Skin viability and microvascular function under localised applications of Heat and Pressure

Soft tissue pressure injuries are localised injuries to surface and deep tissue, caused by sustained compression of skin and muscle between a bony area of the body, and for example, a hospital mattress or medical device. Prolonged cell deformation is known to reduce the structural integrity of the cell cytoskeleton, leading to cascade of cell death, inflammation, oedema and oxidative stress, factors that are like exacerbated by inadequate blood flow and oxygen delivery. Numerous secondary factors are thought to accelerate this cascade, including systemic hypoxia and changes in tissue temperature. By examining the responses of various skin viability markers, both during and after the application of temperature and pressure stimuli, the present study aims to expand understanding of the secondary factors affecting pressure ulcers onset and progression. In the present study, a custom skin deformation device, with an area of 33cm2, was used to apply a combination of pressures (6, 20 and 40mmHg) and temperatures (33, 33, 38°C) at the sacrum of four healthy volunteers (data collection ongoing). A laser doppler flowmetry probe, embedded into the skin deformation device, was used to measure baseline skin blood flow, skin blood flow under pressure, and reactive hyperaemia (RH) on pressure release. All measurements were calculated as a percentage of heat-induced maximal cutaneous vascular conductance (%CVCmax). Changes in stratum corneum and epidermal hydration were calculated using the difference in tissue electrical capacitance (corneometry) measurements before and after skin deformation. The results indicated a significant difference in loaded skin blood flow between the pressures of 6-20mmHg (p=0.045), and 6-40mmHg (p=0.018), decreasing from 30.5 ± 9.1 %CVCmax to 21.8 ± 9.0 %CVCmax and 17.5 ± 6.7 %CVCmax respectively. Furthermore, there was a significant increase (p=0.030) from 16.9 ± 8.2 %CVCmax to 29.8 ± 5.4 %CVCmax in loaded skin blood flow, between the temperatures of 28-38°C. Finally, blood flow saw a significant (p=0.005) increase on pressure release, from a loaded average of 19.7 ± 8.2 %CVCmax to an unloaded average of 29.0 ± 12.0 %CVCmax, however there was no significant effect of pressure level or temperature on reactive hyperemia. Changes in stratum corneum hydration between 28-33°C (p=0.044), and 28-38°C (p=0.019), increased from 20.8 ± 11.3% to 38.8 ± 12.7% and 48.5 ± 15.5% respectively. Differing pressures and temperatures had no significant effect on epidermal hydration. Initial indications from the present study suggest low local tissue temperature reduces tissue blood flow under pressure, thereby potentially reducing oxygen transport to, and metabolites away from, areas of loaded tissue. However, increased local temperature results in greater moisture accumulation on the surface layer of the cutaneous tissues, potentially resulting in a lower structural integrity, and when combined with a higher metabolism, may result in a faster rate of tissue breakdown. On balance, a neutral skin temperature may be best skin to balance the harmful effects pressure on tissue viability, but further investigation is required to fully understand the influence of temperature on each aspect of the pressure injury cascade, including cell cytoskeleton integrity, inflammation, and oedema, as well as blood flow dynamics, oxygen delivery, cell metabolism and oxidative stress.