Relief of cystoid macular edema-induced focal axonal compression with anti-vascular endothelial growth factor treatment

Abstract

Purpose: To evaluate the mechanical compression of retinal nerve fiber layer (RNFL) by intraretinal cysts in macular edema and its relief with anti-vascular endothelial growth factor (anti-VEGF) treatment.

Methods: Optical coherence tomography scans were used to measure RNFL thickness and reflectance at seven preselected points at and around the peak of the edema before and after anti-VEGF treatment in 10 patients (11 eyes) with branch retina vein occlusion (BRVO) and diabetic macular edema (DME). Scans through nonedematous retina and from the fellow eyes were taken as controls. Correlations were sought between the changes in retinal and RNFL thickness, RNFL reflectance, and the size of the intraretinal cysts.

Results: Postinjection RNFL thickness decreased significantly only at peak point of the edema (18.1 +/- 2.7 vs. 13.8 +/- 1.2 mu m; P = 0.038), at its nasal edge (20.1 +/- 2.7 vs. 15.5 +/- 1.4 mu m; P = 0.026), and 500 mu m away from its nasal border (35.7 +/- 6.0 vs. 20.1 +/- 2.7 mu m; P = 0.006) suggesting focal stagnation of the axoplasmic flow owing to compression at its peak point. Significant postinjection decreases in RNFL reflectivity were also noted at peak point of the cyst (164.9 +/- 10.3 vs. 141.5 +/- 12.6 arbitrary units [AU]; P = 0.037), at its nasal edge (166.8 +/- 7.8 vs. 135.1 +/- 10.2 AU; P = 0.02), and 1500 mu m away from temporal edge (160.2 +/- 6.2 vs. 141.1 +/- 6.4 AU; P = 0.022). Cyst proximity to RNFL (D-50 = 50 mu m) was the only determinant significantly affecting the magnitude of the RNFL thickness change after anti-VEGF treatment (P = 0.001).

Conclusions: Intraretinal cysts due to BRVO and DME locally compress overlying axons and induce anatomic changes suggestive of axoplasmic stagnation. This compression can be relieved with anti-VEGF treatment.

Translational Relevance: Focal compression of RFNL by retinal cysts may indicate a need for early treatment of macular edema to prevent axonal loss, especially in patients with low axonal reserve.