Local oxygen content in the skin is increased in chronic venous incompetence

In skin lesions of chronic venous incompetence (CVI) transcutaneous oxygen pressure (tcpO(2)) at the ankle is often reduced. However, in some CVI patients the tcpO(2) during suprasystolic occlusion remains significantly higher than in healthy subjects. The aim of the present study was to investigate which kind of CVI patients develop this phenomenon and whether the higher tcpO(2) during occlusion is caused by a smaller oxygen consumption of the skin or by an increased local oxygen content. The oxygen consumption of the skin was measured by the pO(2) decrease (DeltatcpO(2)/Deltat) after stopping the arterial oxygen supply when the hemoglobin was saturated by oxygen inhalation, i.e., at tcpO(2) values above 120-130 mmHg. By multiplying the tcpO(2) with the mean oxygen solubility coefficient of the skin the content of physically dissolved oxygen is obtained. The decrease of tcpO(2) in the 55- to 45-mmHg range indicates the consumption of oxygen physically dissolved and chemically bound to hemoglobin. It gave a parameter for estimating the local hemoglobin content of the skin. These values and the minimal tcpO(2) after a 5-min arterial occlusion were measured in 14 healthy subjects, in 13 patients with varicose veins, but no skin lesions, in 10 patients with CVI lesions like white atrophy and lipodermatosclerosis and in 16 CVI patients with open venous ulcers. During suprasystolic occlusion tcpO(2) at the ankle remained significantly higher in CVI patients with skin lesions than in the healthy control subjects (25.6 +/- 18.9 versus 8.0 +/- 7.0 mmHg). The steepness of the tcpO(2) decrease caused by cutaneous oxygen consumption in healthy subjects was not significantly different from the CVI patients. In contrast, the decrease of tcpO(2) at the ankle between 55 and 45 mmHg was 1.9 +/- 2.0 mmHg/s in the control group and 0.7 +/- 0.5 mmHg/s in the group with open venous ulcers. These results indicate a higher hemoglobin content in the skin of the CVI patients than in healthy subjects. Obviously, the hemoglobin bound oxygen content in the skin of CVI patients is increased. Thus, a lack of oxygen is unlikely to be the primary reason for the development of skin lesions in CVI.