Retinal Oxygen Saturation in Patients with Primary Open-angle Glaucoma Using a Non-flash Hypespectral Camera

Purpose/Aim: To investigate retinal vessel blood oxygen saturation in patients with primary open-angle glaucoma (POAG) and healthy controls. Materials and Methods: A novel non-flash hyperspectral retinal camera was used to image 17 healthy individuals (mean age 69.3 6.1 years) and 22 patients with stable POAG (mean age 69.2 5.8 years) at 548, 569, 586, 600, 605, and 610 nm wavelengths. POAG patients were grouped as mild-moderate (n = 13) and moderate-severe (n = 9) based on Humphrey 24-2 visual field results (mean deviation [MD] < -6 and MD -6; respectively). Optical density values were extracted using Image-J software for blood oxygen saturation (SO2) determination. Arteriolar and venular SO2 were measured within 1.5 optic nerve head diameters from the disc margin along the vessels in the inferior temporal quadrant of the tested eye per subject. Analysis of variance (ANOVA), student t-test, and Pearson's correlation were used for statistical analysis of the data (p < 0.05). Results: Venular, arteriolar, and arteriovenous (AV) differences in SO2 measurements were not significantly different between controls and the combined POAG groups (p > 0.06 for all). However, mean venular SO2 was significantly higher in the POAG with MD -6 dB when compared to controls and patients with mild glaucoma (p = 0.005). The AV differences were significantly lower in patients with more severe field defect (p = 0.006) compared to the remaining groups. No differences were found in the mean arteriolar SO2 between the groups (p = 0.155). Significant correlations were found only between higher visual field MD values and higher venular SO2 (p = 0.048) but not the remaining SO2 measurements. Conclusion: Patients with POAG and moderate-severe visual field defect had higher venular SO2 compared to those with mild-moderate defect and controls. This would indicate reduced oxygen consumption in more advanced glaucoma likely as a result of ganglion cell degeneration.