Unmasking the pain in a diabetic foot

A woman in her 40s with longstanding type 1 diabetes mellitus (T1DM) and bilateral distal sensory neuropathy presented with persistent right foot pain and hypersensitivity following minor trauma. Examination showed a warm, swollen foot with preserved pulses and allodynia, but no trophic changes, ulcers or deformity. The contralateral foot demonstrated reduced vibration and monofilament sensation consistent with peripheral neuropathy but without pain or vasomotor changes. A temperature difference of less than 2°C was noted between the affected and contralateral foot. Despite minimal findings on initial X-rays (Figure 1) and MRI (Figure 2), symptoms persisted. A three-phase nuclear bone scan (Figure 3) demonstrated focal increased uptake, prompting consideration of complex regional pain syndrome (CRPS) superimposed on diabetic neuropathy, a rare but important differential in people with diabetes and unexplained focal foot pain.1-3 Both conditions can mimic each other in people with diabetes and peripheral neuropathy, presenting with swelling, pain, warmth and functional impairment.3, 4 In this case, the asymmetric pain and sensory hypersensitivity localised to one foot, despite bilateral neuropathy, were key features suggesting CRPS rather than the progression of neuropathic disease. The diagnosis was supported clinically using the Budapest criteria,1 which require disproportionate pain and at least one symptom in three of four domains (sensory, vasomotor, sudomotor/oedema and motor/trophic). Charcot neuroarthropathy often shows progressive joint and bony destruction, but this may be delayed. Diagnostic clarity is frequently hampered by overlapping features, making early differentiation difficult.3, 5 CRPS typically exhibits increased perfusion and soft tissue uptake in the early phases of a three-phase bone scan (Figure 3).2, 4, 6 Delayed SPECT/CT imaging (Figure 4) often reveals focal increased tracer uptake in small tarsal bones such as the navicular and cuneiforms, suggestive of neurogenic inflammation. This pattern contrasts with the diffuse uptake or bony collapse seen in Charcot neuroarthropathy or the sequestration and rim enhancement of osteomyelitis.3 Early multidisciplinary involvement is critical.7-9 This includes input from pain specialists, physiotherapists, psychologists and diabetes teams. Pharmacologic management includes gabapentinoids or tricyclics; physical therapy focuses on mobility and desensitisation techniques; psychological support addresses pain perception and coping strategies.5 Glycaemic control optimisation and tapering of offloading devices are considered to enhance recovery. Education and early intervention are vital in reducing chronicity and disability. The authors declare no conflicts of interest. No funding received for this article. A consent for publication was obtained from the patient.