Tissue Monitoring with Novel Broadband Light Emitting Diode-Based Near-Infrared Spectroscopy Device
Heather A. McMahon, MD, Jonathon B. Olenczak, MD, Christine V. Schaeffer, MD, David C. Lobb, MD, Keita Ikeda, PhD, Robert H. Thiele, MD, Chris A. Campbell, MD.
University of Virginia, Charlottesville, VA, USA.
Purpose: Near-infrared spectroscopy (NIRS) monitoring devices are a widely used adjunct to serial physical exams for microsurgical flap monitoring. Currently available two wavelength NIRS devices do not directly measure tissue ischemia but use the relative amount of oxidized hemoglobin to deoxyhemoglobin to calculate blood oxygen saturation (StO2). Although NIRS devices clinically improve early detection of flap compromise, StO2 readings have significant artifactual variation requiring vigilant clinician interpretation to avoid unnecessary flap re-exploration. We have previously reported the performance characteristics of a three wavelength NIRS device designed to detect the oxidation state of cytochrome aa3, which is a direct measure of cellular ischemia. The device lessened StO2 variation using an established ischemia and reperfusion model, but did not adequately reflect cytochrome aa3 oxidation state. The objective of this study was to compare a broadband NIRS device using white light (> 1000 wavelengths) to the standard two wavelength NIRS device (ViOptix Inc, Freemont CA) commonly employed for flap monitoring by measuring StO2 variability during ischemia and reperfusion and corresponding cytochrome aa3 oxidation – a direct measure of cellular ischemia.
Methods: The two NIRS devices, ViOptix and the broadband NIRS device, were applied to the hands of human volunteers (n = 20) and a blood pressure cuff was placed around the upper arm to occlude arterial and venous flow, as previously described. Measurements were obtained from both devices at baseline, during induced ischemia, and during reperfusion at 30-second intervals. StO2 variability was measured during ischemia and reperfusion between both devices, as was the correlation of broadband-reported cytochrome aa3 oxidation state to StO2 changes.
Results: As demonstrated in Figure 1, StO2 measurements from both devices proportionally decreased during ischemia with similar variability. The broadband device reported cytochrome aa3 changing from an oxidized to reduced state during ischemia, which began even during baseline cuff placement before StO2 decreased. Once the ischemia and reperfusion reporting phases began, cytochrome aa3 oxidation state correlated with StO2 readings from both devices.
Conclusions: The ViOptix and broadband NIRS devices performed similarly with regard to ability to measure StO2 as a surrogate marker of tissue ischemia. However, the use of broadband white light wavelength NIRS monitoring also provided the capability of directly measuring cellular ischemia through cytochrome aa3 oxidation state. Interestingly cytochrome aa3 oxidation-reduction state was sensitive even to minor changes in tissue perfusion. Future work will evaluate clinically critical differences in cellular oxidation reporting in a flap model.
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