Biofilms are found in the majority of chronic wounds and pose a critical health threat, causing nearly 80% of refractory nosocomial infections. They also have a damaging virulence mechanism, which induces resistance to antimicrobials and evasion from the host’s immune system. Over 90% of chronic...
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
- Debride non-viable tissue as needed and episodically to return wound to acute status.
- Optimize nutrition to support healthy collagen growth.
- Consider topical application of growth factors or biologicals if wound tissue is viable but not progressing.
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.
- Use topical therapies with protease inhibitors to decrease degradation of healthy tissue.
- Administer systemic anti-inflammatory drugs as appropriate.
- Use topical antimicrobials judiciously in presence of clinical symptoms in response to wound bioburden; do not use as monotherapy when clinical infection is suspected because true wound infections are nearly impossible to eradicate in this manner.1
- Obtain a culture using literature-validated processes such as qualitative tissue biopsy of healthy appearing tissue; if this is not possible, a swab of wound exudate obtained by using a procedure such as the Levine technique is recommended.2
- Administer targeted antibiotic therapy using sensitivities from qualitative tissue biopsy; this is the gold standard for treating wound infection.1
- Treat with oral or intravenous antibiotics as required, depending on the severity and type of infection; collaborate with infectious disease professionals as needed for complicated infections.2
- Consider atypical wound etiology and workup/referral as necessary if wounds do not respond to treatment as expected (s&n time model).
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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
- Apply topical therapies appropriate for managing the dynamic environment of wounds, such as hydrating dressings for lowly exudating wounds or specialty absorptive for wounds with copious exudate.
- Control edema with NPWT and/or extremity compression to manage wound exudate and excessive moisture in edematous limbs with wounds.
- * Clinicians should note that a sharp increase in wound exudate may be an early indicator of impending infection.1
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
- Surgical excision of the non-viable wound edge is recommended if the wound is not progressing despite addressing the remaining parts of the TIME model.
- Even in the presence of viable tissue and an appropriate treatment plan, stalled wound edges contribute to chronicity of the chronic wound and further increase the likelihood of progression through the spectrum from contamination to infection.2
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.