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OBJECTIVES

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Following completion of this chapter, the student will be able to:

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  • Explain cellular and physiological actions of commonly used modalities on wound healing including thermal agents, electrical stimulation, ultrasound, phototherapies, and compression.

  • Review clinical research evidence of effectiveness of modalities for delayed or nonhealing wounds.

  • Describe application techniques, stimulus parameters, and treatment schedules commonly used when treating chronic wounds with these modalities.

  • Review indications, contraindications, and potential risks of each of the modalities.

  • Use information provided in the chapter to select the best modality for a particular type of chronic wound.

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INTRODUCTION

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The cellular and physiological processes triggered by tissue injury are often divided into three phases, namely, inflammation, proliferation, and remodeling phases (refer to Chapter 2). Briefly, soon after injury, blood loss is minimized through hemostatic changes that involve a cascade of events involving the platelet that result in fibrin clot formation. Chemical mediators released by the activated platelet and mechanical trauma attract leukocytes, including macrophages and neutrophils, to the site of injury where they exit the blood vessel and enter the injured tissue. Phagocytic activities of these inflammatory cells act to debride necrotic and foreign material present in the damaged tissue. Smaller neutrophil, which is a type of polymorphonuclear cell, arrives to the site of injury early in the inflammatory phase and acts to reduce bacteria invasion in the area. White blood cells also release growth factors that have potent mitogenic and chemoattractant properties that are responsible for mediating migration and proliferation of fibroblasts, endothelial cells, and epithelial cells. Fibroblasts and endothelial cells direct collagen synthesis and angiogenesis, respectively, and migration and proliferation of epithelial cells results in the formation of a new epidermal barrier. During the final remodeling phase, turnover and reorganization of collagen and other components of the extracellular matrix optimizes tissue integrity and strength and helps to prevent future wound breakdown.

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Impairments in soft tissue healing are caused by a number of complicating factors that collectively interfere with the normal tissue repair process. Medical, pharmacological, social, and environmental factors that interfere with oxygen perfusion, cause repetitive trauma, promote bacterial growth, or limit the activity of key reparative cells, and ultimately delay the normal healing process. In addition, there is recent experimental evidence that delayed healing is associated with chronic inflammation that causes elevated levels of inflammatory mediators that promote tissue destruction and interfere with new tissue formation.1 Therefore, therapies that halt the destructive chronic inflammatory process and help restore the normal balance of tissue promoters and inhibitors can accelerate closure of chronic wounds.

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To determine the best modality for the treatment of a particular chronic wound, it is imperative to have an awareness of the experimental research evidence available that provides information about the cellular and systemic effects of these modalities on the biological systems in general and on the processes of wound healing specifically. Understanding how and where ...

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