Speckle Study: In Arterial, Mixed and Diabetic Foot Ulcers

The most common underlying etiologic factors responsible for chronic delayed healing among lower extremity wounds encountered in the outpatient clinic are chronic venous insufficiency (CVI), diabetic neuropathy, and arterial insufficiency (AI). One or more of these factors can be identified in more than 90% of chronic lower extremity ulcers, and treatment protocols have been designed to manage wounds of each type to maximize healing potential. It is important to remember that multiple factors may coexist in any individual patient with a chronic wound, complicating management and hindering the healing process. Recently, it has been reported that the neuroischemic diabetic foot ulcer is now more common than nonischemic neuropathic diabetic foot ulcers, as arterial insufficiency promoted by poorly controlled diabetes complicates already impaired healing present in patients with diabetes.

Chronic leg ulcers are painful, debilitating wounds that place a significant burden on the patient, their family, and healthcare resources. Treating leg ulcers can present a significant challenge to clinicians, who currently have a limited range of treatments at their disposal. The mainstay of treatment is compression bandaging, ambulation and elevation at rest. In patients with mobility deficits, or in those who are unable to tolerate compression bandaging, ulcers may deteriorate and never heal. Accordingly, there is a need for novel, alternative devices or strategies that can be used to complement or replace compression therapy.

Numerous pathophysiological and metabolic factors can affect wound healing and result in a poor outcome. They include local causes such as oedema, ischemia, tissue hypoxia, infection, necrosis and growth factor imbalance, as well as systemic causes including metabolic disease, nutritional status general perfusion disturbances and pre-existing illness. These factors alter the wound repair environment, impede healing and increase the risk of chronic wound development. All healing processes including, inflammatory cell influx, fibroblast migration, and collagen and extracellular matrix deposition, are delayed in this situation, leading to prolonged wound healing.

Any wound management should assist the healing process and optimise the patient's blood flow to the wound area4. An acute wound in a stable patient with normal blood flow should heal successfully. Anything that compromises tissue oxygen delivery, such as poor vascularisation, will impede healing. There is a strong scientific basis for oxygen treatment as prophylaxis against infection; to facilitate wound closure and to prevent amputation in wounded patients. Oxygen delivery is a critical element for the healing of wounds. Hypoxemia, caused by disrupted vasculature, is a key limiting factor against wound healing.

The link between compromised circulation and ulceration is well established and well described. Chronic venous insufficiency is a direct cause of ulceration.

Diabetic foot ulcer is a major complication of diabetes mellitus, and probably the major component of the diabetic foot. Diabetes mellitus is one such metabolic disorder that impedes the normal steps of the wound healing process. Many studies show a prolonged inflammatory phase in diabetic wounds, which causes a delay in the formation of mature granulation tissue and a parallel reduction in wound tensile strength.

Treatment of diabetic foot ulcers should include: blood sugar control, removing dead tissue from the wound, dressings, and removing pressure from the wound through techniques such as total contact casting. Surgery in some cases may improve outcomes. Hyperbaric oxygen therapy may also help but is expensive. It occurs in 15% of people with diabetes and precedes 84% of all diabetes-related lower-leg amputations.