The purpose of this study was to evaluate outcomes of persons with UT grade 2A neuropathic diabetic foot wounds treated with an acellular matrix. Data were abstracted for 17 consecutive patients with diabetes--76.5% males, aged 61.5 +/- 8.5 years with a mean glycated haemoglobin of 9.2 +/- 2.2% presenting for care at a large, multidisciplinary wound care centre. All patients received surgical debridement for their diabetic foot wounds and were placed on therapy consisting of a single application of an acellular matrix graft (GraftJacket; Wright Medical Technologies, Arlington, TN, USA) with dressing changes taking place weekly. Outcomes evaluated included time to complete wound closure and proportion of patients achieving wound closure in 20 weeks. Acellular matrix therapy was used as initial therapy and was sutured or stapled in place under a silicone-based non adherent dressing. Therapy was then followed by a moisture-retentive dressing until complete epithelialisation. In total, 82.4% of wounds measuring a mean 4.6 +/- 3.2 cm(2) healed in the 20-week evaluation period. For those that healed in this period, healing took place in a mean 8.9 +/- 2.7 weeks. We conclude that a regimen consisting of moist wound healing using an acellular matrix dressing may be a useful adjunct to appropriate diabetic foot ulcer care for deep, non-infected, non-ischaemic wounds. We await the completion of further trials in this area to confirm or refute this initial assessment.
The etiology of neuropathic diabetic foot wounds can be summarized by the following formula: pressure x cycles of repetitive stress = ulceration. The final pathway to ulceration consists of an inflammatory response, leading to tissue breakdown. Mitigation of this response might reduce the risk of ulceration. This proof-of-concept trial evaluates whether simple cooling of the foot can safely reduce the time to thermal equilibrium after activity. After a 15-min brisk walk, the six nondiabetic volunteers enrolled were randomly assigned to receive either air cooling or a 10-min 55 degrees F cool water bath followed by air cooling. The process was then repeated with the intervention reversed, allowing subjects to serve as their own controls. There was a rise in mean +/- SD skin temperature after 15 min of activity versus preactivity levels (87.8 degrees +/- 3.9 degrees versus 79 degrees +/- 2.2 degrees F; P = .0001). Water cooling immediately brought the foot to a point cooler than preactivity levels for all subjects, whereas air cooling required an average of nearly 17 min to do so. Ten minutes of cooling required a mean +/- SD of 26.2 +/- 5.9 min to warm to preactivity levels. No adverse effects resulted from the intervention. We conclude that cooling the foot may be a safe and effective method of reducing inflammation and may serve as a prophylactic or interventional tool to reduce skin breakdown risk.
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