Modelling the skin's microvascular function under localised applications of heat and pressure at the posterior heel

Introduction: The heel is one of the two most common sites for pressure injuries (PI), the other being the sacrum (Linden and Riordan, 2006). It is considered a particularly vulnerable area due to low adiposity, bone prominences, as well as the influence of vascular dysfunction in disease, and normal biological aging of the local tissue (Delmore et al., 2015). There is only a small amount of tissue covering the posterior surface of the calcaneum which leads to particularly high interface pressures between the heel and the supporting surfaces (Mayrovitz, Macdonald and Smith, 1999) .The high interface pressure leads to damage of the microcirculation of the soft tissues overlaying the calcaneum, resulting in tissue ischaemia and necrosis (Ousey, 2009). Methods: In the present study, a custom skin deformation device, with an area of 33cm2, was used to locally apply a combination of pressures (6, 20, 60 and 100mmHg) and temperatures (33, 38°C) at the left posterior heel of eight healthy male volunteers (mean age, 24 ± 2 years). A laser doppler flowmetry probe, embedded into the skin deformation device, was used to measure baseline skin blood flow, loaded skin blood flow (LSBF), and reactive hyperaemia (RH; quantified as aera under curve) on pressure release. Skin Blood Flow measures are all expressed as cutaneous vascular conductance (CVC = Flux/MAP). The relationship between local temperature (33-38°C) and pressure (6-100mmHg) application of LSBF and RH was then assessed via non-linear regression. (Burk and Grap, 2012) Results: LSBF saw a significant reduction (p<0.003) as the applied pressure increased, falling from 2.1 ± 0.1au at 6mmHg, to 0.8 ± 0.01au at 20mmHg, to 0.2 ± 0.13au at 60mmHg, and finally to 0.2 ± 0.15au at 100mmHg. There were significant differences observed between all LSBF apart from the values for 60 and 100mmHg, which had a mean difference of only 0.01au. Temperature had a significant (p=0.015) effect on LSBF, which increased from 0.6 ± 0.1au at 33°C to 1.0 ± 0.17au at 38°C. RH, saw a significant (p=0.003) increase between the temperatures of 33 and 38°C, increasing from 9.0 ± 5.9 to 17.9 ± 12.9. Significant differences (p<0.001) were also observed between the body’s hyperaemic response to the pressures of 20 to 60 and 100mmHg, increasing from 7.4 ± 2.67 to 18.8 ± 11.2au and 21.6 ± 11.5au. RH data demonstrated a quadratic increase with increasing interface pressures at both 33°C and 38°C, plateauing at 90mmHg irrespective of temperature. When interpolated, LSBF demonstrated a quadratic decline with increasing pressure at 33°C, and a power decline with increasing pressure at 38°C, predicting LSBF to shut down completely at 45mmHg, and 55mmHg, respectively. Conclusions: This study characterized the relationship between local temperature (33-38°C) and pressure application (6-100mmHg) on LSBF and RH. Burk, R. S. and Grap, M. J. (2012) ‘Backrest position in prevention of pressure ulcers and ventilator-associated pneumonia: Conflicting recommendations’, Heart and Lung: Journal of Acute and Critical Care, 41(6), pp. 536–545. doi: 10.1016/j.hrtlng.2012.05.008. Delmore, B. et al. (2015) ‘Risk Factors Associated with Heel Pressure Ulcers in Hospitalized Patients’, Journal of Wound, Ostomy and Continence Nursing, 42(3), pp. 242–248. doi: 10.1097/WON.0000000000000134. Linden, M. and Riordan, B. (2006) ‘Ostomy Wound Management’, Ostomy Wound Management, 51(3), pp. 1–26. Mayrovitz, H. N., Macdonald, J. and Smith, J. R. (1999) ‘Blood perfusion hyperaemia in response to graded loading of human heels assessed by laser-Doppler imaging’, Clinical Physiology, 19(5), pp. 351–359. doi: 10.1046/j.1365-2281.1999.00184.x. Ousey, K. (2009) ‘Heel ulceration - An exploration of the issues’, Journal of Orthopaedic Nursing, 13(2), pp. 97–104. doi: 10.1016/j.joon.2009.06.001.