Assessing The Role And Impact Of Enzymatic Debridement
- Volume 17 - Issue 7 - July 2004
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Over the last few decades, many technological advances have occurred in the field of wound healing, resulting in a variety of wound dressings, ointments, creams, debriding agents, growth factors and bioengineered skin grafts. While one does not have to be a wound care specialist to treat complicated wounds, it is important to have a basic knowledge of normal wound healing and the etiology of a chronic or nonhealing wound, an understanding of the wound products available, and the ability to adapt to an ever-changing wound.
Chronic, delayed or non-healing wounds demonstrate an impaired response due to the presence of bacteria, necrotic tissue, growth factor deficiencies, increased inflammatory cytokines, abnormal matrix metalloproteinase regulation, poor oxygenation of the wound and the development of cellular senescence. Recognizing the involved factor(s) that are preventing the wound from healing is the key to knowing what product to use to optimize the chemical processes that allow for wound bed preparation and facilitate healing.
The exudate from chronic wounds affects wound healing in a variety of mechanisms. Exudate inhibits the proliferation and function of key resident cells and contains proteases that break down extracellular matrix proteins.1-3 Extracellular matrix components, including fibronectin, accumulate within the wound for up to a year in the life of a non-healing diabetic foot ulcer.4 With inflammatory wounds, such as venous ulcers, there is enough exudate to interfere with healing or hamper the effectiveness of therapeutic products like growth factors and bioengineered skin. In addition, fibroblasts and keratinocytes may become altered, becoming unresponsive to certain signals, including growth factors.5-9 Studies have shown these cells are not only senescent (aged), but also demonstrate decreased proliferative rates.
Understanding The Importance
Of Wound Bed Preparation
Wound bed preparation has been defined as the global management of the wound to accelerate endogenous healing or to facilitate the effectiveness of other therapeutic measures.10 This includes the use of sharp, mechanical and enzymatic debridement to convert a chronic wound into an acute wound.
When we remove necrotic, devitalized tissue, we are creating an injury response that changes the molecular environment into a healing wound environment. This is the goal of wound bed preparation. Reestablishing a rejuvenation of the cellular response, decreasing bacterial burden and decreasing the amount of growth inhibiting exudate are all necessary to allow the wound to progress to healing. However, despite our best efforts at debridement, one must still address the underlying factors that have caused the chronic wound. (See “Chronic Wound Characteristics” below.)
Chronic Wound Characteristics
• Necrotic, fibrotic tissue within the wound bed
• Poor blood flow
• Recurrent tissue/wound breakdown
• Degeneration of fibronectin, vitronectin
• Lack of granular tissue
• Lack of epithelialization
• Elevated levels of cytokines
• Elevated levels of matrix metalloproteinases (MMPs)
• Elevated levels of proteases
• Decreased levels of inhibitors for MMPs (TIMPs)
• Decreased levels of protease inhibitors
• Decreased growth factor activity
• Decreased mitotic activity
• Increased presence of senescent cells
• High levels of bacterial content
• High levels of multi-drug resistant organisms
• Presence of bio-films
• Increased likelihood of osteomyelitis
• Increased likelihood of amputation
Reviewing The Various Types Of Debridement
Debridement certainly remains the critical first step in the process of wound healing. However, there is no specific methodology that one can universally apply to every wound. One must weigh many considerations before selecting the appropriate course of debridement.