Clinical Experience with Wound Biofilm and Management: A Case Series
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At his first office visit, he had 3 to 4+ bilateral lower extremity pitting edema with hemosiderin staining and three full-thickness stasis ulcers, one on his right shin and one on his proximal right calf measuring approximately 0.1 cm depth and one on his distal right calf with depth of approximately 0.3 cm. Specific chronicity was uncertain but Mr. D reported reoccurring problems with weeping ulcerations. Initial treatment included silver alginate dressing and compression. Close contact was maintained with his cardiologist during the time that his lower extremity edema was initially mobilized. At first, all ulcers demonstrated significant improvement using 20 mm Hg to 30 mm Hg compression provided by elastic wrap. Although the more superficial wounds closed during the first several weeks, the deeper shin ulcer stalled, with a clinically significant film build-up noted on the wound bed. The film appeared as a cloudy, translucent film on the wound surface through which larger granular buds protruded. Mr. D tolerated careful sharp removal of the film during each visit. However, the film redeveloped between monthly visits and the ulcer showed minimal decrease in diameter or depth. Initially, the visible slime was removed with scalpel and sharp forceps. Mr. D was instructed to cleanse the wound daily with a 0.057% sodium hypochlorite antiseptic before applying a new dressing. At Mr. D’s appointment the following month, the wound was without significant film and the ulcer depth had begun to decrease. At Mr. D’s next monthly visit, the ulcer depth had reduced to skin level and the wound had begun to re-epithelialize.
Case 4. Mr. V was 54 years old with a history of hypertension, chronic venous stasis disease, and deep vein thrombosis. He was admitted to acute care for management of lower extremity cellulitis. Initial assessment revealed bilateral lower extremity 4+ pitting edema with actively exudating ulcerations on both calves and his left dorsal foot. The ulcers were covered with a thick, opaque, wet scab-like layer. The left dorsal foot ulcer is seen in Figure 4a. Mr. V was receiving systemic antibiotics, diuretics, and warfarin sodium (a potent blood thinner). An arterial ultrasound ruled out significant impairment to distal arterial flow.
Initial wound therapy included application of mafenide acetate covered with oil emulsion gauze, absorbent cotton pad, gauze wrap, and compression wrap. Neither this management strategy nor rubbing a sterile gauze pad on the wound facilitated film removal or prevented its redevelopment. However, the film could be removed with forceps and scalpel. Removal was somewhat akin to trying to pull a suction-pad bath mat from a wet tub — the film appeared to be stuck to the wound bed without being a part of it (as slough is). Interestingly, the wound areas cleared of film with this method of sharp debridement but did not bleed despite the patient being anti-coagulated; this is very different from how this same wound would appear after sharp debridement of adherent slough (see Figure 4c). Skillful film removal can inflict minimal harm to the wound bed, and in some wounds, thick film can be removed completely (see Figure 4d).
Through this small case series of patients, it has been shown that links may exist between biofilm, ischemia, persistent inflammation, moisture, and wound recalcitrance and that signs of biofilm in chronic wounds may be visually evident. Biofilm is bacteria-derived living material (as opposed to slough being host-derived dead tissue) that often has a cloudy, translucent and viscous, gel-like appearance. It often forms above granulation tissue, and as such it may interfere with epithelialization.
1. Fux CA, Costerton JW, Stewart PS, Stoodley P. Survival strategies of infectious biofilms. TRENDS in Microbiol. 2005;13(1):34–40.
2. Costerton JW, Geesey GG, Cheng KJ. How bacteria stick. Scientific American. 1978;238(1):86–95.
3. Donlan RM, Costerton JW. Biofilms: survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev. 2002;15(2):167–193.
4. Kievit TR, Iglewski BH. Bacterial quorum sensing in pathogenic relationships. Infect Immun. 2000;68(9):4839–4849.
5. Enoch S, Harding K. Wound bed preparation: the science behind the removal of barriers to healing. WOUNDS. 2003;15(7):213–229.
6. Costerton JW. A short history of the development of the biofilm concept. In: Ghannoum M, O’Toole GA (eds). Microbial Biofilms. Washington, DC: ASM Press;2004:4–19.
7. Purevdorj-Gage LB, Stoodley P. Biofilm structure, behavior and hydrodynamics. In: Ghannoum M, O’Toole GA (eds). Microbial Biofilms. Washington, DC: ASM Press;2004:160–173.
8. Starkey M, Gray KA, Chang SI, Parsek MR. A sticky business: the extracellular polymeric substance matrix of bacterial biofilms. In: Ghannoum M, O’Toole GA (eds). Microbial Biofilms. Washington, DC: ASM Press;2004:174–191.
9. Sheffield PJ. Tissue oxygen measurements. In: Davis JC, Hunt TK (eds). Problem Wounds. The Role of Oxygen. New York, NY: Elsevier; 1988:17–51.
10. Rooke T. TcPO2 in non-invasive vascular medicine. Blood Gas News. 1998;7(2):21–23.
11. Sarkisova S, Patrauchan MA, Berglund D, Nivens DE, Franklin MJ. Calcium-induced virulence factors associated with the extracellular matrix of mucoid Pseudomonas aeruginosa biofilms. J Bacteriol. 2005;187(13):4327–4337.
12. Chaw KC, Manimaran M, Francis EHT. Role of silver ions in destabilization of intermolecular adhesion forces measured by atomic force microscopy in Staphylococcus epidemidis biofilms. Antimicrob Agents Chemother. 2005;49(12):4853–4859.
13. Percival SL, Bowler PG. Biofilms and their potential role in wound healing. WOUNDS. 2004;16(7):234–240.
14. Roberts FA, Richardson GJ, Michalek SM. Effects of Porphyromonas gingivalis and Escherichia coli lipopolysaccharides on mononuclear phagocytes. Infect Immun. 1997;65(8):3248–3254.
15. Rabehi L, Irinpoulou T, Cholley B, Haeffner-Cavaillon N, Carreno M-P. Gram-positive and Gram-negative bacteria do not trigger monocytic cytokine production through similar intracellular pathways. Infect Immun. 2001;69(7):4590–4599.
16. Wolcott RD, Rhoads DD, Dowd SE. Biofilms and chronic wound inflammation. J Wound Care. 2008;17:333–341.
17. Cappelli G, Tetta C, Canaud B. Is biofilm a cause of silent chronic inflammation in haemodialysis patients? A fascinating work hypothesis. Nephrol Dialysis Transplant. 2005;20:266–270.
18. Tsuneda S, Aikawa H, Hayashi H, Yuasa A, Hirata A. Extracellular polymeric substances responsible for bacterial adhesion onto solid surface. FEMS Microbiol Letters. 2003;223:287–292.
19. Lindfors J. A comparison of an antimicrobial wound cleanser to normal saline in reduction of bioburden and its effect on wound healing. Ostomy Wound Manage. 2004;50(8):28–41.
20. Shakeri S, Kermanshahi RK, Moghaddam MM. Assessment of biofilm cell removal and killing and biocide efficacy using the microtiter plate test. Biofouling. 2007;23(2):79–86.
21. Hunt TK, Hennestall RB, Pines E, et al. Impairment of microbicidal function in wounds: correction with oxygen. In: Hunt TK (ed). Soft and Hard Tissue Repair, Biological and Clinical Aspects. New York, NY: Praeger;1984:455–468.