Assessment of tissue oxygen saturation during a vascular occlusion test using near-infrared spectroscopy: the role of probe spacing and measurement site studied in healthy volunteers

INTRODUCTION: To assess potential metabolic and microcirculatory alterations in critically ill patients, near-infrared spectroscopy (NIRS) has been used, in combination with a vascular occlusion test (VOT), for the non-invasive measurement of tissue oxygen saturation (StO(2)), oxygen consumption, and microvascular reperfusion and reactivity. The methodologies for assessing StO(2 )during a VOT, however, are very inconsistent in the literature and, consequently, results vary from study to study, making data comparison difficult and potentially inadequate. Two major aspects concerning the inconsistent methodology are measurement site and probe spacing. To address these issues, we investigated the effects of probe spacing and measurement site using 15 mm and 25 mm probe spacings on the thenar and the forearm in healthy volunteers and quantified baseline, ischemic, reperfusion, and hyperemic VOT-derived StO(2 )variables. METHODS: StO(2 )was non-invasively measured in the forearm and thenar in eight healthy volunteers during 3-minute VOTs using two InSpectra tissue spectrometers equipped with a 15 mm probe or a 25 mm probe. VOT-derived StO(2 )traces were analyzed for base-line, ischemic, reperfusion, and hyperemic parameters. Data were categorized into four groups: 15 mm probe on the forearm (F(15 mm)), 25 mm probe on the forearm (F(25 mm)), 15 mm probe on the thenar (T(15 mm)), and 25 mm probe on the thenar (T(25 mm)). RESULTS: Although not apparent at baseline, probe spacing and measurement site significantly influenced VOT-derived StO(2 )variables. For F(15 mm), F(25 mm), T(15 mm), and T(25 mm), StO(2 )ownslope was -6.4 ± 1.7%/minute, -10.0 ± 3.2%/minute, -12.5 ± 3.0%/minute, and -36.7 ± 4.6%/minute, respectively. StO(2 )upslope was 105 ± 34%/minute, 158 ± 55%/minute, 226 ± 41%/minute, and 713 ± 101%/minute, and the area under the hyperemic curve was 7.4 ± 3.8%·minute, 10.1 ± 4.9%·minute, 12.6 ± 4.4%·minute, and 21.2 ± 2.7%·minute in these groups, respectively. Furthermore, the StO(2 )parameters of the hyperemic phase of the VOT, such as the area under the curve, significantly correlated to the minimum StO(2 )during ischemia. CONCLUSIONS: NIRS measurements in combination with a VOT are measurement site-dependent and probe-dependent. Whether this dependence is anatomy-, physiology-, or perhaps technology-related remains to be elucidated. Our study also indicated that reactive hyperemia depends on the extent of ischemic insult.