Evidence-based protocol for diabetic foot ulcers.
ABSTRACT Diabetic foot ulcers are the single biggest risk factor for nontraumatic foot amputations in persons with diabetes. Foot ulcers occur in 12 to 25 percent of persons with diabetes and precede 84 percent of all nontraumatic amputations in this growing population. Because of the high incidence of foot ulcers, amputations remain a source of morbidity and mortality in persons with diabetes. Strict adherence to evidence-based protocols as described herein will prevent the majority of these amputations.
The collective experience of treating patients with neuropathic diabetic foot ulcers in four major diabetic foot programs in the United States and Europe was analyzed.
The following protocol was developed for patients with diabetic foot ulcers: (1) establishment of good communication among the patient, the wound healing team, and the primary medical doctor; (2) comprehensive, protocol-driven care of the entire patient, including hemoglobin A1c, microalbuminuria, and cholesterol as well as early treatment of retinopathy, nephropathy, and cardiac disease; (3) weekly objective measurement of the wound with digital photography, planimetry, and documentation of the wound-healing process using the Wound Electronic Medical Record, if available; (4) objective evaluation of blood flow in the lower extremities (e.g., noninvasive flow studies); (5) débridement of hyperkeratotic, infected, and nonviable tissue; (6) use of systemic antibiotics for deep infection, drainage, and cellulitis; (7) off-loading; (8) maintenance of a moist wound bed; (9) use of growth factor and/or cellular therapy if the wound is not healing after 3 weeks with this protocol; and (10) consideration of the use of vacuum-assisted therapy in complex wounds.
In diabetic foot ulcers, availability of the above modalities, in combination with early recognition and comprehensive treatment, ensures rapid healing, minimizes morbidity and mortality rates, and eliminates toe and limb amputations in the absence of ischemia and osteomyelitis.
- SourceAvailable from: Chinaka Nwaehujor[Show abstract] [Hide abstract]
ABSTRACT: The seeds of Garcinia kola are used in ethnopharmacological practice to cure cough, catarrh, wounds and sores. In this study, the seeds were extracted with 80% methanol and distilled water after de-fatting with n-hexane. The ethyl acetate fraction of the methanol extract yielded 2.4% w/w abundance. Repeated fractionation of the ethyl acetate fraction yielded a major fraction identified as Kolaviron and a second pure compound identified as Garcinia hydroxybiflavanonol, (GB1). The ethyl acetate fraction containing GB1 showed significant wound healing properties. The influence of GB1 on wound healing in diabetes was studied using the excision wound and dead wound space experimental models in STZ-induced diabetic rats. Topical application of GB1 caused a significant (p<0.05) concentration-dependent reduction in wound diameter and epithelialization period of excision wounds. On day 18, GB1 topically treated rats showed 87.82% and 94.08% wound contraction in 15%- and 30%-ointments respectively compared to Neomycin-bacitracin powder (CicatrinR) (15%- ointment) treated rats (92.75%). The WC50 values showed that GB1 (30%) produced a better wound closure rate (8.8 days) than neomycin-bacitracin powder (9.1 days). In the dead space wound model, oral administration of GB1 caused a significant (p<0.05) and dose-related increase in the weight of granuloma tissue with highest dose producing 101.32±6.78 (74.71%) protection while ASA produced (110.48±5.53) 90.28% as compared to the negative control 57.81±7.73. Also, an increase was observed in the hydroxyproline content which was dose-dependent. GB1 also significantly lowered malondialdehyde levels when compared with negative control. These effects of GB1 may find a beneficial application in therapies of variousdiabetic patients especially in wound healing.
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ABSTRACT: Large scale clinical trials have demonstrated that an intensive antihyperglycemic treatment in diabetes mellitus (DM) in individuals reduces the incidence of micro- and macrovascular complications, e.g. nephropathy, retinopathy, DM-accelerated atherosclerosis, myocardial infarction, or limb amputations. Here, we investigated the effect of short- and long-term insulin administration on mitochondrial function in peripheral tissues of streptozotocin (STZ)-induced hyperglycemic rats. In addition, the in vitro effect of methylglyoxal (MG), advanced glycation end products (AGEs) and human diabetic plasma on mitochondrial activity was investigated in skeletal muscle and liver mitochondria and in rat skin primary fibroblasts. Hyperglycemic STZ rats showed tissue-specific patterns of energy deficiency, evidenced by reduced activities of complexes I, II and/or IV after 30 days of hyperglycemia in heart, skeletal muscle and liver; moreover, cardiac tissue was found to be the most sensitive to the diabetic condition, since energy metabolism was impaired after 10 days of the hyperglycemia. Insulin-induced tight glycemic control was effective in protecting against the hyperglycemia-induced inhibition of mitochondrial enzyme activities. Furthermore, the long-term hormone replacement (30 days) also increased these activities in kidney from STZ-treated animals, where the hyperglycemic state did not modify the electron transport activity. Results from in vitro experiments indicate that mitochondrial impairment could result from oxidative stress-induced accumulation of MG and/or AGEs. Further investigations demonstrated that human plasma AGE accumulation elicits reduced mitochondrial function in skin fibroblast. These data suggest that persistent hyperglycemia results in tissue-specific patterns of energy deficiency and that early and continuous insulin therapy is necessary to maintain proper mitochondrial metabolism.Biochimica et Biophysica Acta 07/2011; 1812(11):1460-71. DOI:10.1016/j.bbadis.2011.06.017
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ABSTRACT: Diabetic foot syndrome (DFS) is a late-stage complication of type 2 diabetes which originates from interplay among impaired tissue regeneration, vasculopathy, neuropathy and inflammation all on the background of insulin resistance. Despite astonishing mortality rate pharmacological approach in management of diabetic ulceration is almost non-existent. Foot pressure relief, wound debridement and infection control remain widely accepted options in the treatment of DFS. We hypothesize that resveratrol treatment and subsequent activation of SIRT1 pathway might be highly beneficial for patients with DFS. This prediction is based on multiple lines of evidence implicating resveratrol and sirtuins in restoration of insulin sensitivity, microcirculation, tissue regeneration, function of peripheral nerves and production of cytokines. Stabilized "nutraceutical" formulations of resveratrol with high absorption rate are essential to examine its potential medical benefits since dietary polyphenols are known to be rapidly metabolized by gut microflora and oxidized during absorption. Clinical trials with nutraceutical formulations and placebo are required to understand if resveratrol indeed holds the promise for treatment of DFS.Medical Hypotheses 06/2011; 77(3):364-7. DOI:10.1016/j.mehy.2011.05.016