Seat Pressure Changes after Eight Weeks of Functional Electrical Stimulation Cycling: A Pilot Study

Pressure ulcers (PUs) are among the most common secondary conditions associated with spinal cord injury (SCI). According to the Model SCI System Statistical Center, approximately 15% of individuals with SCI will develop a PU within the first year of injury and approximately 27% over the first 25-year period post injury.1 Additionally, 40% to 80% of those who develop a PU will have a recurrence.2 PUs are also among the most troublesome as they potentially interfere with activities of daily living, occupational duties, and rehabilitation programs. In severe cases, PUs may be life threatening. Monetarily, they account for approximately 25% of the cost associated with SCI in the United States, totaling 1.6 billion dollars annually and 70,000 dollars per full-thickness PU.3,4 PUs are also commonly known as pressure sores, pressure wounds, or decubitus ulcers. Typically, PUs result from constant pressure on the skin in areas of the body where there is a boney prominence near the surface, such as ischial tuberosities, sacrum, greater trochanters, and calcaneus and olecranon processes.3 Although there are many factors that play a role in the development of PUs, such as immobility, malnutrition, decreased blood circulation, and poor hygiene, the primary cause is the restriction of blood supply to soft tissue as a result of tissue compression between the external barrier to the skin (ie, bed, wheelchair seat, etc) and the internal bony prominence.5 When compression is sustained, the decrease in blood supply and oxygen to the local tissue results in tissue damage.6,7 Sprigle and Sonenblum assert that even though the underlying causes of PU are quite complex, with multiple factors influencing tissue breakdown, PUs do not occur without forces or pressure being placed on soft tissue. Because the loading is the defining characteristic of PUs, it is reasonable to believe that the magnitude and duration of loading are key factors.8 PUs are divided into 4 stages with increasing degree of severity. In stage 1, the skin is not broken but is red or discolored. The redness or change in color does not fade within 30 minutes after pressure is removed. In stage 2, the epidermis or topmost layer of the skin is broken, creating a shallow open sore. Drainage may or may not be present. For stage 3, the break in the skin extends through the dermis (second skin layer) into the subcutaneous and fat tissue. The wound is deeper than in stage 2. Finally, in stage 4, the breakdown extends into the muscle and can extend as far down as the bone. Usually lots of dead tissue and drainage are present.9 Persons with SCI are particularly at risk due to their reliance on wheelchairs and their loss of sensation, which hinders their ability to feel pressure. The atrophied state of the gluteal muscles also decreases the amount of soft tissue and vascularity, which predisposes individuals with SCI to PUs.7 Because of prolonged sitting due to paralysis, high pressure areas such as the ishium, greater trochanters, and the sacrum are especially at risk. Pressure relief techniques such as wheelchair pushups and directional trunk leaning in combination with mechanical pressure relief via tilt-in-space wheelchairs are designed to help decrease the risk of PUs. Likewise, a variety of seat cushions containing foam, gel, air, or a combination of these have been devised to maintain a healthy seat-buttocks interface. However, PUs remain a frequent problem for many of the 1.4 million wheelchair users in the United States.10 In fact, the incidence of PUs is reported to be as high as 38% in acute care, 23% in long-term care, and 17% in home environments.11 Garber and Rintala conducted a 3-year retrospective study on VA Medical Center out-patient veterans with SCI and found that 39% had been treated for PUs. Their study illustrates the magnitude of the problems of PUs associated with community-dwelling veterans with SCI.12 Electrical stimulation has been used over the past 4 decades in an attempt to assist in the prevention of PUs. Strategies include altering the contour of the buttocks to enhance its surface interface with the seat and increasing the blood flow and soft tissue area of the gluteus maximus.13–16 In 1989, Levine and associates applied bilateral electrical stimulation to the guteal muscles and found simultaneous reduction of pressure under the ischial tuberosities with redistribution of pressure to lower risk areas of the seat.13 This demonstrated that relatively low levels of electrical stimulation could positively alter the seating interface. Later, Levine and colleagues studied the effectiveness of reducing seat pressure through the reconfiguration of the shape of the buttocks during low-level electrical stimulation of the gluteal muscles.17 Again the result was reduced seat pressure. The authors theorized that reduced seat pressure may assist in the prevention of PUs. Ferguson et al applied electrical stimulation to the quadriceps muscles and found that the greater the knee extension movement, the more significant the decreases in pressure at the ischial tuberosity.18 A decade later, Bogie and Triolo used implanted neuromuscular stimulation of the gluteal muscles to assist individuals with standing and transfer activities.14 In addition, they measured seat interface pressures and found that after 8 weeks of electrical stimulation, the ischial regions of the buttocks showed decreased pressure in a seated position. This alteration was matched with increases in tissue oxygen levels in the ischial area. These changes provided evidence that neuromuscular electrical stimulation can benefit tissue health.14 Curtis and colleagues studied the use of intermittent electrical stimulation on the triceps surae of rats for 5 to 10 seconds every 10 minutes and found that it was effective in reducing deep muscle tissue damage caused by 28% and 38% body-weight pressures.16 Van Londen and associates completed a similar study on humans and found that the seat–buttocks interface pressure decreased whether the gluteal muscles were electrically stimulated simultaneously or alternately.19 Functional electrical stimulation (FES) cycling has been proposed as an activity that may decrease the risk of PUs through the promotion of increased blood flow and thickening of the gluteus maximus.20 Petrofsky et al compared the incidence of PUs in persons who performed FES cycling over a 2-year period with a non–FES cycling control group and found that the FES cycling group developed 90% fewer PUs.21 Nevertheless, research is lacking concerning the effects of FES cycling on seat pressure and its association with PUs. The purpose of this pilot study was to measure the effects of home-based FES cycling on the average and maximal seat pressure of wheelchair-reliant individuals with SCI.