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Background <p>Advanced Charcot neuro-osteoarthropathy involving the hindfoot is associated with severe deformity, instability, ulceration, infection, and major lower-limb amputation. Non-traumatic calcaneal fracture associated with diabetic Charcot hindfoot collapse is uncommon and difficult to treat because of neuropathy, impaired bone quality, tendon imbalance, soft tissue compromise, and a high risk of fixation failure. Reports describing long-term functional limb preservation in patients with advanced Charcot hindfoot collapse associated with severe metabolic bone impairment remain limited.</p> Case presentation <p>A 63-year-old Japanese woman with a 36-year history of type 1 diabetes mellitus presented with progressive right hindfoot deformity and ulceration without major trauma. Radiographs and computed tomography demonstrated advanced Charcot hindfoot collapse with a non-traumatic calcaneal fracture classified as Eichenholtz stage III and Brodsky type 3B. Preoperative evaluation demonstrated severe vitamin D deficiency and elevated bone turnover markers. The patient underwent corrective osteotomy of the calcaneus, Achilles tendon Z-lengthening, internal fixation with headless compression screws, autologous iliac bone grafting, and circular external fixation. A staged postoperative unloading protocol was used, followed by gradual protected loading. Sequential metabolic therapy was administered after surgery. Bone union was achieved at approximately 3 months, and the external fixator was removed at 3.5 months. During long-term follow-up, glycaemic control and bone mineral density improved. At 8 years after surgery, the patient remained ambulatory with preserved plantigrade alignment and without recurrent ulceration, infection, fixation failure, or amputation. The American Orthopaedic Foot &amp; Ankle Society ankle-hindfoot score was 94. Interpretation of pain scores was limited by profound diabetic neuropathy.</p> Conclusions <p>This case illustrates an integrated multidisciplinary limb-salvage strategy combining mechanical reconstruction, staged postoperative offloading, and metabolic optimisation in a patient with advanced diabetic Charcot hindfoot deformity complicated by severe metabolic bone impairment. The favourable long-term outcome should be interpreted as hypothesis-generating rather than evidence for the efficacy of any individual adjunctive therapy.</p>

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Integrated mechanical and metabolic limb salvage for advanced diabetic Charcot hindfoot collapse with non-traumatic calcaneal fracture: an 8-year follow-up case report

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  • 发表日期：

    2026年7月9日

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  • Koji Nozaka,
  • Hiroshi Aonuma,
  • Kenta Tominaga,
  • Naohisa Miyakoshi

摘要

Background

Advanced Charcot neuro-osteoarthropathy involving the hindfoot is associated with severe deformity, instability, ulceration, infection, and major lower-limb amputation. Non-traumatic calcaneal fracture associated with diabetic Charcot hindfoot collapse is uncommon and difficult to treat because of neuropathy, impaired bone quality, tendon imbalance, soft tissue compromise, and a high risk of fixation failure. Reports describing long-term functional limb preservation in patients with advanced Charcot hindfoot collapse associated with severe metabolic bone impairment remain limited.

Case presentation

A 63-year-old Japanese woman with a 36-year history of type 1 diabetes mellitus presented with progressive right hindfoot deformity and ulceration without major trauma. Radiographs and computed tomography demonstrated advanced Charcot hindfoot collapse with a non-traumatic calcaneal fracture classified as Eichenholtz stage III and Brodsky type 3B. Preoperative evaluation demonstrated severe vitamin D deficiency and elevated bone turnover markers. The patient underwent corrective osteotomy of the calcaneus, Achilles tendon Z-lengthening, internal fixation with headless compression screws, autologous iliac bone grafting, and circular external fixation. A staged postoperative unloading protocol was used, followed by gradual protected loading. Sequential metabolic therapy was administered after surgery. Bone union was achieved at approximately 3 months, and the external fixator was removed at 3.5 months. During long-term follow-up, glycaemic control and bone mineral density improved. At 8 years after surgery, the patient remained ambulatory with preserved plantigrade alignment and without recurrent ulceration, infection, fixation failure, or amputation. The American Orthopaedic Foot & Ankle Society ankle-hindfoot score was 94. Interpretation of pain scores was limited by profound diabetic neuropathy.

Conclusions

This case illustrates an integrated multidisciplinary limb-salvage strategy combining mechanical reconstruction, staged postoperative offloading, and metabolic optimisation in a patient with advanced diabetic Charcot hindfoot deformity complicated by severe metabolic bone impairment. The favourable long-term outcome should be interpreted as hypothesis-generating rather than evidence for the efficacy of any individual adjunctive therapy.