The current and ongoing explosion of wound-dressing technologies can be traced to the work of Bull et al1 on occlusive dressings in 1948. This work was expanded in the 1960s by Winter2 when he demonstrated that porcine wounds epithelialized faster in a moist versus a dry environment. His findings were later confirmed and expanded to human subjects by Hinman.3
In the past several decades, we have seen the variety and types of dressings that are available for wound management literally explode in number. A comprehensive guide to wound dressings by Hess4 lists 280 frequently used wound-care products. With available dressings easily numbering in the hundreds, and many new products entering the market each year, it is easy to see why wound management has become a clinical specialty.
With the ever-increasing number of wound dressings and their complex chemical compositions, wear characteristics, indications, and contraindications, the clinician is often left asking, "How do I possibly make the best dressing selection for my patient?" At first glance, this question is quite overwhelming and seems impossible to answer. However, with careful analysis and knowledge of current research on acute and chronic wound healing, an algorithm for dressing selection does emerge.
At this point in time, chronic and acute wounds appear to have distinct biochemical characteristics.5 To most appropriately dress a wound, we must first consider whether it is an acute or chronic wound. To make this differentiation, the clinician must understand the difference between an acute and a chronic wound.6 While wound-healing science is in its infancy, we do have evidence that acute and chronic wounds differ in a number of ways. The definition of an acute versus a chronic wound provides insight into the overall difference between these two entities. Namely, an acute wound heals by progressing through an orderly sequence of biochemical steps, while the chronic wound results from an interruption of this orderly process. Hence, chronic wounds are characterized by a persistent inflammatory response that disrupts the normal progression of the reparative process. A number of factors may contribute to this persistent inflammatory response, including high levels of bacteria, repetitive trauma, and the increased number and activity of tissue-matrix enzymes. As a result, dressings that target these specific problems are being developed and marketed for chronic wound care.
The Evolution of a Framework Building on the aforementioned work of Winter2, who first demonstrated the benefits of moist wound healing, as well as the work of others who have demonstrated the detrimental effects of high microorganism number7 and necrosis8 on wound healing, a framework has evolved to guide wound-management practices. This framework, wound-bed preparation9, can be used to assist with the selection of wound dressings. This concept emerged out of the need for clinicians to articulate a paradigm for wound management, and it provides a useful model for comprehensive wound care for both the acute and chronic wound.
The three primary principles of the wound-bed-preparation concept are: 1) management of edema, 2) reduction of necrosis, and 3) control of microorganism level. Management of edema includes the idea that moisture levels in the wound should be balanced to optimize healing (that is, cell migration) and prevent the excessive accumulation of fluid. Reduction of necrosis targets harnessing endogenous systems (enzymes) to remove necrotic tissue in conjunction with dressings and debridement technologies. Finally, bioburden management is aimed at reducing wound-bed microorganism levels through facilitating the body’s normal immune response and using cleansing/debridement technologies and appropriate topical or systemic antimicrobials.
Taken together, these two bodies of information can guide the wound-care practitioner through dressing selection. Gone are the days of plain gauze dressings for every wound with the only question being "to add saline or not to add saline." We have all become familiar with the basic categories of dressings—alginates, films, foams, gauze, hydrogels, and hydrocolloids—and the various permutations on these themes of mixing different categories to produce composite dressings. Utilization of these dressings singly and in combination can address some of the components of wound-bed preparation. However, two other categories of dressings—one new and the other a twist on an old idea—have evolved to deal with the unique characteristics of the complicated/infected acute wound and the biochemical changes inherent in the chronic wound. These categories include: antimicrobial dressings and wound-matrix dressings.
New Wound-Dressing Technologies:
Antimicrobial Dressings Silver Dressings The efficacy of topically applied antimicrobials for open wounds remains questionable. No definitive study exists to provide broad support for topical therapy. However, a number of reports indicate more rapid healing times in the presence of select antimicrobial dressings.10 Currently, the buzzword in antimicrobial dressings is silver, silver, and more silver. It seems that every conference is discussing, and every dressing company has, a silver-based dressing. The evolution of these dressings appears to be related to the increasing prevalence of antibiotic-resistant organisms. These newer silver products provide an advantage over older preparations in that lower concentrations of silver are required for microbial control and occlusive to semiocclusive technologies, and absorptive materials can be combined with silver to provide a dressing with multiple functions.
