Following completion of this chapter, the student will be able to:
- Explain cellular and physiological actions of commonly used modalities on wound healing. 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.
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. 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.
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 ability of cells involved in tissue response to stimuli will 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 may accelerate closure of chronic wounds.
To determine the best modality for the treatment of that 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 these modalities work within the healing processes allows the clinician to make a better choice of modality on this condition.
Both superficial hot and cold therapies are commonly used to treat musculoskeletal conditions following injuries.