Are Tissue Replacements Cost Effective?
- Volume 16 - Issue 7 - July 2003
- 25467 reads
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Yes, these authors say tissue replacements can facilitate shorter healing times and reduce the risk of complications from chronic wounds.
By Jason R. Hanft, DPM, Andre Williams, DPM, Constantine Kyramarios, DPM, and Kerry Temar, DPM, MS
The goals in treating diabetic foot ulcers are to obtain wound closure as quickly as possible, lower the probability of amputation and decrease recurrent ulcerations. Timely healing is important because the longer a diabetic foot ulcer remains unhealed, the greater the risk for infection, hospitalization and progression of the ulcer to require limb amputation.
Diabetic wounds can become chronic and non-healing for multiple reasons. Infection, biomechanical abnormalities, systemic illnesses, poor nutrition and vascular insufficiency have all been documented as causes for non-healing ulcers.1 The wound bed of chronic wounds also has characteristics which impede wound healing, contributing to the vicious cycle of the continued non-healing state. Elevated proteases, senescent fibroblasts, accumulation of exudate, necrotic tissue, chronic inflammation, bacterial contamination and the absence of growth factors have all been demonstrated to occur in the wound bed of chronic ulcers.2
Tissue replacements offer a viable alternative to other wound care products as they actually change the physiology and chemistry of the wound bed. They are also advantageous over split thickness skin grafts as they do not create an additional wound or increase morbidity.
Once you have determined and addressed the etiology of the wound, tissue replacements are an excellent treatment option that you use either alone or adjunctively with other treatment modalities. There are currently two tissue replacements approved for use on lower extremity wounds. Their composition varies from bovine collagen to human-derived fibroblasts. The efficacy and success rate of each product is slightly different. However, the function is essentially the same. The goal of each product is to initiate the wound healing process by providing certain components of a wound which are required to heal, such as fibroblasts, protease inhibitors and growth factors. Tissue replacements also provide a lattice for migration of epithelial tissue across the wound surface.
Each product mentioned below has different indications. New products are constantly being engineered for the treatment of burns, diabetic wounds, trophic ulcers and venous stasis wounds. It is up to each individual practitioner to stay informed on the latest products available.
A Closer Look At Apligraf
Apligraf® (graftskin, Novartis, Organogensis) is a bilayered living skin substitute. It has both an epidermis and dermis, with living keratinocytes and fibroblasts derived from neonatal foreskin.3 The epidermal layer is formed by human keratinocytes and has a well-differentiated stratum corneum. The dermal layer is composed of human fibroblasts in a bovine type collagen lattice. It does not contain Langerhans’ cell, melanocytes, macrophages, lymphocytes, blood vessels or hair follicles. Therefore, it will not illicit an immune response.4
The Food and Drug Administration approved Apligraf for the treatment of diabetic foot wounds and venous leg ulcers. The exact mechanism of action is unknown, but researchers believe it works to promote healing by providing immediate coverage and by stimulating healing via cytokines, matrix proteins and cell-to-cell interactions.5 Epithelialization occurs from the edge of the wound and from islands within the wound bed.
Apligraf is supplied as a circular disk approximately 7.5 cm in diameter and is intended for single-use. The cost of Apligraf is $1,000 to $1,200 per use.
In a 2000 study by Attilasoy, a higher percentage of wounds were healed with Apligraf (55 percent) compared to the control (40 percent). Chronic venous leg ulcers were healed to complete closure with an average of 1.41 applications of Apligraf.5 Diabetic ulcers treated with Apligraf once a week for a maximum of four weeks reduced the median time to complete wound closure from 91 days in the control group to 38.5 days in the Apligraf group.6