Abstract

Despite improved treatment, a significant number of diabetic foot ulcers do not heal and eventually lead to amputation (1–5). The important local factors determining the healing rate of ulcers are pressure at the site of the ulcer, adequacy of blood supply, and infection. It is generally accepted that for optimal healing, infection needs to be treated. However, the definition of infection is arbitrary, and, in many borderline cases, clinicians will be uncertain whether antibiotic therapy is indicated. Edmonds et al. (6) showed, in a study of clinically uninfected diabetic foot ulcers, that, even in the absence of overt infection, antibiotic therapy reduced hospitalization and amputation. Conceptually, a high bacterial load by itself can retard ulcer healing by causing a wound environment not conducive to healing. Important factors that may play a role in this regard include secretion of metalloproteinases and their tissue inhibitors from the bacteria, compounds that can cause local tissue destruction (7). Little is known, however, about the effect of bacterial load on the healing rate of neuropathic diabetic foot ulcers. In this study, instead of arbitrarily deciding clinically whether infection was present, a quantitative microbiological method was used to examine the relationship between bacterial load in the wounds of diabetic neuropathic ulcers and the subsequent ulcer healing rate. Wound fluid was obtained from 32 patients (22 male and 10 female) with neuropathic ulcers at the plantar surface of the foot. Patients were referred to the High Risk Diabetic Foot Clinic at the Diabetes Centre of Royal Prince Alfred Hospital in Sydney, Australia. The mean ± SD age of the cohort was 60.0 ± 9.0 years with a diabetes duration of 14.6 ± 10.1 years and an A1C of 7.9 ± 1.4% (normal 50 V and ankle brachial …

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