Studies on sitting pressure and buttock microcirculation : aiming at developing an alarm in the prevention of pressure ulcers in patients with spinal cord injuries

Sammanfattning: Pressure ulcers in patients with spinal cord injuries are a major problem, the prevalence in this group being reported as high as 20 – 30 percent. Most pressure ulcers develop around the pelvic girdle, and the key-contributing factor in the development of pressure ulcers is ischaemia due to longstanding pressure. Loss of mobility and lack of sensation below the level of injury are prominent risk factors for the development of pressure ulcers. Although many factors are known to contribute to pressure ulcer development, the exact aetiology is not completely clear. Prevention is suggested as the best way to deal with the problem. The studies in this thesis investigate some aspects of the physiology of sitting in patients with spinal cord injuries and healthy controls, aiming at developing a pressure ulcer alarm device to aid in the prevention of pressure ulcers. Methods used are laser Doppler perfusion imaging (LDPI) for measurement of superficial skin blood flow, as well microdialysis and a microelectrode (Licox®) to measure direct and indirect signs of ischaemia. In addition sitting pressures are mapped. The main findings are that patients with spinal cord injuries have almost four-fold mean maximum sitting pressures 43 and 49 N/cm2, left and right buttock) compared with healthy controls 12 and 13 N/cm2, left and right buttock). In the subcutaneous fat in healthy individuals, the tissue oxygen pressure decreases significantly during 30 minutes of sitting on a wheel chair cushion 13,7 mmHg) compared with 30 minutes of sitting on a hard surface 19,8 mmHg) implying that the tissues deep in the skin are exposed to a reduction in blood supply. This is also confirmed by a decrease in extracellular glucose during sitting for 30 minutes on a hard surface 1,8 mmol/L) and on a wheel chair cushion 1,7 mmol/L). The post-sitting reactive hyperaemia is dependent on duration of sitting in both patients and healthy subjects. It seems to be attenuated in patients in the sitting position but intensified while lying prone. Furthermore, four repeated loadings on a hard surface 15 minutes of sitting followed by five minutes of rest) without allowing the tissues to return to resting perfusion results in a significantly increasing reactive hyperaemia for each loading in healthy subjects, suggesting that it is important to unload the buttock skin completely before the next sitting period starts. This thesis also describes the construction of an alarm device that measures surface interface pressures during sitting continuously in eight predefined points, to alert the user by an audible signal after a given period of time when the pressure has reached a dangerously high level. It is concluded that the reactive hyperaemia that is observed in the buttock skin after sitting, as well as the reduction in glucose and oxygen in adipose tissue during sitting, are due to a reduction in blood supply relative or absolute ischaemia) caused by a compression of the vasculature by the ischial tuberosities. These findings imply a multilayer aetiology in pressure ulcer development. The altered hyperaemic reaction in patients with spinal cord injuries after sitting is possibly related to alterations in sympathetic activity due to the cord lesion. Lastly, the alarm device is supposed to be an aid to pressure ulcer prevention in patients with spinal cord injuries who lack normal sensory feedback.