By Gregory Schultz, PhD
In my recent WoundSource webinar on the assessment and treatment of chronic wounds and biofilms, I discussed the pathogenesis of chronic wounds and offered a biofilm-based wound care protocol to promote healing.
by the WoundSource Editors
Bioburden in chronic wounds can be a principal contributor to inflammation, clinical wound infection, and further delayed wound healing. Clinically diagnosing infection in chronic wounds can be problematic because most individuals susceptible to developing chronic wounds are subject to physiological states that often blunt typical infectious responses in various ways.1 These responses include pain, erythema, febrile state, leukocytosis, edema and increased wound exudate, wound odor, etc. For example, a patient with a neuropathic ulcer and diabetes mellitus may not report pain or fever or present with leukocytosis but will have increased edema and wound exudate. A patient with an ischemic ulcer of peripheral arterial disease may report pain, erythema, fever, and leukocytosis but not have perfusion sufficient to produce edema or increased wound exudate.1 It is imperative to understand how to concurrently manage factors that can contribute to infection, as well as assess for symptoms and implement interventions to prevent infection.
Each letter in the mnemonic of the TIME (tissue, infection/inflammation, moisture, edge ) model of wound bed preparation represents a factor that contributes to the pathophysiology of the chronic wound. Let’s review how each factor contributes to wound bioburden (the problem) and the associated interventions that can assist with managing bioburden and addressing infection (the solution).
Non-viable tissue must be eradicated while growth of healthy tissue is supported. Non-viable tissue is a breeding ground for bacteria, and its presence causes production of proinflammatory cytokines that damage proliferative cells such as fibroblasts and growth factors such as vascular endothelial growth factor (VEGF), which are responsible for collagen and vascular tissue formation, respectively.1
Wounds become chronic as a result of perpetuation of inflammatory states in response to a multitude of factors, including host factors (immunosuppression, malnutrition) and extrinsic factors such as bacterial burden and topical therapies.1 Depending on a combination of these factors and how they are managed at a given time in treatment, wounds can progress in both directions along the spectrum from contamination, colonization, critical colonization, infection, and sepsis.
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Moisture in excess causes maceration, which as we have noted previously is non-viable tissue; this perpetuates the cycle of non-viable tissue and its contribution to presence of bioburden. In addition, a lack of moisture delays or prevents epithelialization because wound bed dehydration hampers keratinocyte migration.2
Epithelialization in full-thickness wounds begins when healthy granulation tissue is available for migrating keratinocytes and ends when keratinocytes from opposing wound edges meet. This phenomenon is known as contact inhibition. Unfortunately, this process also occurs when wound edges become stalled by undermining or rolled wound edges (epibole) where epithelial cells meet and cellular signaling causes the body to “think” the edge wound is closed, but migration occurs in a shelf-like formation versus bridging across the wound bed. This can happen when there is insufficient viable tissue to support epithelization, and this is why reduction of bioburden to decrease subsequent tissue necrosis is crucial.1
Managing bioburden can prevent perpetuation of chronic inflammation related to the presence of pathogens and subsequent wound infection. Implementing interventions to reduce bioburden is key to progression through the inflammatory phase into the proliferative phase of wound healing (S&N, TIME model PDF ). For a summary of interventions complementary to the TIME model for wound bed preparation, please review the previous practice accelerator installment.
1. Bryant RA, Nix DP. Acute & Chronic Wounds: Current Management Concepts, 5th ed. St. Louis, MO: Elsevier Health Sciences; 2015.
2. European Wound Management Association (EWMA). Position Document: Wound Bed Preparation in Practice. London: MEP Ltd; 2004. Available at: http://ewma.org/fileadmin/user_upload/EWMA.org/Position_documents_2002-2.... Accessed June 8, 2018.
The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, Kestrel Health Information, Inc., its affiliates, or subsidiary companies.