Particular dressings may also be selected according to effects on microbial control, inflammatory cytokine suppression, and epithelialization.11,12 High-content silver dressings may provide enhanced microbial control, but they appear to inhibit epithelialization. On the other hand, lower-content silver dressings may not provide the same level of microbial control but do not inhibit epithelialization. Recent research findings also indicate that silver dressings may be efficacious in treating dermatitis, as silver appears to suppress inflammation through the induction of programmed cell death in immune cells.
All silver dressings or preparations release ionic silver that is thought to interfere with microbial respiratory enzymes, protein synthesis, and DNA replication.11 However, newer products use different delivery and binding technologies. One of the newer methods for delivering silver uses what is termed nanocrystalline silver technology. Silver is bound in smaller particles with a high ratio of exposed surface area. This binding technology provides for increased availability for ionization in wound fluid and subsequent exposure to microbes in the wound bed. There is some concern about the possibility of microbes developing silver resistance, since such low levels of silver are utilized by these dressings. These low levels are quite close to the minimum inhibitory concentration for microbes and may allow organisms to survive and mutate.
Cadexomer Iodine Dressings New formulation technology is also allowing iodine to be used more efficiently to control microorganisms in the wound bed while minimizing potential toxicity to the wound-bed cells.11 This technology provides a slow, time release of active iodine to the wound bed as wound fluid is absorbed by the iodine-polymer complex. Sustained release of iodine from this polymer optimizes its antimicrobial effects while preventing the accumulation of active iodine in tissues at levels toxic to wound-bed cells.13
Toxicity studies have not demonstrated any local or systemic adverse effects. Because of its slow release formulation and rapid excretion by the kidneys, cadexomer iodine is not thought to pose a threat to healing tissues or the central nervous system.14 The cadexomer molecule is broken down by amylase enzymes in the wound fluid, thus limiting its absorption into the blood vascular system. In animal studies, cadexomer iodine did not produce sensitization/allergic reactions.
Other positive benefits of this technology include no evidence of microbial resistance, good fluid-handling capabilities, and an immune-stimulating effect. Recent research also indicates that cadexomer iodine may stimulate human macrophages, thus facilitating the wound-healing process.15
Polyhexamethylene Biguanide Another antimicrobial dressing that is available to the wound-care clinician is one that has bidirectional fluid-handling properties (can absorb or hydrate the wound bed) and uses 0.3% polyhexamethylene biguanide (PHMB) as the antimicrobial constituent. PHMB is a broad-spectrum antimicrobial dressing that can provide wide coverage to the wound-bed tissues.16 In addition, the design of this dressing allows for the donation of fluid to the wound bed or its extraction depending on intrinsic fluid levels. The dressing matrix donates fluid to dry areas of the wound, as well as absorbs fluid from overly hydrated areas.
Wound-Matrix Dressings The understanding of the processes involved in wound-matrix synthesis and repair has rapidly progressed in the past decade or so due to the ongoing technological revolution in cell and molecular biology. We are beginning to understand in greater detail the chemical composition of the extracellular matrix of various tissues and how cells that reside in these matrices interact with matrix components. The importance of matrix components in guiding cell migration, proliferation, and function is also being recognized. For example, it is currently known that collagen not only provides tensile strength for tissues but acts as a storage depot for growth factors that orchestrate tissue synthesis and repair.17 Another example is the glycoprotein or sugar protein fibronectin, which is an important attachment site for fibroblasts as they migrate through the extracellular matrix.18 Other important findings in the area of tissue-matrix function include the elucidation of a number of specific enzymes that play a role in normal extracellular tissue-matrix remodeling.5 A number of these enzymes have been shown to become hyperactive in chronic wounds, leading to the destruction of the extracellular tissue matrix and the growth factors that orchestrate wound healing.
As a result of these new discoveries, a new category of wound dressings has evolved to enhance the function of the extracellular tissue matrix and the cells that reside there. Collagen-based dressings in powder, dried matrices, alginate, hydrogel, and hydrocolloid formulations have evolved to provide support for fibroblast migration and function and growth-factor binding. These collagen-based dressings act as a temporary scaffolding for cells and are reabsorbed or removed as the wound heals. Newer technology includes a collagen (55%) and chemically processed cellulose (45%) blend that works to bind growth factors and bind/disable tissue enzymes (metallomatrix proteinases) that destroy the extracellular matrix in chronic wounds.19 This preparation also provides fluid-handling capabilities to control wound exudates. Other products include hydrogels that contain fibronectin that also provide a temporary attachment site for fibroblasts as they migrate into a wound bed.
