Heel‐Skin Microvascular Blood Perfusion Responses to Sustained Pressure Loading and Unloading

Abstract

The present seminal findings may serve as a guide to develop sorely needed microvascular tests to help classify heel breakdown risk on a patient-by-patient basis.

Preventing pressure ulcers by assessment of the microcirculation in tissue exposed to pressure

“…The theory is based on the view that the circulation transports oxygen and metabolites to and from the cells and that pressure disturbs the transport function leading to local tissue ischemia that is made worse by toxic metabolites that accumulate in the tissue (Dinsdale, 1974, Kosiak, 1961. Studies based on this theory include measurements of skin blood flow in both animals and humans (Bennett et al, 1981, Mayrovitz and Smith, 1998, Sae-Sia et al, 2007, Sanada et al, 1997, Schubert and Fagrell, 1991.…”

Heel skin hyperaemia: direct compression versus vascular occlusion

“…Another mechanically linked possibility is that tissue recovery after 5-min of compression might be delayed thereby limiting vessel re-expansion rate and extending refill time. However, previous observations of heel tissue recovery in which heels were loaded with a range of pressures and durations argue against this as a significant factor (Mayrovitz & Smith, 1998). Another mechanical factor that might conceivably render the postload hyperaemia peak greater than the postocclusion hyperaemia is the slight downward rotation of the foot when the heel support pressure was reduced to zero.…”

“…Heel interface pressures (IP) usually exceed arterial diastolic pressure and often are close to or greater than arterial systolic blood pressure (Mayrovitz & Sims, 2002). Systematic studies of the hyperaemic response to variable magnitudes and durations of heel loading have shown a nonlinear relation between postloading hyperaemia and the loadduration product (Mayrovitz et al, 1997;Mayrovitz & Smith, 1998;. Comparisons between postloading hyperaemia and maximum possible hyperaemia achieved by tissue heating, showed that heel loading of only 5 min resulted in unexpectedly high hyperaemic flows that were 80% of the maximum.…”

Physiology and prevention of heel ulcers: The state of science

“…Loading was done with subjects supine and one heel on a transparent plate through which heel blood perfusion data were obtained during loading. 30 Heel perfusion was rapidly and significantly reduced on loading (P < 0.01) with the greatest reduction within the central heel area; perfusion remained uniformly depressed throughout the loading interval while off-loading was associated with a rapid onset hyperemia which exceeded baseline (P < 0.01) for 10 minutes.…”

“…Higher pressures do not influence the amplitude in skin microvascular response, but result in a longer delay to maximal hyperemia. 28 Mayrovitz and his colleagues 29 explored the hyperemic response of heel skin.…”