Burn Prevention

It is the wound microenvironment, which is altered in the chronic wound, perpetuates its chronicity. These changes are best described with a comparison to normal healing (Table 3). With normal healing, the phases of wound healing proceed in the standard overlapping fashion, carefully orchestrated to maintain a homeostatic balance of the key factors.

Acute inflammation of the injured tissue activates the process. Inflammatory cells are present but to a controlled degree. The devitalized tissue is removed by a local controlled protease release. The protease activity is tightly controlled and balanced by antiproteases and growth factors increase.

Table 4. TISSUE INJURY
Adequate Wound Environment	Chronically Abnormal Wound Environment
available nutrients available oxygen	repeated wound traumas malnutrition infection hypoperfusion
Acute Inflammation	Acute Inflammation *Chronic Inflammation stopping normal healing
activate neutrophils, macrophages increased growth factors cell proliferation debridement of non-viable tissue by proteases new tissue formation is continuous resolution of proteases and protease inhibitors balance if proteases and protease inhibitors wound immune defenses control bacterial content	increased neutrophils increased proteases excess of inflammatory degrading cytokines excess of matrix degrading proteases deficiency of protease inhibitors degradation of growth factors impaired epitheliaization wound fluid inhibits healing breakdown of new tissue synthesis increased bacterial content increased exudates
Wound closure by normal wound healing	*Non-healing Wound with perpetuation chronic inflammation

* In the acute wound, wound fluid stimulates new tissue formation likely through growth factors. Wound immune defenses are adequate enough to prevent recurrent infection or an excessive bacterial burden which will impede healing. Extracellular matrix is produced in large quantities and matrix components are needed for re-epithelialization and wound contraction. The healing process proceeds to wound closure followed by wound remodeling. Some wounds may heal slowly, e.g. diabetic ulcer, but the healing process is continuous.

In the chronic wound, acute inflammation occurs but the healing process cannot proceed due to the etiologic factors described. A chronic excessive inflammation then develops which is not controlled. Increased wound protease activity, especially metalloproteinases is present which is out of control. Protease inhibitor activity is decreased. The proteases proceed to degrade any new extracellular matrix. The absence of new matrix makes further healing extremely difficult. The proteases not only rapidly degrade new collagen, fibronectin and other matrix proteins, but also rapidly degrade growth factors needed to stimulate the healing process. In addition, the ability of the cells to response to growth factors is decreased. Wound fluid inhibits cell proliferation. Not only is matrix degraded but there is also inadequate synthesis. Decreased epithelial migration is due to the lack of the extracellular matrix needed to facilitate this process. Increased bacterial content is usually present. Evidence of infection may not be present, but frequently the bacterial load can impede healing. The chronic inflammatory process leads to the release of more inflammatory cytokines, oxidants, and proteases which perpetuate the chronic inflammation.