Effect of High Voltage Stimulation on Pressure Ulcers
Objective. To investigate the effect of high voltage monophasic stimulation (HVMS) on pressure ulcer healing.
Methods. Fifty-eight patients with pressure ulcers were included and ultimately allocated into two comparative groups. Patients in group A and B were treated pharmacologically (a local bath of potassium permanganate, compresses of fibrolan, colistin, iruxol, and wet dressings containing 10% sodium chloride). Patients in group A were additionally treated with HVMS (100 μs, 100 Hz, 100 V) once daily, five times a week for 6 weeks.
Results. The relative changes in total surface area were (85.38% in group A versus 40.08% in group B); length (71.22% in group A versus 30.38% in group B); width (76.09% in group A versus 32.48% in group B); and volume (20.69% in group A versus 9.39% in group B). The Gilman Index (0.64 cm in group A versus 0.28 cm in group B) indicated a difference in favor of group A (P ≤ 0.001). More efficient decrease of pus and greater granulation growth were observed in group A.
Conclusion. HVMS appears to be a promising and useful treatment modality for pressure ulcers.
Pressure ulcers are typically associated with individuals of compromised mobility, the elderly, and people with spinal cord injuries. A pressure ulcer is any lesion caused by unrelieved pressure resulting in damage of underlying tissue involving the skin, fat, fascia, muscle, and bone.
Pressure ulcers develop following a prolonged period of compression of the tissue between a bony prominence and a surface, which causes the occlusion of capillaries and leads to ischemia. According to Grey et al, an external pressure of 50 mmHg may rise to 200 mmHg at a bony prominence. The described mechanical forces are much higher than the physiological (32 mmHg) capillary pressure. Continuous compression (more than 2–3 hours) can reduce blood flow, which causes ischemia. The ischemic state causes tissue necrosis, which ultimately leads to pressure ulcer formation.
Significant etiological factors in pressure ulcers include paralysis and sensory loss, soft tissue atrophy, and skin maceration attributable to incontinence. Other contributing factors include advanced age, poor diet, smoking, anemia, vitamin deficiency, and hypoproteinemia. Depending on the depth of tissue injury, pressure ulcers can lead to serious complications, such as osteomyelitis, septicemia and even death.
Pressure ulcers present a massive financial burden not only for the healthcare system, but also for patients. Hirshberg et al reported an average hospital charge of $48,934 per patient for the management of ulcers, which did not include the cost of treatment before hospitalization or the cost of pharmaceuticals. Bennett et al noticed that the cost of treating a pressure ulcer varies in the United Kingdom from £1.064 (Stage I) to £10.551 (Stage IV). Cost increases coincide with ulcer stage because the time to heal is longer and due to the fact that the incidence of complications is higher in more severe cases. The total cost in the United Kingdom is £1.4 to £2.1 billion annually (4% of total National Health Service [NHS] expenditure). Thus, a need exists for an effective therapy that decreases the healing time and severity of ulcers, is easy to use, and is cost efficient.
The application of various forms of electrical current to augment wound healing has been reported. As early as 1668, electrically charged gold leaf was applied to smallpox lesions to prevent scar formation. Charged gold leaf has also been used for its hemostatic effect in vascular surgery and to heal diabetic and ischemic skin ulcers.
Although the mechanism responsible for the apparent facilitation of the wound healing process is not readily apparent, Becker has suggested the existence within the body of a direct current electrical system that is responsible for controlling tissue healing. Becker theorized that when the body is injured, the inherent electrical balance of the body is disturbed, resulting in a shift in current flow within this system. Becker referred to this shift in current flow as the "current of injury," which he believes is generated by the injured tissue and is responsible for initiating the healing process. Becker suggested that the ability of anodal electrical current to facilitate healing is based on the current amplifying the magnitude of the body's current of injury, which acts as a signal to initiate and maintain the healing process. A recent review article reports that electrical fields may stimulate and direct epithelial cell proliferation and cell migration at the wound edge, and thus promote wound healing.
Another possible benefit of electrical stimulation of an open wound is apparent bactericidal effect that has been reported.
The present study investigates the effect of high voltage monophasic stimulation (HVMS) on pressure ulcer healing. Study endpoints were the Gilman Index and other measured parameters as predictors of healing.