To deliver quality care and to follow best practices, the clinician will need to remain abreast of research findings that define normal wound-healing processes and the pathological changes in these processes that lead to chronic wounds. An understanding of this information will guide our selection of best products, and more importantly, define the best practice for wound management.
Teresa Conner-Kerr, PhD, PT, CWS, CLT, is the new professor and chair of the Department of Physical Therapy in the School of Health Sciences at Winston-Salem State University, Winston-Salem, NC. She can be reached at connerkerrt@wssu.edu
References 1. Bull JP, Squire J, Topley E. Experiments with occlusive dressings of a new plastic. Lancet. 1948;213–215.
2. Winter GD. Formation of the scab and the rate of epithelialization of superficial wounds in the skin of the young domestic pig. J Wound Care. 1995;4:366–367.
3. Hinman CD, Maibach H. Effect of air exposure and occlusion on experimental human skin wounds. Nature. 1963;200: 377–378.
4. Hess CT. Clinical Guide to Wound Care. New York, NY: Lippincott, Williams & Wilkins; 2004.
5. Yager D, Zhang L, Liang H, et al. Wound fluids in human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. J Invest Dermatol. 1996;107: 743–748.
6. Bowler PG, Duerden BI, Armstrong DG. Wound microbiology and associated approaches to wound management. Clin Microbiol Rev. 2001;14:244–269.
7. Daltrey DC, Rhodes B, Chattwood JG. Investigation into the microbial flora of healing and nonhealing decubitus ulcers. J Clin Pathol. 1981;34:701–705.
8. Steed DL, Donohoe D, Wester MW, et al. Effect of extensive debridement and treatment on the healing of diabetic foot ulcers. J Am Coll Surg. 1996;183:61–64.
9. Schultz GS, Sibbald RG, Falanga V, et al. Wound bed preparation: systematic approach to wound management. Wound Repair Regen. 2003;11 Suppl 1:S1–S28.
10. Mertz PM, Oliveira-Gandia MF, Davis SC. The evaluation of cadexomer iodine wound dressing on methicillin resistant Staphylococcus aureus (MRSA) in acute wounds. Dermatol Surg. 1999;25: 89–93.
12. Bhol KC, Schechter PJ. Topical nanocrystalline silver cream suppresses inflammatory cytokines and induces apoptosis of inflammatory cells in a murine model of allergic contact dermatitis. Br J Dermatol. 2005;152:1235–1242.
13. Zhou LH, Nahm WK, Badiavas E, et al. Slow release iodine preparation and wound healing: in vitro effects consistent with lack of in vivo toxicity in human chronic wounds. Br J Dermatol. 2002;146: 365–374.
14. Iodosorb Ointment (PL 14038/0008) Data Sheet. London: Smith & Nephew. Available at: http: //wound.smith-nephew.com/uk/Standard.asp?NodeId=2746. Accessed March 1, 2006.
15. Moore K, Thomas A, Harding KG. Iodine released from the wound dressing Iodosorb modulates the secretion of cytokines by human macrophages responding to bacterial lipopolysaccharide. Int J Biochem Cell Biol. 1997;29:163–171.
16. Cazzaniga A, Serralta V, Davis S, et al. The effect of an antimicrobial gauze dressing impregnated with .2-percent polyhexamethylene biguanide as a barrier to prevent pseudomonas aeruginosa wound invasion. Wounds. 2002;14:169–176.
17. Nishi N, Matsushita O, Yuube K, et al. Collagen-binding growth factors: production and characterization of functional fusion proteins having a collagen-binding domain. Proc Natl Acad Sci USA. 1998;95:7018–7023.
18. Repesh LA, Fitzgerald TJ, Furcht LT. Fibronectin involvement in granulation tissue and wound healing in rabbits. J Histochem Cytochem. 1982;30:351–358.
19. Veves A, Sheehan P, Pham HT. A randomized, controlled trial of Promogran (a collagen/oxidized regenerated cellulose dressing) vs standard treatment in the management of diabetic foot ulcers. Arch Surg. 2002;137:822–827.
The Evolution of a Framework
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