Tissue oxygenation and skin blood flow in the diabetic foot: responses to cutaneous warming

We previously reported an unexpected statistically significant decline in the mean transcutaneous partial pressure of oxygen (TcPO2) with cutaneous warming from 37 degrees C to 44 degrees C on the plantar diabetic foot, as opposed to the expected increase seen at the dorsal sites. To elucidate this relationship we compared changes with cutaneous warming in TcPO2 and skin circulation measured by laser Doppler flowmetry on the right plantar foot surface of 20 consecutive subjects. Neuropathy by monofilament testing was present in 55% of the cases. Right dorsal foot TcPO2 increased with cutaneous warming from 37 degrees C to 44 degrees by a mean change of +43.6+/-20.7 mmHg (+/- standard deviation) in 95% of the cases. In 42% of cases right plantar first metatarsal head TcPO2 fell with warming from 37 degrees C to 44 degrees C by a mean change of -10.7+/-7.6 mmHg. In the remaining 58% of cases right plantar first metatarsal head TcPO2 rose by 6.8+/-6.3 mmHg. In 95% of cases right plantar great toe laser Doppler perfusion units (LDPU) increased with warming from 36 degrees C to 44 degrees C by a mean change of +50.4+/-37.1. Blood flow measured by laser Doppler flowmetry increased in 95% of the subjects with heating. The finding that blood flow was increased with warming contradicts the hypothesis that arterioles in the plantar great toe cannot vasodilate in response to thermal stimuli. This finding supports the hypothesis that the decline in TcPO2 with warming might be due to an increase in epidermal oxygen consumption that exceeds the increase in oxygen delivery due to increased blood flow. The pathological mechanisms behind microvascular dysfunction in skin microcirculation in the diabetic foot need further investigation.