Heel skin hyperaemia: Direct compression versus vascular occlusion

Vulnerability of the heel to ulceration in bed-bound persons is related to direct pressure-induced blood flow decreases. Periodic pressure reduction is a clinical strategy to help prevent ulcers by allowing flow-repayment hyperaemia that has a magnitude and duration thought to be related to the duration of the prior interval of ischaemia. However, there are reasons to question whether effects of flow stoppages caused by direct tissue loading are similar to those because of ischaemia without superimposed direct pressure. This question was investigated by comparing posterior heel skin blood flow responses via laser-Doppler perfusion monitoring of 27 supine-lying subjects in whom blood flow was reduced by 5-min of direct heel loading on a support surface and by 5-min of ankle-cuff compression. Results showed that blood flow reductions were the same for both methods but the hyperaemia was significantly greater when flow reduction was produced by direct heel loading. This was true for ratio of peak hyperaemic flow to baseline (8·20 ± 1·32 s versus 4·68 ± 0·80 s, P≤0·001), hyperaemic to baseline 3-min flow-time area ratios (4·70 ± 0·65 s versus 1·95 ± 0·29 s, P≤0·001) and for total hyperaemia durations (352 ± 39 s versus 181 ± 14 s, P<0·001). These findings raise new questions regarding the precise physiological effects of heel and tissue loading in general, the factors that contribute to the hyperaemic response and their clinical impact and interpretation. Possible sources of the observed greater post-loading hyperaemia responses are discussed