Transcutaneous oxygen tension (tcPO2) of the legs and feet was measured at 37 and 44°C in 21 patients with diabetes mellitus, 9 of whom had peripheral neuropathy. At 37°C, tcPO2 in the legs and feet of diabetic patients with peripheral neuropathy was significantly higher (P < .02) than in control subjects and diabetic patients without neuropathy. Whereas tcPO2 in the legs of control subjects and nonneuropathic diabetic patients was > in the feet (P < .02), this leg-to-foot difference was absent in diabetic patients with neuropathy. After an increase in skin temperature to 44°C, tcPO2 increased in the legs and feet of all three groups, but the increase was smallest in diabetic patients with neuropathy and greatest in control subjects. In neuropathic (P < .02) and nonneuropathic (P < .02) diabetic patients, tcPO2 was significantly lower than in control subjects. These data are consistent with a loss of vasoconstrictor tone in the blood vessels perfusing skin and subcutaneous tissue at 37°C and an inability of these vessels to vasodilate and increase blood flow at 44°C in diabetic patients in general and neuropathic diabetic patients in particular. This inability to increase tcPO2 after an increase in temperature and possibly other vasodilatory stimuli may contribute to the pathogenesis of nonhealing ulcers, protracted infections, and gangrene, which characterize the diabetic foot.

This content is only available via PDF.