How To Identify Underlying Causes Of Problem Wounds
- Volume 16 - Issue 2 - February 2003
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Recent advancements in technology have led to numerous adjunctive therapies for healing chronic wounds. In many cases, though, we can achieve healing in a short period of time once we identify the underlying factors that inhibit proper healing. With this in mind, let’s take a closer look at some of these common impediments.
While wound hypoxia is the most common obstacle we see, it is also the most difficult hurdle in facilitating wound healing. You can measure wound hypoxia with transcutaneous oxygen pressure (TcPO2). A TcPO2 reading of less than 40mmHg has been correlated with poor wound healing.
Wound hypoxia impairs all three phases of wound healing. Low oxygen tension predisposes wounds to bacterial invasion by impeding oxygen-depending intracellular bacterial killing. Some antimicrobial agents require adequate amounts of oxygen in their antimicrobial activity. Vancomycin and aminoglycosides, such as gentamicin, tobramycin, amikacin and netilmicin, are examples of the oxygen dependent agents that do not kill microorganisms effectively if there is low oxygen tension.
The effect of wound hypoxia on the proliferative phase has been well documented. Low oxygen tension deceases ATP production, which is necessary for every cellular function. Replication of fibroblasts, epidermal and endothelial cells also decrease. Therefore, the whole secondary healing process (i.e. angiogenesis, collagen synthesis and epithelialization) becomes significantly impaired.
Tissue perfusion can be decreased by many disorders, including poor cardiac output, focal ischemia, peripheral vascular disease, atherosclerosis, chronic infection or tobacco consumption. You should make very attempt to improve tissue perfusion by identifying the etiology and making an adequate referral as necessary.
Reviewing Causal Factors For Infections
Wound infection has been shown to impair wound contraction in both acute and chronic wounds by several mechanisms. Some bacteria are believed to release endotoxins that inhibit the migration of keratinocytes and fibroblasts into the wound. Proteases from bacteria can degrade fibrin and growth factor in the wound. Infection causes prolonged elevation of inflammatory mediators and cytokines, resulting in a prolonged inflammatory response to the wound.
The presence of bacteria is not the only cause of impairment as the necrotic tissue left in the wound also inhibits the healing process. Foreign debris in the wound will serve as a growth medium for bacteria and increase the probability of infection. It will also promote pro-inflammatory mediators and proteinases that destroy endogenous growth factors, and degrade the glycosaminoglycan matrix needed for wound healing.
Therefore, one should not treat an infection with antimicrobials alone. Indeed, good wound debridement is essential as it helps to:
• reduce the bacterial load;
• decrease inhibitors of growth factors; and
• stimulate the production of growth factors from cells involved in healing.
When Other Medications Affect Healing
There are numerous medications known to inhibit wound healing. Steroids are known to interfere with angiogenesis and fibrogenesis. They also inhibit wounds from contraction.
Oral or topical administration of vitamin A has been proposed to reverse the effect of steroids on wounds. Nonsteroidal antiinflammatory drugs (NSAIDs) are also commonly used by patients who have chronic diabetic ulcers. Researchers have shown that NSAIDs decrease collagen production. While the mechanism is unknown, it is believed to be associated with impaired prostaglandin metabolism.
It is important to review the patient’s medication list. Doing so can help you identify possible medications that are inhibiting wound healing and allows you to make appropriate substitutions and/or discontinue problematic medications until the wound shows signs of improved healing.