Closing Difficult Wounds
Non-healing skin ulcerations of the lower extremities affect millions of people in the United States and impose tremendous medical, psychosocial and financial impact. These wounds may be secondary to a myriad of etiologies including pressure, metabolic, trauma, venous, arterial etiologies and diabetic neuropathy.1 The Wound Healing Society defines chronic ulcerations as wounds that have “failed to proceed through an orderly and timely process to produce anatomic and functional integrity, or proceeded through the repair process without establishing a sustained anatomic and functional result.”2 This prolonged and sometimes interrupted healing process affects the patient’s quality of life due to impaired mobility and substantial loss of productivity, and is a significant management challenge to healthcare professionals.3 The relapsing course may also be reflected in the astounding economic burden that chronic ulcerations have placed upon healthcare. The attributable cost for the treatment of chronic ulcerations has been conservatively estimated at $3.6 billion dollars per year.4 Medicare expenditures for lower-extremity ulcer patients were, on average, three times higher than expenditures for Medicare patients in general.5 In addition, a lack of immediate attention to these wounds can often serve as a prelude to serious health problems due to associated infections that may lead to amputations or induce life-threatening situations.1,6 Wound repair is an orchestra of highly integrated cellular and biochemical responses to injury.7 Certain pathophysiologic and metabolic conditions can alter this normal course of events, leading to delayed or impaired healing that may result in chronic, non-healing wounds.7,8 Integrating technological advances with our understanding of the complex cellular and biochemical mechanisms of wound healing has led to the development of various advanced wound healing modalities such as hyperbaric oxygen, topical growth factors, bioengineered skin and tissue equivalents, and negative pressure wound therapy (NPWT).7,9-13 What Studies Have Suggested About Using NPWT Negative pressure wound therapy (see “What You Should Know About NPWT” below) can often be both a catalyst to secondary wound healing and a bridge between debridement and definitive closure.24 The optimal subatmospheric pressure for wound healing, as shown in animal models, appears to be approximately 125 mmHg, utilizing an alternating pressure cycle of five minutes of suction followed by two minutes of no suction.29 Although the exact mechanism of the action of NPWT on wound healing is not clear, studies suggest that applying subatmospheric pressure may optimize blood flow, decrease local tissue edema, remove excessive fluid and pro-inflammatory exudates, facilitate the removal of bacteria from the wound, and promote a moist wound healing environment.24,29,30 In addition, researchers have noted the application of subatmospheric pressure helps increase the rate of cell division, angiogenesis, local elaboration of growth factors and subsequent formation of granulation tissue.22,24,29-31 In a simulated NPWT application on a computer wound model, Saxena, et. al., studied the effects of negative pressure-induced material deformations.32 They compared the morphology of deformation of the computerized wound model with histologic sections of wounds treated with NPWT. They demonstrated that most elements stretched by subatmospheric pressure experience deformations of 5 to 20 percent strain, which are similar to in vitro strain levels shown to promote cellular proliferation.32 Furthermore, they noted that the deformation illustrated by the computer wound model was similar in morphology to the surface undulations observed in histologic cross-sections of the wounds.32 Chen, et. al., examined the effects of NPWT on the microcirculation of full thickness wounds in rabbit ears and postulated that NPWT stimulates angiogenesis by promoting capillary blood flow velocity, increasing capillary caliber and blood volume, and stimulating endothelial proliferation.