Pathway to Retinal Oximetry

Retinal oxygen metabolism is thought to be affected in diabetic retinopathy. The aim of this study was to test whether retinal vessel oxygen saturation is different in patients with diabetic retinopathy from that in healthy controls. The retinal oximeter is based on a fundus camera. It estimates retinal vessel oxygen saturation from light absorbance at 586 nm and 605 nm. Retinal vessel oxygen saturation was measured in one major temporal retinal arteriole and venule in healthy volunteers and in patients with diabetic retinopathy. Oxygen saturation in the retinal arterioles of healthy volunteers was 93 ± 4% and 58 ± 6% in venules (mean ± SD, n=31). The corresponding values for all diabetic patients (n=20) were 101 ± 5% and 68 ± 7%. The difference between healthy volunteers and diabetic patients was statistically significant (p < 0.001 for arterioles and venules). Three subgroups of diabetic patients (background retinopathy, macular oedema and pre-proliferative/proliferative retinopathy) all had higher saturation values than the healthy volunteers (p < 0.05 for arterioles and venules). Retinal vessel oxygen saturation is higher in patients with diabetic retinopathy than in healthy controls. Possible explanations include shunting of blood through preferential channels, bypassing non-perfused capillaries in the capillary network. Parts of the retinal tissue may be hypoxic while blood in larger vessels has high oxygen saturation.

To measure hemoglobin oxygen saturation (SO(2)) in retinal vessels and to test the reproducibility and sensitivity of an automatic spectrophotometric oximeter. Specialized software automatically identifies the retinal blood vessels on fundus images, which are obtained with four different wavelengths of light. The software calculates optical density ratios (ODRs) for each vessel. The reproducibility was evaluated by analyzing five repeated measurements of the same vessels. A linear relationship between SO(2) and ODR was assumed and a linear model derived. After calibration, reproducibility and sensitivity were calculated in terms of SO(2). Systemic hyperoxia (n = 16) was induced in healthy volunteers by changing the O(2) concentration in inhaled air from 21% to 100%. The automatic software enhanced reproducibility, and the mean SD for repeated measurements was 3.7% for arterioles and 5.3% venules, in terms of percentage of SO(2) (five repeats, 10 individuals). The model derived for calibration was SO(2) = 125 - 142 . ODR. The arterial SO(2) measured 96% +/- 9% (mean +/- SD) during normoxia and 101% +/- 8% during hyperoxia (n = 16). The difference between normoxia and hyperoxia was significant (P = 0.0027, paired t-test). Corresponding numbers for venules were 55% +/- 14% and 78% +/- 15% (P < 0.0001). SO(2) is displayed as a pseudocolor map drawn on fundus images. The retinal oximeter is reliable, easy to use, and sensitive to changes in SO(2) when concentration of O(2) in inhaled air is changed.

Longstanding diabetes mellitus results in a disturbed microcirculation. A new imaging oximeter was used to investigate the effect of this disturbance on retinal vessel oxygen saturation. The haemoglobin oxygen saturation was measured in the retinal arterioles and venules of 41 diabetic patients (65 +/- 12.3 years) with mild non-proliferative through proliferative diabetic retinopathy (DR). Twelve individuals (61.3 +/- 6.2 years, mean +/- standard deviation) without systemic or ocular disease were investigated as controls. Measurements were taken by an imaging oximeter (oxygen module by Imedos GmbH, Jena). This technique is based on the proportionality of the oxygen saturation and ratio of the optical density of the vessel at two wavelengths (548 nm and 610 nm). Whereas there were no significant differences in the arterial oxygen saturation between controls and diabetic retinopathy at any stage, the venous oxygen saturation increased in diabetic patients with the severity of the retinopathy: controls 63 +/- 5%, mild non-proliferative DR 69 +/- 7%, moderate non-proliferative DR 70 +/- 5%, severe non-proliferative DR, 75 +/- 5%, and proliferative DR 75 +/- 8%. The increase of retinal vessel oxygen saturation in diabetic retinopathy points to a diabetic microvascular alteration. This may be due to occlusions and obliterations in the capillary bead and the formation of arterio-venous shunt vessels. On the other hand, hyperglycaemia-induced endothelial dysfunction, with subsequent suppression of the endothelial NO-synthase and disturbance of the vascular auto-regulation, may contribute to retinal tissue hypoxia.