Charcot neuro-osteoarthritis (CNO) is a serious diabetic complication linked to peripheral neuropathy. It involves inflammation, progressive destruction of bones and joints, deformity, and sometimes ulceration and amputation of the lower extremities.1 Diagnosis depends on clinical signs, such as local hyperthermia, and medical imaging, especially radiography and magnetic resonance imaging.1,2 The reported prevalence of CNO ranges from about 0.08% in the overall diabetic population to as much as 13% in high-risk groups with neuropathy.3 However, studies using X-ray indicate that nearly 30% of the patients with diabetic neuropathy may have CNO, yet roughly a quarter of them are misdiagnosed.1,3 CNO development involves both neurotraumatic and neurovascular mechanisms.1,4 The prognosis depends heavily on early diagnosis and effective offloading, especially with a total contact cast (TCC), along with multidisciplinary care.5 Below, we present a case that illustrates the challenges described above.

A 46-year-old man with longstanding type 2 diabetes mellitus, managed with basal and premixed insulin, as well as oral hypoglycemic agents, presented in January 2025 with swelling, erythema, and mild pain in the left foot. No trauma was reported. A general practitioner diagnosed an ankle sprain and advised conservative management. Radiography showed blurred trabecular patterns and minor cortical erosions. The patient’s glycated hemoglobin level was 7.1% (reference range [RR], 4.3%–5.9%).

As the symptoms worsened, in February 2025, the patient presented to an emergency department with a fever of 38.5 °C. On examination, he had tense, erythematous skin, and seropurulent discharge near the medial ankle. Laboratory tests showed a C-reactive protein level of 110 mg/l (RR <⁠5 mg/l), leukocytosis (leucocytes, 14 × 109/l; RR, 4–109/l), and a procalcitonin concentration of 0.4 ng/ml (RR, 0.1–0.5 ng/ml). Incision and drainage were performed, and empirical oral clindamycin was started.

One week later, at the Diabetic Foot Outpatient Clinic of the University Hospital in Krakow, multiple penetrating ulcers with exposed tendons were observed (Figure 1A). Probe-to-bone testing was negative, but marked erythema and swelling persisted. Radiography findings were consistent with the fragmentation phase of CNO: trabecular resorption, intra-articular fractures, and loss of tarsometatarsal congruence (stage II according to the Eichenholtz classification; Figure 1B and 1C). Surgical debridement was carried out, and advanced silver-based dressings were applied. Complete offloading using a wheelchair and crutches was advised, along with twice-daily antiseptic irrigations. The culture confirmed methicillin-susceptible Staphylococcus aureus, and targeted therapy with oral amoxicillin-clavulanate was initiated. The diagnosis of active-phase CNO (zones 3 and 4; stage II) was confirmed. Temperature monitoring was considered unreliable due to concurrent ulceration. Antibiotics were prescribed for 14 days, with notable improvement after 1 week: the fever subsided, swelling and erythema diminished, and the wounds began to heal.

Figure 1. Clinical and radiologic presentation of Charcot neuro-osteoarthropathy in a patient with type 2 diabetes mellitus; A – first visit: extensive penetrating ulcers with pronounced erythema; B – anteroposterior X-ray view showing destructive lesions with features of fragmentation (arrow); C – lateral X-ray view showing marked osteolysis and subluxation of the tarsometatarsal joint (arrow); D – second visit: partial improvement with granulation tissue at the base of the lesions; E – third visit: further shallowing of the ulcers; F – final visit: complete wound closure

By April 2025, the ulcers had healed, granulation tissue covered the wound bed, and swelling reduced significantly (Figure 1D and 1E). Radiography showed stable lytic changes without progression. Offloading was transitioned to a prefabricated removable device (instant TCC), vacuum-sealed for a close fit. The safety and efficacy of this treatment is supported by clinical studies, and they are comparable to those of traditional TCC (as per the International Working Group on the Diabetic Foot guidelines).2 Dressings were changed to the healing-promoting Technology Lipido-Colloid with Nano-Oligosaccharide Factor matrix.6 By June 2025, complete wound closure was achieved (Figure 1F). Mild swelling persisted, but the temperature difference between the affected and contralateral foot decreased from 3.2 °C to 1.5 °C. Radiography demonstrated stabilization with a preserved plantigrade foot and no progression of deformity. The patient remained under follow-up, with the disease classified as transitional toward the inactive phase. Custom footwear and insoles were planned, partially reimbursed by the National Health Fund.

This case highlights diagnostic challenges of CNO. The patient was initially misdiagnosed as having an ankle sprain, which delayed appropriate treatment. Radiography later confirmed fragmentation-phase disease. Multimodal therapy—comprising surgical debridement, advanced dressings, targeted antibiotics, and progressive offloading—led to wound closure and radiologic stabilization within 6 months, despite the delayed diagnosis. A late diagnosis of CNO poses the risk of deformity and amputation.1,6 Conversely, early offloading often results in remission within 5–8 months for most patients.3

A swollen and warm foot in a diabetic patient with neuropathy should always raise a suspicion of CNO. Early diagnosis, including the use of medical imaging, reduces the risk of bone destruction, deformity, ulceration, and amputation. Early implementation of comprehensive offloading and multidisciplinary management are crucial for the prognosis.