.6×10. 9. ). Mean post op WCC at 1 week was 8.8×10. 9. (range 5.1–12.7×10. 9. ) and 1 month was 7.1×10. 9. (range 3.7–10.4×10. 9. ). Organisms cultured included enterobacter, staphylococcus species, stenotrophomonas, acinetobacter, group B streptococcus, enterococcus, escherichia coli, pseudomonas, morganella morganii and finegoldia magna. Infection eradication as a single stage procedure with primary would closure and healing was achieved in 10 out of 11 cases (90.9%). No additional procedures were required in these cases. Conclusions. Our results support the use of a calcium sulphate bio composite with antibiotic as an adjuvant for effective local infection control in cases with implant related bone sepsis. The technique is well tolerated with no systemic or local side effects. Our results show that a single stage implant removal, debridement and
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:
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).
