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Electrical Stimulation as a Therapy for Wound Healing

IP.com Disclosure Number: IPCOM000005898D
Publication Date: 2001-Nov-14
Document File: 10 page(s) / 31K

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Abstract

A means of providing chronic direct and/or alternating electrical stimulation to a chronic wound(s) with one or more microstimulators that can be implanted with a minimal surgical procedure is described herein. Prior research suggests that stimulation of chronic wounds may promote effective wound healing through the promotion of circulation, wound contraction, epidermal migration, edema reduction, and tensile strength improvement. Electrical stimulation may also help trigger an immune response to a chronic wound and may have direct bactericidal effects.

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Electrical Stimulation as a Therapy for Wound Healing

Summary & Background

Several diseases commonly lead to the formation of pressure ulcers and other chronic non-healing wounds. Diabetes mellitus is chief among these. In the United States, 12-15 million people suffer from diabetes mellitus. This is closely followed by patients with peripheral vascular disease (PVD), which has an incidence of 10-18% in people over age 70.

Pressure ulcers (a.k.a. pressure sores) are caused by excessive pressure that deprives the skin and underlying tissues of adequate nutrition. The Agency for Health Care Policy and Research (AHCPR) cites the prevalence of pressure ulcers as 3-30% in acute care facilities, 66% in elderly fracture patients, and 33% in critical care facilities. The prevalence of pressure ulcers in skilled nursing facilities (i.e., long-term care centers) is 23%.

The incidence of chronic wounds appears to be higher in persons suffering from disease conditions, such as diabetes, and/or physical disabilities due to mobility impairments, such as those that result from spinal cord injury (SCI). Little is known about how changes in the homeostatic mechanisms of persons having either of these conditions predispose them to wounds, or how they affect wound repair. Though the categories of chronic wounds that are prevalent in both conditions vary, there may be similar etiologies. For diabetic wounds, both neurological abnormalities and vasculopathy have been postulated in explaining the pathogenesis of the diabetic ulcer. In persons with SCI, changes in sensory innervation and circulation provide a spectrum of metabolic changes that can predispose to the development of chronic wounds.

Phases of Wound Healing

There are three sequential phases of wound healing:

1. Inflammatory Phase - usually lasts 3-10 days

This phase prepares the wound for healing and cleans up debris. The inflammatory phase includes Vasoconstriction, Vasodilation, Clot Formation, Phagocytosis, and Neovascularization. Clinically, the wound site demonstrates edema, erythema, warmth, and pain. Initially, the surrounding tissues undergo vasoconstriction to slow or stop blood loss; this lasts only 5-10 minutes. During and following this time, platelets aggregate along the vasculature (a.k.a., endothelium) and form platelet plugs. Also following initial vasoconstriction, the non-injured vessels dilate and capillary permeability increases for approximately an hour. During this time, plasma leaks and forms fibrin plugs which block lymphatic flow. White blood cells (a.k.a. leukocytes) cluster together at the margins of the wound. Polymorphonuclear leukocytes begin digestion (a.k.a. phagocytosis) of debris and foreign substances in order to prevent or fight infection. (Clinically, this leads to pus formation.) Mononuclear leukocytes (i.e. monocytes and macrophages) aid in phagocytosis (through excretion of digestive products, e.g., ascorbic acid, hydrogen peroxide, lactic acid) and initiate the t...