Pressure ulcers are a significant health care problem in all patient care settings. They are a lifelong, serious complication of spinal cord injury (SCI) that has the potential to interfere with physical, psychological and social well-being, and overall quality of life. According to the Institute of Medicine, SCI research should prioritize the elimination of SCI-related complications, such as pressure ulcers.1
Pressure ulcers are wounds caused by unrelieved pressure from forces perpendicular (compression) or tangential (shear) to the tissue surface.1
This constant force can interfere with the pressure in capillaries and therefore, affect the exchange and elimination of nutrients and metabolites. Prolonged circulatory interference ultimately leads to cell death and in severe cases individuals can develop septic shock and ultimately organ failure.1
Pressure ulcers rank as the second highest cause of re-hospitalization after traumatic SCI.2
It is estimated that approximately 25–40% of patients with SCI will develop a pressure ulcer in their lifetime and that at 2-year follow-up the prevalence of pressure ulcers is 8.9%.1,3
Patients with SCI may have many factors that are associated with pressure ulcer formation, including paralysis, loss of sensation to pain and pressure, poor nutrition, anemia, and skin maceration related to incontinence. Healing time for pressure ulcers can vary greatly.
As Gardner et al.4
point out, there are several moderating variables that impact healing, including tissue perfusion, bacterial burden, and nutritional status, but few studies have provided data regarding these variables. Poor nutritional status has been correlated with the healing of pressure ulcers.5,6
Biochemical parameters useful in assessing nutritional status include prealbumin, total protein, albumin, hemoglobin, and hematocrit. According to the Consortium for Spinal Medicine, specific nutritional factors associated with wound healing include micronutrients such as zinc, vitamin C, vitamin A, and vitamin E.7
Treatment of these ulcers involves relieving pressure, improving nutrition and skin hygiene, treating infections, removing necrotic tissues, and applying the appropriate dressings. However, some cases are not responsive to the above treatment.
Electrical stimulation (ES) is thought to enhance soft tissue healing, but this is based chiefly on evidence from animal studies and very few rigorously controlled studies conducted in humans.
While the mechanisms that explain how ES promotes wound healing are poorly understood, some believe that ES imitates the natural electrical current that occurs in skin when it is injured.4
It has been shown that ES induces cellular actions in almost every phase of the wound healing cascade, including the stimulation of several fibroblast activities, such as enhanced collagen and deoxyribonucleic acid synthesis, adenosine triphosphate production and calcium influx, and an increased number of growth factor receptor sites.8 In vitro
studies on macrophages, epithelial cells, and fibroblasts have demonstrated that ES promotes the migration and activation of key cells within the wound site. Additionally, in vivo
studies involving animal models have shown that ES results in more collagen deposition, enhanced angiogenesis, greater wound tensile strength, and a faster wound contraction rate.8
ES has also been shown to improve tissue perfusion and reduce edema formation, indirectly stimulating healing by improving oxygen delivery to the tissue.9
There have been relatively few controlled studies conducted regarding the use of ES specifically for the healing of recalcitrant pressure ulcers. In Regan et al.
review of therapeutic interventions for pressure ulcers, the ES studies focus on comparing the rate of healing with ES to either sham/placebo groups or to standard wound care groups. There is no discussion on the use of ES for recalcitrant wounds that have failed to respond to standard wound care and have persisted for longer than 11 months. Houghton et al.8
provide a recent single-blind randomly assigned study that compares healing rates for standard wound care versus ES plus standard wound care for pressure ulcers, but their study includes Stage II and non-recalcitrant wounds. In addition, their standard wound care group had a disproportionate amount of Stage II versus Stage III and IV wounds when compared to the Standard Wound Care (SWC) + Electrical Stimulation Treatment (EST) group. When you consider that all Stage II wounds were fully healed within 3 months for both groups, the comparison between both groups becomes skewed.