Assessment of a Wound Cleansing Solution in the Treatment of Problem Wounds
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Problem wounds are rarely affected by a single factor.1 Delay in closure of a wound can result from problems such as poor perfusion, infection, pressure, and chronic venous hypertension.
To support wound healing, systemic factors and local factors should be addressed.1–4 Local barriers to healing must be removed before attempting wound closure.
Sometimes a wound may present as healthy and granulating and yet does not heal. This could be due to the wound bed containing nonviable (senescent) cells or cells of the wrong phenotype. In either case, they are not responding to biochemical signals in a manner conducive to the wound healing process, leading to so called weak or problem wounds.1–6
The importance of individual matrix metalloproteinases (MMP) in the epithelialization process is not fully understood. Commonly, many MMP-9 positive neutrophils are observed in close proximity to the negative MMP-9 epithelium. Excess MMP-9 in a wound may deprive the keratinocytes of signals by extracellular matrix molecules. Additionally, MMP-9 can degrade a1-proteinase inhibitor, which can result in elevated neutrophil elastase activity. Thus, MMP-9 can contribute to unfavorable conditions in several ways and lead to delayed epithelialization.
IL-8 is a member of the α-chemokine family and is a potent neutrophil chemoattractant. Neutrophils, as “early responders” to wounds and infections, release enzymes to remodel the extracellular matrix of the tissues through which they migrate to reach the site of the wound. It is proposed that the host’s cellular response to IL-8 enhances angiogenesis, but if these cells are of the wrong phenotype, wound healing could be delayed.3,6
There have been several studies investigating the contents of both problem and acute wound fluid in order to distinguish their differences.5–7 Protease activity appears to be the major area of disparity between fluid types.
Chronic or problem wounds may develop due to an underlying disease that is complicated by relevant cofactors.5–9 Wound healing may also be delayed due to the underlying disease, eg, chronic venous stasis, chronic lymphatic congestion, or arterial circulation disorders on a macro or micro level.
Chronic wounds that are not (clinically) infected are assumed to be colonized.9 In the process of becoming chronic, the pathogens present in wounds are of different etiology, independent of the actual cause of the wound condition and may present with similar issues.9–11
More attention must be paid to the complex synergistic biotope in a problem wound.11 Local reduction and/or elimination of isolated species is not useful and is frequently counter productive.10
An optimal wound healing environment is free of debris and nonviable tissue. The presence of necrotic tissue influences the wound environment and increases the risk for infection, even when aseptic wound management is carried out.1,12
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