Successful wound care involves optimizing patient local and systemic conditions in conjunction with an ideal wound healing environment. Many different products have been developed to influence this wound environment to provide a pathogen-free, protected, and moist area for healing to occur. Newer products are currently being used to replace or augment various substrates in the wound healing cascade. This review of the current state of the art in wound-healing products looks at the latest applications of silver in microbial prophylaxis and treatment, including issues involving resistance and side effects, the latest uses of negative pressure wound devices, advanced dressings and skin substitutes, biologic wound products including growth factor applications, and hyperbaric oxygen as an adjunct in wound healing. With the abundance of available products, the goal is to find the most appropriate modality or combination of modalities to optimize healing. 1. Introduction The field of wound care seemingly contains as many different treatment options and modalities as the number of practitioners caring for wounds. While many clinicians rely on and obtain good results with older “tried and true” treatments, there continues to be a constant flow of new products and technologies to add to the wound care armamentarium. Some of these products are updated and improved variations of previous treatments, while others are the result of entirely new fields of study. As with any new product, oftentimes the race to introduction into clinical use precedes adequate controlled study, and the efficacy is then defined by clinical experience. This can lead to unanswered questions regarding appropriate use and indications. This paper will discuss several new technologies in burn and wound care. Silver dressings are time honored in wound care, but new forms of delivery aim to increase the efficacy while minimizing side effects. We will also review some of the latest literature on emerging bacterial resistance to these products. Negative pressure wound devices are relatively new in wound care treatment, and their indications are continually expanding to encompass aspects of wound management that previously had very few options. Advanced wound dressing products can help alter the wound environment to optimize healing conditions. With the advent of biosynthetics and tissue engineering, skin substitutes are being created that not only provide novel effective temporary coverage of wounds, but are also changing the paradigm of wound management. By supporting the wound with growth factors
M. Trop, M. Novak, S. Rodl, B. Hellbom, W. Kroell, and W. Goessler, “Silver-coated dressing acticoat caused raised liver enzymes and argyria-like symptoms in burn patient,” Journal of Trauma, vol. 60, no. 3, pp. 648–652, 2006.
W. Stanford, B. W. Rappole, and C. L. Fox, “Clinical experience with silver sulfadiazine, a new topical agent for control of pseudomonas infections in burns,” Journal of Trauma, vol. 9, no. 5, pp. 377–388, 1969.
H. Q. Yin, R. Langford, and R. E. Burrell, “Comparative evaluation of the antimicrobial activity of Acticoat Antimicrobial Barrier Dressing,” Journal of Burn Care and Rehabilitation, vol. 20, no. 3, pp. 195–200, 1999.
J. B. Wright, K. Lam, and R. E. Burrell, “Wound management in an era of increasing bacterial antibiotic resistance: a role for topical silver treatment,” American Journal of Infection Control, vol. 26, no. 6, pp. 572–577, 1998.
Y. Huang, X. Li, Z. Liao et al., “A randomized comparative trial between Acticoat and SD-Ag in the treatment of residual burn wounds, including safety analysis,” Burns, vol. 33, no. 2, pp. 161–166, 2007.
J. Fong, F. Wood, and B. Fowler, “A silver coated dressing reduces the incidence of early burn wound cellulitis and associated costs of inpatient treatment: comparative patient care audits,” Burns, vol. 31, no. 5, pp. 562–567, 2005.
E. E. Tredget, H. A. Shankowsky, A. Groeneveld, and R. Burrell, “A matched-pair, randomized study evaluating the efficacy and safety of acticoat silver-coated dressing for the treatment of burn wounds,” Journal of Burn Care and Rehabilitation, vol. 19, no. 6, pp. 531–537, 1998.
P. K. Lam, E. S. Y. Chan, W. S. Ho, and C. T. Liew, “In vitro cytotoxicity testing of a nanocrystalline silver dressing (Acticoat) on cultured keratinocytes,” British Journal of Biomedical Science, vol. 61, no. 3, pp. 125–127, 2004.
M. E. Innes, N. Umraw, J. S. Fish, M. Gomez, and R. C. Cartotto, “The use of silver coated dressings on donor site wounds: a prospective, controlled matched pair study,” Burns, vol. 27, no. 6, pp. 621–627, 2001.
