Pressure ulcers often occur at sites subjected to pressure and wetness. Although skin wetness is a risk factor for pressure ulcers, the mechanisms and effects of wetness versus urine constituents on skin breakdown is unclear. The hypothesis that wetness reduces skin hardness and, thereby, increases vulnerability of underlying blood vessels to pressure-induced flow reductions was tested in this study.
Pads saturated with water and with a water solution mixed with the main chemical constituents of urine (synthetic urine; s-urine) were applied to forearm skin of 10 healthy subjects for 5.5 hours. Skin hardness, blood flow change caused by 60 mm Hg of pressure, erythema, and temperature were compared among dry, water, and s-urine test sites.
10 healthy women.
Research Center, Nova Southeastern University, Health Professions Division, Fort Lauderdale, FL.
S-urine and water caused significant reductions in initial hardness and caused greater initial perfusion decreases during pressure load when compared with dry sites. Skin temperature and erythema were lower at wet sites when compared with dry sites.
The findings of this study are consistent with the concept that sustained skin wetness increases vulnerability to pressure-induced blood flow reduction. The effect appears to be mainly dependent on wetness, but urine constituents may exacerbate the effect. In addition, wetness-related skin cooling may play a role. In the healthy subjects studied, the blood flow decrease was not sustained due to perfusion recovery under pressure. Skin wetness would likely have more sustained effects in patients with compromised recovery mechanisms. Measures to diminish skin exposure to wetness in these patients, whatever the wetness source, are an important consideration in a multifaceted strategy to reduce the risk of pressure ulcers.
Harvey N. Mayrovitz, PhD, is a Professor of Physiology at Nova Southeastern University, College of Medical Sciences, Fort Lauderdale, FL. Nancy Sims, RN, LMT, MLDT, is a coordinator of Lymphedema Therapy, North Broward Hospital District Wound Healing Lymphedema Center, Fort Lauderdale, FL.
Support for this study was provided by a Nova Southeastern University, Health Professions Division Research Grant.
Submitted March 6, 2000; accepted in revised form May 26, 2000.