Prevention of diabetic foot ulceration: new evidences for an old problem

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Diabetic patients have a 15 % lifetime risk of developing a foot ulcer and have a 15 % risk of developing a lower extremity amputation. Amputation is preceded by nonhealing foot wounds in 85 % of cases [1]. The ulcerated diabetic foot may be considered the complication of the peripheral neuropathy (PN) and/or peripheral arterial disease (PAD). Several studies showed that diabetic patients with PN are at risk of foot ulceration and indeed true neuropathic ulceration is found in almost 50 % of the patients with a new foot ulcer according to eurodiale [2]. Those with PAD are at risk of foot amputation and ischemic lesions are found in the other 50 % of patients with foot ulceration. However true ischemic ulcers are observed only in 15 % of cases. The remaining 35 % have both PAD and PN present at the same time: neuroischemic ulcers [2]. Many factors may be responsible of the appearance of an ulcer in those patients: intrinsic factors related to the progressive appearance of limited joint mobility, soft tissue stiffness, early and persistent windlass mechanism [3] presence of structural foot deformities as hammer toes, hallux valgus or pes cavus. Metatarsal heads are prominent. This results in increased pressure underneath the metatarsal heads, which will make the plantar forefoot more susceptible to breakdown, also because patients are unaware of this abnormal pressure because of the neuropathy. However, there are also other contributing factors leading to diabetic foot ulcer formation, such as arterial occlusive disease, foot trauma, history of previous amputations, and callus due to the increased plantar pressures caused by abnormal mechanical loading of the foot [4]. A sequence of