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Index: WOUNDS. 2012;24(5):132–137.

  Abstract: Although excessive exudate has been associated with poor wound healing outcomes, exudate is still not well understood in the pathophysiology of chronic wounds. Wound exudate is believed to be the result of wounds that are trapped in a persistent, hyper inflammatory state. Biofilm, bacteria of multiple species living in community, has multiple well-defined molecular pathways that produce hyper inflammation. The exudate that is produced in wounds is a potentially important nutrient source for biofilm; therefore, rapidly removing exudate may rob the biofilm of important nutrients and suppress its negative effects.

Methods. A hydroconductive fiber dressing that possesses excellent capillary action properties was utilized to rapidly remove wound exudate in 10 patients. Results. The data demonstrate an average 62% reduction in wound volume for these 10 wounds over a 4-week period. Two wounds completely closed during the 2 weeks, and all but 1 wound significantly improved. Only 6 of the 10 wounds showed fewer bacteria at the end of the 4-week study period, suggesting there is not a 1:1 correlation with reduction in the number of bacteria in the wound and wound healing. Conclusion. Rapid removal of the nutrient source from wound biofilm, while not diminishing the number of bacteria, may suppress a biofilm’s negative effects on wound healing.

Introduction

  Exudate, a fluid rich in protein and other nutrients that oozes out of blood vessels due to inflammation, is not well understood in the pathophysiology of chronic wounds. There is agreement as to how exudate forms, but a consensus does not exist as to why exudate occurs, and more importantly, what it means to the nonhealing wound.¹ This study will attempt to explore possible roles that exudate may play as a barrier to wound healing.

  Increased exudate has negative connotations for wound healing. Antibiotics and biocides can decrease exudate, as can the management of edema and inflammation, but most management strategies rely on methods to remove exudate locally after it has formed. Through trial and error, it has been firmly established that chronic wounds heal better if exudate is managed aggressively.^2,3 Therefore, it becomes critical for clinicians to understand exudate at the cellular and biochemical level.

  Chronic wounds are stuck in a chronic, hyper inflammatory state. Biochemically, there is a 100- to 1000-fold increase in proinflammatory cytokines, such as gamma interferon, tumor necrosis factor-alpha (TNF-a), interleukin 1, interleukin 6, interleukin 8, and many others.^4–8 At the cellular level, the most notable abnormality is an increase in polymorphonuclear cells, up to 1000 times greater than normal levels.⁹ Additionally, it is important to note that these neutrophils have lost their chemotactic abilities and cannot be cleared by macrophages.¹⁰ This results in retention of neutrophils in a wound bed that will eventually die and release elastase, metalloproteinase-8 (MMP-8), and other matrix metalloproteinases (MMPs) into the local wound milieu.¹¹ There are many well-defined molecular mechanisms demonstrating that bacteria in biofilm phenotype can, and do, produce all of these biochemical and cellular effects in many host tissue environments.¹²

  Biofilm transformation begins when a free-floating bacterium (planktonic) attaches to a surface. The bacterium divides and quickly coats itself with a self-secreted matrix of sugary polymers (extracellular polymeric substance [EPS]). The EPS binds the group of bacteria to the host surface and protects the society from white blood cells, antibodies, and compliment, as well as antibiotics and biocides.