Retinal vessel oximetry in children with inherited retinal diseases

Abstract

AbstractBackgroundAlterations in retinal oxygen metabolism have already been confirmed in eldery subjects with retinitis pigmentosa (RP). Hovewer, whether this is a also a feature in children affected by RP has not been studied yet. The aim of our study was to compare retinal oxymetry (RO) parameters whithin children with inherited retinal diseases (IRDs), as well as agains those of carriers and healthy controls.MethodsA total of 68 children (136 eyes) of were examined: 16 with IRDs (32 eyes) were compared to those of 11 IRD carriers (22 eyes) and of 41 healthy children (82 eyes). RO was performed with the oxygen saturation tool of the Retinal Vessel Analyser (RVA; IMEDOS, Germany). The mean oxygen saturations, within 1.0–1.5 optic disc diameters from the disc margin, in the retinal arterioles (A‐SO2;%) and venules (V‐SO2;%) were estimated and their difference (A‐V SO2;%), was calculated. The corresponding arterioles (D‐A;μm) and venules (D‐V;μm) were evaluated, as well. For statistical evaluation ANOVA‐based linear mixed‐effects models were calculated with SPSS®.ResultsThe V‐SO2 showed a statistically significant increase in RP eyes (67.00 ± 7.48%) when compared to healthy controls (59.07 ± 11.98%, p=0.03), but also to children with other IRDs and to carriers (p ≤ 0.03). The A‐V SO2 showed a statistically significant decrease in RP eyes (32.62 ± 4.03%), when compared to eyes suffering from macular dystrophies (MD, 44.35 ± 10.55%, p = 0.05) or cone‐rod‐dystrophies (CRD, 43.29 ± 10.55, p = 0.03). The D‐V, even if not reaching statistically significant level, showed a trend for RP to be slightly attenuated (102.31 ± 8.20 μm) when compared to controls (108.76 ± 20.87 μm; p = 0.07).ConclusionThese data indicate that children suffering RP show early metabolic alterations. With aging and progression of RP the sign of vascular attenuation seems to be a secondary effect of neurovascular remodeling. Here, RO seems to be a useful screening tool for metabolic dysfunction within a family affected from RP.