Promotion of Wound Healing with Electrical Stimulation

Document Type

Article

Language

eng

Publication Date

9-1996

Publisher

Lippincott Williams & Wilkins

Source Publication

Advances in Wound Care

Source ISSN

1076-2191

Abstract

Clinicians involved in the conservative care of chronic wounds have many treatment interventions from which to choose, including debridement/irrigation, dressings, pressure-relieving devices, hyperbaric or topically applied oxygen, whirlpool/pulsed lavage, ultrasound, topical antibiotics, and cytokine growth factors. All except the last two interventions are physical treatments that create a wound-tissue environment conducive to healing. Unfortunately, many chronic wounds heal very slowly, do not heal, or worsen despite the best efforts of caregivers to promote tissue repair.

An intervention commonly used to treat chronic wounds, especially by physical therapists, is electrical stimulation (ES). The rationale for use of this method is based on the fact that the human body has an endogenous bioelectric system that enhances healing of bone fractures and soft-tissue wounds. When the body's endogenous bioelectric system fails and cannot contribute to would repair processes, therapeutic levels of electrical current may be delivered into the wound tissue from an external source. The external current may serve to mimic the failed natural bioelectric currents so that wound healing can proceed.

Certain chemotaxic factors found in wound substrates contribute to tissue repair processes by attracting cells into the wound environment. Neutrophil, macrophage, fibroblast, and epidermal cells involved in wound repair carry either a positive or negative charge. When these cells are needed to contribute to autolysis, granulation tissue formation, anti-inflammatory activities, or epidermal resurfacing, ES may facilitate galvanotaxic attraction of these cells into the wound tissues and thereby accelerate healing.

Comments

Advances in Wound Care, Vol. 9, No. 5 (September/October 1996): 42-45. Permalink.

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