Dry skin, interdigital fissuring and forefoot plantar hyperkeratosis are all signs and symptoms that may predispose patients to forefoot ulcerations. A diabetic lower extremity examination may seem routine but documenting and addressing these seemingly small changes may deter the devastating effects of peripheral neuropathy. Moisture balance therapy, accommodative shoe gear and routine diabetic foot care remain important factors in the preventative care of the diabetic population.
Essential Principles In Treating Diabetic Forefoot Ulcers
- Volume 26 - Issue 8 - August 2013
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How Diabetes Affects Wound Healing
Diabetes mellitus is a progressive metabolic disorder characterized by an abnormal hyperglycemic state, which often negatively affects wound healing by producing abnormal granulation tissue as a result of altered protein and lipid metabolism.21 As a result, wound healing phases are delayed, specifically re-epithelialization and remodeling, due to the predominately abnormal collagen metabolism and collagen cross-linking necessary for wound healing.22 These changes generate a highly inflexible wound bed and unstable framework prone for tissue breakdown and reulceration.22 The presence of diabetic autonomic neuropathy exacerbates these changes due to the patients’ loss of thermoregulatory abilities. Similar to the subtle changes that occur with motor neuropathy, indications of autonomic dysregulation are frequently disregarded during physical examination. Advanced testing such as the quantitative sudomotor axon reflex test (QSART) and the thermoregulatory sweat test (TST) are modalities clinicians can use to quantify the body’s sudomotor function and sweat response, and confirm the extent of autonomic neuropathy.23 These tests usually occur at a testing center under the supervision of a qualified neurologist.
The natural physiological process of wound healing consists of four phases: hemostasis, inflammation, proliferation and remodeling. This process is well orchestrated with overlapping between each phase. Hemostasis occurs within the first hour of injury and begins with vasoconstriction of blood vessels and the clotting of platelets. Inflammation may take up to seven days. This phase is mediated with neutrophils and monocytes that clear out bacteria, promote chemotactic factors and release growth factors at the site of injury. Proliferation begins early in the injury and will last for about 20 days. This development begins the process of angiogenesis in which macrophages, growth factors and angiotensin initiate the formation of granular tissue. The last phase, remodeling, involves extensive remodeling of collagen and epithelial tissues to organize the construct into a stronger, more rigid scar.24
The pathophysiology of wounds in the diabetic foot does not follow the aforementioned pattern.25 Instead, diabetic wound healing is significantly impacted and strongly influenced by two forces: intrinsic and extrinsic factors.26,27 Intrinsic factors include hyperglycemia, altered immune function, abnormal expression of growth factors, tissue remolding and cells undergoing phenotypic changes.26 Extrinsic factors consist of trauma and abnormal load forces to the foot. The insensitive, neuropathic foot falls casualty to recurring trauma, injury and mechanical stress. Thickening of the basement membrane impairs wound healing and increases the incidence of forefoot ulceration.27
The standard treatment for diabetic forefoot ulcerations involves a multifocal approach. These measures include a thorough history and physical, optimizing glycemic control, assessing vascular supply, aggressive wound debridement, infection control, maintaining wound moisture control, and appropriate offloading.28