L. C. Argenta, M. J. Morykwas, M. W. Marks, A. J. DeFranzo, J. A. Molnar, and L. R. David, “Vacuum-assisted closure: state of clinic art,” Plastic and Reconstructive Surgery, vol. 117, no. 7, pp. 127S–142S, 2006.
M. L. Venturi, C. E. Attinger, A. N. Mesbahi, C. L. Hess, and K. S. Graw, “Mechanisms and clinical applications of the vacuum-assisted closure (VAC) device: a review,” American Journal of Clinical Dermatology, vol. 6, no. 3, pp. 185–194, 2005.
H. M. Quah, A. Maw, T. Young, and D. J. Hay, “Vacuum-assisted closure in the management of the open abdomen: a report of a case and initial experiences,” Journal of Tissue Viability, vol. 14, no. 2, pp. 59–62, 2004.
D. Herscovici, R. W. Sanders, J. M. Scaduto, A. Infante, and T. DiPasquale, “Vacuum-assisted wound closure (VAC therapy) for the management of patients with high-energy soft tissue injuries,” Journal of Orthopaedic Trauma, vol. 17, no. 10, pp. 683–688, 2003.
J. R. Heugel, K. S. Parks, S. S. Christie, J. F. Pulito, D. H. Zegzula, and N. A. Kemalyan, “Treatment of the exposed Achilles tendon using negative pressure wound therapy: a case report,” Journal of Burn Care and Rehabilitation, vol. 23, no. 3, pp. 167–171, 2002.
J. Noordenbos, C. Doré, and J. F. Hansbrough, “Safety and efficacy of TransCyte for the treatment of partial-thickness burns,” Journal of Burn Care and Rehabilitation, vol. 20, no. 4, pp. 275–281, 1999.
R. H. Demling and L. DeSanti, “Closure of partial-thickness facial burns with a bioactive skin substitute in the major burn population decreases the cost of care and improves outcome,” Wounds, vol. 14, no. 6, pp. 230–234, 2002.
J. F. Hansbrough, D. W. Mozingo, G. P. Kealey, M. Davis, A. Gidner, and G. D. Gentzkow, “Clinical trials of a biosynthetic temporary skin replacement, dermagraft-transitional covering, compared with cryopreserved human cadaver skin for temporary coverage of excised burn wounds,” Journal of Burn Care and Rehabilitation, vol. 18, no. 1 I, pp. 43–51, 1997.
V. Falanga, D. Margolis, O. Alvarez et al., “Rapid healing of venous ulcers and lack of clinical rejection with an allogeneic cultured human skin equivalent,” Archives of Dermatology, vol. 134, no. 3, pp. 293–300, 1998.
F. Cianfarani, R. Tommasi, C. M. Failla et al., “Granulocyte/macrophage colony-stimulating factor treatment of human chronic ulcers promotes angiogenesis associated with de novo vascular endothelial growth factor transcription in the ulcer bed,” British Journal of Dermatology, vol. 154, no. 1, pp. 34–41, 2006.
R. Marques da Costa, F. M. Ribeiro Jesus, C. Aniceto, and M. Mendes, “Randomized, double-blind, placebo-controlled, dose-ranging study of granulocyte-macrophage colony stimulating factor in patients with chronic venous leg ulcers,” Wound Repair and Regeneration, vol. 7, no. 1, pp. 17–25, 1999.
M. Cruciani, B. A. Lipsky, C. Mengoli, and F. De Lalla, “Are granulocyte colony-stimulating factors beneficial in treating diabetic foot infections? A meta-analysis,” Diabetes Care, vol. 28, no. 2, pp. 454–460, 2005.
S. A. L. Bennett and H. C. Birnboim, “Receptor-mediated and protein kinase-dependent growth enhancement of primary human fibroblasts by platelet activating factor,” Molecular Carcinogenesis, vol. 20, no. 4, pp. 366–375, 1997.
D. L. Steed, M. W. Webster, J. J. Ricotta et al., “Clinical evaluation of recombinant human platelet-derived growth factor for the treatment of lower extremity diabetic ulcers,” Journal of Vascular Surgery, vol. 21, no. 1, pp. 71–81, 1995.
