A Closer Look At Topical Therapies In Wound Care
Ischemia. Oxygen is essential to all phases of wound healing as it is necessary for cellular metabolism and production of energy in the form of adenosine triphosphate. Adequate tissue oxygenation promotes angiogenesis, prevents infection and induces keratinocyte and fibroblast maturation and proliferation. This leads to re-epithelialization and formation of collagen, which aids in wound contraction.7 Ischemia in the form of peripheral vascular disease is a common complication of those afflicted with diabetes mellitus. Microvascular changes are apparent in the way of capillary size reduction and basement membrane thickening.8 This poor oxygen environment or hypoxic state often clinically appears as a dry or necrotic wound.
Peripheral sensory neuropathy. Peripheral sensory neuropathy is another contributor to a chronic DFU. In one study that looked at the causal pathway of DFUs, researchers estimated that in 78 percent of the cases, peripheral sensory neuropathy was present.9 The thinking is that peripheral sensory neuropathy initiates the development of the DFU, beginning with the patient being unable to sense pain. This leads to repetitive trauma in areas of peak pressures, disrupting normal tissues or making existing ulcerations progressively worse.10
This propagates a vicious cycle that often goes unrecognized until significant clinical changes are visible in the DFUs. Researchers have noted a decrease in important chemotactic neuropeptides (nerve growth factor, substance P and calcitonin gene-related peptide) in patients with peripheral sensory neuropathy.3 In addition, authors have shown that patients with peripheral sensory neuropathy also have deceased levels of lymphocyte infiltration.11 As such, these wounds often get “trapped” in the inflammatory phase, leading to exudative types of wounds.
Infection. After any injury or break in the skin, microorganisms can easily access deeper tissues. It is important to classify the wound into one of four categories: colonized, contaminated, with local infection or with deep infection. The large, irregular heel ulceration at left should raise concern for the potential of deep infection. Recognizing the stage of bacterial invasion helps the physician choose the proper therapy for management of infection.
If one does not adequately remove the microorganisms from the wound, the bacteria and endotoxins produced will lead to a prolonged inflammatory phase. This also often leads to increased production of inflammatory cytokines, proteases and metalloproteases that, when unregulated, will lead to degradation of the extracellular matrix.12 Other concerns include the formation of biofilms, aggregates of bacteria that often produce an extracellular polysaccharide matrix, which protects the bacteria from traditional antibiotic topical and systemic therapies.13
While we have described only a few factors that affect wound healing, one should understand there are countless causes of delayed wound healing. These factors do not act independently but rather in tandem. This makes wound healing a complex challenge. One should emphasize having a strong understanding of the underlying pathology of the DFU and perform a good clinical examination of the wound as well.
What About Enzymatic Debridement?
When it comes to topical therapy treatment of DFUs, it is helpful to categorize wounds into one of three categories: dry/necrotic, exudative or infected. Depending on the type of wound, the clinician can choose appropriate topical therapy. Topical therapies ideally should be comfortable, provide protection to the wound itself and create an optimal wound healing environment.14