Clinical approach to wounds: débridement and wound bed preparation including the use of dressings and wound-healing adjuvants.

This is a clinical review of current techniques in wound bed preparation found to be effective in assisting the wound-healing process. The process begins with the identification of a correct diagnosis of the wound's etiology and continues with optimizing the patient's medical condition, including blood flow to the wound site. Débridement as the basis of most wound-healing strategies is then emphasized. Various débridement techniques, including surgery, topical agents, and biosurgery, are thoroughly discussed and illustrated. Wound dressings, including the use of negative pressure wound therapy, are then reviewed. To properly determine the timing of advance therapeutic intervention, the wound-healing progress needs to be monitored carefully with weekly measurements. A reduction in wound area of 10 to 15 percent per week represents normal healing and does not mandate a change in the current wound-healing strategy. However, if this level of wound area reduction is not met consistently on a weekly basis, then alternative healing interventions should be considered. There is a growing body of evidence that can provide guidance on the appropriate use of such adjuvants in the problem wound. Several adjuvants are discussed, including growth factor, bioengineered tissues, and hyperbaric medicine.

Ineffective treatment of keloids with interferon alpha-2b.

BACKGROUND: Keloids are exuberant, disfiguring scars that result from an abnormal healing process. Current established treatment strategies include surgical resection, triamcinolone steroid injection, pressure therapy, silicone therapy, and radiotherapy. None of these therapies, either alone or in combination, offers consistent recurrence-free rates above 70 to 80 percent. The antiproliferative, antifibrotic cytokine, interferon alpha-2b, may be useful in keloid management because of its ability to interfere with collagen synthesis and fibroblast proliferation. METHODS: To determine the efficacy of interferon alpha-2b in keloid management, the authors prospectively evaluated the effects of interferon alpha-2b as postexcisional adjuvant therapy for keloids. Thirty-nine keloids in 34 patients were photographed, measured, and surgically excised. The wound bed was injected twice with either interferon alpha-2b (treatment group; n = 13 keloids) or triamcinolone (control group; n = 26 keloids) at surgery and 1 week later. The patients were followed up in the plastic surgery clinic. RESULTS: The trial protocol was terminated at midtrial surveillance. Among the 13 keloids that were treated with postoperative intralesional interferon alpha-2b, seven recurred (54 percent recurrence rate). In contrast, in the 26 keloids that received triamcinolone (control group), only four recurred (15 percent recurrence rate). Recurrence in either group did not correlate with location of the keloid or race. CONCLUSION: Interferon does not appear to be effective in the clinical management of keloids.

Keloid pathogenesis and treatment.

BACKGROUND: Keloid management can be difficult and frustrating, and the mechanisms underlying keloid formation are only partially understood. METHODS: Using original and current literature in this field, this comprehensive review presents the major concepts of keloid pathogenesis and the treatment options stemming from them. RESULTS: Mechanisms for keloid formation include alterations in growth factors, collagen turnover, tension alignment, and genetic and immunologic contributions. Treatment strategies for keloids include established (e.g., surgery, steroid, radiation) and experimental (e.g., interferon, 5-fluorouracil, retinoid) regimens. CONCLUSION: The scientific basis and empiric evidence supporting the use of various agents is presented. Combination therapy, using surgical excision followed by intradermal steroid or other adjuvant therapy, currently appears to be the most efficacious and safe current regimen for keloid management.