Table 1.
Initial Clinical Characteristics of Eligible Patients with Acute Branch Retinal Vein Occlusion.
Fig 1.
Subfoveal hemorrhage in eyes with BRVO.
Fundus photograph (A) and the magnified image (B) of an inset in (A), and the OCT image (C) corresponding to the arrow in (A). On the color fundus photograph, subfoveal hemorrhage appears as a mat red lesion at the fovea (arrow in B). On the OCT section, subfoveal hemorrhage was detected as homogenous hyperreflective, or amorphous moderately hyperreflective material in the subretinal space (arrow in C).
Table 2.
Initial and Final Findings in Eyes With or Without Subfoveal Hemorrhage Associated with Branch Retinal Vein Occlusion.
Fig 2.
Foveal damage seen in three representative eyes with old BRVO.
Color fundus photographs (A, D, G) and the corresponding magnified images (B, E, H) show gray-flat, or yellowish-fibrotic degeneration at the foveal areas of eyes with old BRVO. Consistent with the foveal degeneration seen in the fundus photographs, the vertical optical coherence tomography sections (C, F, I) of the foveal area show defects in the external limiting membrane and ellipsoid lines (arrows in C, F, I) or hyperreflective subretinal material (arrowhead in I).
Fig 3.
Formation process of foveal damage in an eye with BRVO accompanying subfoveal hemorrhage.
Retrospective observation of color fundus photographs (A–D) demonstrates that the foveal areas of damage (solid arrows) are affected by the subfoveal hemorrhage seen in the acute phase of BRVO (dotted arrows).
Fig 4.
Foveal damage due to BRVO-associated subfoveal hemorrhage in two eyes not treated with ranibizumab.
Fundus photographs (A–D) show BRVO in a 64-year-old female (follow-up period of 15 months). Retinal and subfoveal hemorrhages are completely absorbed (A–D), however, the final photograph (D) shows a mild degenerative change at the fovea (solid arrow in D). Vertical OCT sections of foveal areas (E–H) show that foveal and subfoveal hemorrhages are detected as homogenous hyperreflective, or amorphous moderately hyperreflective material in the outer retina and the subretinal space (dotted arrows in E, F), and the foveal external limiting membrane (ELM) and ellipsoid lines affected by the hemorrhage are lost (between the arrowheads in G, H). Initial and final visual acuity (Snellen equivalents) of the eye was 20/40, and 20/100, respectively. Fundus photographs (I–L) show BRVO in a 56-year-old male (follow-up period of 20 months). Color fundus photographs at chronic phase (K, L) show severe foveal damage has formed (solid arrow). Vertical OCT sections of the foveal areas (M–P) show that the foveal and subfoveal hemorrhages are detected in the outer retina and the subretinal space (dotted arrows in M, N), and the foveal ELM and ellipsoid lines, and consistent with that, the locations of the longstanding subfoveal hemorrhage are lost (between arrowheads in O, P). Initial and final visual acuity (Snellen equivalents) of the eye were 20/100 and 20/67, respectively.
Fig 5.
Minimal foveal damage in two eyes with BRVO-associated subfoveal hemorrhage that were treated with ranibizumab.
(A–D, and I–L) Fundus photographs show BRVO with subfoveal hemorrhage (solid arrows) in an 81-year-old female, and a 65-year-old female respectively. (E–H, and M–P) OCT images of the foveal areas show the subfoveal hemorrhage is detected as homogenous hyperreflective material in the subretinal spaces (dotted arrows). (D, H and L, P) Each final photograph and OCT image is obtained just after the third IVR. IVR appears to accelerate the absorption of retinal hemorrhage, with rapid reduction of macular edema. Subfoveal hemorrhage is resolved quickly after the intervention. There are no foveal degenerative changes evident via fundus photography (D and L), and no defects or only minimal defects in the photoreceptor-layers are evident in the OCT sections (H and P). Initial visual acuity (Snellen equivalents) of the eyes were 20/66 and 20/40 respectively, and in both cases VA improved to 20/20 after IVR treatment.
Table 3.
Initial and Final Findings in Eyes with Branch Retinal Vein Occlusion With or without Subfoveal Hemorrhage and IVR Therapy.
Fig 6.
Associations between final visual acuity (VA) and other ocular parameters in the IVR(-) and IVR(+) groups.
The scatter diagrams show the correlations between final VA foveal retinal thickness (A), duration of subfoveal hemorrhage (B), and defect lengths in foveal ELM (C), and ellipsoid lines (D) at the final visit. Final VA was not significantly correlated with final foveal retinal thickness in either group (A), however, it was significantly correlated with the length of the foveal defect in the ELM (C) and ellipsoid lines (D) in both groups (P < 0.001 in all cases). In addition, final VA was correlated with the duration of subfoveal hemorrhage (B) in the IVR(-) group (r = 0.468, P = 0.003) and in the IVR(+) group (r = 0.348, P = 0.022).
Table 4.
Factors Associated with Foveal Photoreceptor Damage at the Final Visit in Eyes with Branch Retinal Vein Occlusion.
Table 5.
Final Ocular Measurements According to Initial Macular Perfusion Status of Eyes with Branch Retinal Vein Occlusion.