Can Ultrasound Debridement Facilitate Biofilm Removal From Diabetic Foot Ulcers?

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Author(s): 
Melinda Bowlby, DPM, and Peter Blume, DPM, FACFAS

A patient with diabetes mellitus has a 15 to 25 percent chance of developing a diabetic foot ulcer during his or her lifetime.1 Once the patient with diabetes develops an ulcer, there is an even higher rate of ulcer recurrence at 50 to 70 percent over five years.1

   Diabetic foot ulcers are notoriously slow to heal and often lead to complications such as life-threatening infection and amputation.1 Traditionally, the mainstays of wound care include debridement, ensuring adequate vascular perfusion, eradicating infection and offloading diabetic foot ulcers.2

   An often underestimated cause in the delay of wound healing is the development of biofilm. Researchers have estimated that 60 percent of chronic wounds are covered with biofilm.3 Biofilm occurs when bacteria colonize a wound and become encased in a protective coating of polysaccharides and lipids, termed glycocalyx, which is resistant to the patient’s immune system, systemic and topical antibiotics.1 Bacterial cells make up approximately 5 to 30 percent of biofilm and are typically polymicrobial.4 Biofilm thickness varies from a few micrometers to a few millimeters and bacteria encased in biofilm are approximately 1,000 times more resistant to antibiotics than in the planktonic form.4,5 Independent biofilm colonies form interconnected and sophisticated networks.6

   Both Pseudomonas aeruginosa and Staphylococcus aureus, two common pathogens in diabetic foot ulcers, are known to form these structures.6 Methicillin-resistant Staphylcoccus aureus (MRSA) also lives in biofilm, further increasing the virulence of the bacteria.6 Biofilm can begin forming within hours and complex structures can form on a wound within two to four days.6 Biofilm clusters can break free and migrate to colonize new areas of the wound.4 Bacteria in biofilm communicate with each other through signaling molecules, termed quorum sensing.4 Pseudomonas aeruginosa uses quorum sensing for defense and can actually paralyze and lyse neutrophils.4

   Wound healing is delayed in the presence of biofilm for a number of reasons. Biofilm causes chronic inflammation with the prolonged presence of neutrophils.4 The neutrophils prevent keratinocyte migration and release destructive reactive oxygen species and proteinases.4 Keratinocytes produce more matrix metalloproteinases in biofilm, which leads to destruction of the extracellular matrix and decreases growth factors.4

   A microscope is often not necessary to detect biofilm as the presence of slough, shininess to an ulcer, malodor or necrotic tissue is likely an indication that biofilm is present.7 Superficial wound swab cultures often do not detect bacteria within biofilms, making swabs of little value.6 Deep tissue culture remains the most effective way of determining biofilm pathogens.6 Effective oral antibiotic treatment would require a much higher dose than what would be required if bacteria were not encased in biofilm, making antibiosis difficult.4 Topical antibiotics would also need to be polymicrobial and often do not penetrate the thick biofilm membrane.4

An Overview Of Surgical Debridement

Debridement is essential to wound bed preparation for removing necrotic tissue, bacteria and biofilm in wounds. Forms of debridement include autolytic (endogenous proteolysis), mechanical (wet to dry dressings), enzymatic (collagenases), biological (maggots) and surgical.9

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