Abstract and Introduction
Abstract
Objective. To investigate the effect of high voltage monophasic stimulation (HVMS) on pressure ulcer healing.
Methods. Fifty-eight patients with pressure ulcers were included and ultimately allocated into two comparative groups. Patients in group A and B were treated pharmacologically (a local bath of potassium permanganate, compresses of fibrolan, colistin, iruxol, and wet dressings containing 10% sodium chloride). Patients in group A were additionally treated with HVMS (100 μs, 100 Hz, 100 V) once daily, five times a week for 6 weeks.
Results. The relative changes in total surface area were (85.38% in group A versus 40.08% in group B); length (71.22% in group A versus 30.38% in group B); width (76.09% in group A versus 32.48% in group B); and volume (20.69% in group A versus 9.39% in group B). The Gilman Index (0.64 cm in group A versus 0.28 cm in group B) indicated a difference in favor of group A (P ≤ 0.001). More efficient decrease of pus and greater granulation growth were observed in group A.
Conclusion. HVMS appears to be a promising and useful treatment modality for pressure ulcers.
Introduction
Pressure ulcers are typically associated with individuals of compromised mobility, the elderly, and people with spinal cord injuries. A pressure ulcer is any lesion caused by unrelieved pressure resulting in damage of underlying tissue involving the skin, fat, fascia, muscle, and bone.
Pressure ulcers develop following a prolonged period of compression of the tissue between a bony prominence and a surface, which causes the occlusion of capillaries and leads to ischemia. According to Grey et al, an external pressure of 50 mmHg may rise to 200 mmHg at a bony prominence. The described mechanical forces are much higher than the physiological (32 mmHg) capillary pressure. Continuous compression (more than 2–3 hours) can reduce blood flow, which causes ischemia. The ischemic state causes tissue necrosis, which ultimately leads to pressure ulcer formation.
Significant etiological factors in pressure ulcers include paralysis and sensory loss, soft tissue atrophy, and skin maceration attributable to incontinence. Other contributing factors include advanced age, poor diet, smoking, anemia, vitamin deficiency, and hypoproteinemia. Depending on the depth of tissue injury, pressure ulcers can lead to serious complications, such as osteomyelitis, septicemia and even death.
Pressure ulcers present a massive financial burden not only for the healthcare system, but also for patients. Hirshberg et al reported an average hospital charge of $48,934 per patient for the management of ulcers, which did not include the cost of treatment before hospitalization or the cost of pharmaceuticals. Bennett et al noticed that the cost of treating a pressure ulcer varies in the United Kingdom from £1.064 (Stage I) to £10.551 (Stage IV). Cost increases coincide with ulcer stage because the time to heal is longer and due to the fact that the incidence of complications is higher in more severe cases. The total cost in the United Kingdom is £1.4 to £2.1 billion annually (4% of total National Health Service [NHS] expenditure). Thus, a need exists for an effective therapy that decreases the healing time and severity of ulcers, is easy to use, and is cost efficient.
The application of various forms of electrical current to augment wound healing has been reported. As early as 1668, electrically charged gold leaf was applied to smallpox lesions to prevent scar formation. Charged gold leaf has also been used for its hemostatic effect in vascular surgery and to heal diabetic and ischemic skin ulcers.
Although the mechanism responsible for the apparent facilitation of the wound healing process is not readily apparent, Becker has suggested the existence within the body of a direct current electrical system that is responsible for controlling tissue healing. Becker theorized that when the body is injured, the inherent electrical balance of the body is disturbed, resulting in a shift in current flow within this system. Becker referred to this shift in current flow as the "current of injury," which he believes is generated by the injured tissue and is responsible for initiating the healing process. Becker suggested that the ability of anodal electrical current to facilitate healing is based on the current amplifying the magnitude of the body's current of injury, which acts as a signal to initiate and maintain the healing process. A recent review article reports that electrical fields may stimulate and direct epithelial cell proliferation and cell migration at the wound edge, and thus promote wound healing.
Another possible benefit of electrical stimulation of an open wound is apparent bactericidal effect that has been reported.
The present study investigates the effect of high voltage monophasic stimulation (HVMS) on pressure ulcer healing. Study endpoints were the Gilman Index and other measured parameters as predictors of healing.
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