D. J. Margolis, C. Bartus, O. Hoffstad, S. Malay, and J. A. Berlin, “Effectiveness of recombinant human platelet-derived growth factor for the treatment of diabetic neuropathic foot ulcers,” Wound Repair and Regeneration, vol. 13, no. 6, pp. 531–536, 2005.
D. P. Shackelford, E. Fackler, M. K. Hoffman, and S. Atkinson, “Use of topical recombinant human platelet-derived growth factor BB in abdominal wound separation,” American Journal of Obstetrics and Gynecology, vol. 186, no. 4, pp. 701–704, 2002.
O. C. Velazquez, “Angiogenesis and vasculogenesis: inducing the growth of new blood vessels and wound healing by stimulation of bone marrow-derived progenitor cell mobilization and homing,” Journal of Vascular Surgery, vol. 45, no. 6, pp. 39–47, 2007.
O. M. Tepper, R. D. Galiano, J. M. Capla et al., “Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures,” Circulation, vol. 106, no. 22, pp. 2781–2786, 2002.
C. J. M. Loomans, E. J. P. De Koning, F. J. T. Staal et al., “Endothelial progenitor cell dysfunction: a novel concept in the pathogenesis of vascular complications of type 1 diabetes,” Diabetes, vol. 53, no. 1, pp. 195–199, 2004.
M. Ii, H. Takenaka, J. Asai et al., “Endothelial progenitor thrombospondin-1 mediates diabetes-induced delay in reendothelialization following arterial injury,” Circulation Research, vol. 98, no. 5, pp. 697–704, 2006.
S. R. Thom, V. M. Bhopale, O. C. Velazquez, L. J. Goldstein, L. H. Thom, and D. G. Buerk, “Stem cell mobilization by hyperbaric oxygen,” American Journal of Physiology, vol. 290, no. 4, pp. H1378–H1386, 2006.
L. J. Goldstein, K. A. Gallagher, S. M. Bauer et al., “Endothelial progenitor cell release into circulation is triggered by hyperoxia-induced increases in bone marrow nitric oxide,” Stem Cells, vol. 24, no. 10, pp. 2309–2318, 2006.
K. A. Gallagher, L. J. Goldstein, S. R. Thom, and O. C. Velazquez, “Hyperbaric oxygen and bone marrow-derived endothelial progenitor cells in diabetic wound healing,” Vascular, vol. 14, no. 6, pp. 328–337, 2006.
S. R. Jones, K. M. Carpin, S. M. Woodward et al., “Hyperbaric oxygen inhibits ischemia-reperfusion-induced neutrophil CD18 polarization by a nitric oxide mechanism,” Plastic and Reconstructive Surgery, vol. 126, no. 2, pp. 403–411, 2010.
K. T. Khiabani, S. A. Bellister, S. S. Skaggs, L. L. Stephenson, C. Nataraj, and W. A. Zamboni, “Reperfusion-induced neutrophil CD18 polarization: effect of hyperbaric oxygen,” Journal of Surgical Research, vol. 150, no. 1, pp. 11–16, 2008.
A. Gabriel, M. L. Porrino, L. L. Stephenson, and W. A. Zamboni, “Effect of L-arginine on leukocyte adhesion in ischemia-reperfusion injury,” Plastic and Reconstructive Surgery, vol. 113, no. 6, pp. 1698–1702, 2004.
W. A. Zamboni, H. P. Wong, L. L. Stephenson, and M. A. Pfeifer, “Evaluation of hyperbaric oxygen for diabetic wounds: a prospective study,” Undersea and Hyperbaric Medicine, vol. 24, no. 3, pp. 175–179, 1997.
M. L？ndahl, P. Katzman, A. Nilsson, and C. Hammarlund, “Hyperbaric oxygen therapy facilitates healing of chronic foot ulcers in patients with diabetes,” Diabetes Care, vol. 33, no. 5, pp. 998–1003, 2010.
A. Abidia, G. Laden, G. Kuhan et al., “The role of hyperbaric oxygen therapy in ischaemic diabetic lower extremity ulcers: a double-blind randomized-controlled trial,” European Journal of Vascular and Endovascular Surgery, vol. 25, no. 6, pp. 513–518, 2003.