Cath Lab Digest

M any wounds healing by secondary intention become indolent, extending periods of patient discomfort and inconvenience and increasing healthcare costs and staff workload. Although wounds cease to heal for many reasons, perhaps the most common emanates from the effects of wound bioburden,1 due to invasive infection, the sheer quantity of colonizing microbes, the mixture of species in the wound base, or the effect of their toxins. The indiscriminate use of antibiotics, either systemic and topical, for all open wounds would raise healthcare costs and contribute to the development or selection of multi-resistant micro-organisms; therefore, systemic antibiotics are not an option for prophylactic use in all open wounds and are reserved for proven cases of wound infection. However, proof of infection is fundamentally restricted to acknowledging clinical signs and symptoms in collaboration with qualitative microbiology.
The use of qualitative microbiology alone is flawed because the relative impact of bacteria in any particular context on the body must be considered, creating the potential for either over-treatment or under-treatment depending on the diagnostic skills of the clinician. Based on the results of an audit, nurses'2 and other clinicians'3 ability to diagnose is highly variable, suggesting that wounds that become indolent due to bioburden (ie, critical colonization) but that do not exhibit the classically considered signs of infection may go untreated, even though they might benefit from a topical or systemic antimicrobial strategy. It should be noted that the term critical colonization - defined as a transition state between bacterial surface colonization that does not impair the healing process and invasion of the bacteria into viable tissue - is largely conceptual, although Fumal and colleagues4 have shown supportive evidence .
Additionally, understanding the intricacies of the microbiology of open wounds is further complicated by the need to interpret laboratory results in various contexts. The wound's anatomical position, duration, shape, or presentation; the patient's level of health and control of underlying pathologies; the presence of infection-potentiating factors such as foreign bodies, hematoma, and necrotic tissue; the sources and frequency of exogenous contamination; the considered virulence of the individual micro-flora species; and the potential synergism between different species all require consideration. Add to this the complicated task of correctly identifying tissue types and interpreting the reasons why the wound is exhibiting certain signs and symptoms and the range of opinions on how to proceed clinically becomes self-evident.

The Healing Process
The wound healing process can be divided into three phases: inflammation, proliferation, and maturation. Each stage has signature events or cells. Inflammation includes coagulation through fibrin mesh and platelet plug, vasodilation and release of pro-inflammatory markers, platelet degranulation and release of proliferative growth factors, and the rapid infiltration of neutrophils (polymorphonuclear white cells) for non-specific bacterial killing. Monocytes also enter the wound and activate to become macrophages with a longer lifespan than the neutrophils; these are able to phagocytose damaged tissue, contaminating microbes and spent neutrophils. Macrophages also send out cytokines to attract fibroblasts necessary for the proliferative stage.
In the proliferative stage, fibroblasts deposit collagen and, along with a massive influx of new blood vessels and ground substance of proteoglycans and glycosaminoglycans, form granulation tissue. During this time, myofibroblast activity is believed to incite wound contraction, significantly reducing the area to be filled. Keratinocytes change their phenotype and start moving across the granulation to form a new epithelium.