BACKGROUND: Formation of collateral pathways by veins on the optic nerve head is sometimes observed during the resolution of a central retinal vein occlusion (CRVO). However, no cases have been reported in which the formation and involution of these collateral pathways were documented during the resolution of a CRVO. CASE: A 56-year-old man with a nonischemic CRVO was followed over a 10-year period by ophthalmoscopy, fluorescein angiography (FA), and indocyanine green angiography (IA). OBSERVATIONS: Initial examination revealed only mild arteriosclerosis and the absence of optociliary veins (OCV) in the right eye. Approximately 9 years later, the patient returned with a nonischemic CRVO, and FA demonstrated a prolongation of the retinal circulation time to 12.1 seconds (normal < 11.0 seconds). Monitoring of this patient while undergoing treatment disclosed the development of OCV on the optic nerve head and gradual decrease in the retinal hemorrhage. FA showed that the retinal circulation time was shortening and recovering to normal. IA verified an outflow through the OCV into choroidal veins. Later, ophthalmoscopy showed a narrowing of the diameter of the OCV. CONCLUSIONS: We suggest that the OCV developed to drain blood from the retinal veins into the vortex veins through choroidal veins to compensate for the slowing of retinal blood outflow. The reperfusion of the central retinal vein was accompanied by the narrowing of the OCV.
BACKGROUND: Formation of collateral pathways by veins on the optic nerve head is sometimes observed during the resolution of a central retinal vein occlusion (CRVO). However, no cases have been reported in which the formation and involution of these collateral pathways were documented during the resolution of a CRVO. CASE: A 56-year-old man with a nonischemic CRVO was followed over a 10-year period by ophthalmoscopy, fluorescein angiography (FA), and indocyanine green angiography (IA). OBSERVATIONS: Initial examination revealed only mild arteriosclerosis and the absence of optociliary veins (OCV) in the right eye. Approximately 9 years later, the patient returned with a nonischemic CRVO, and FA demonstrated a prolongation of the retinal circulation time to 12.1 seconds (normal < 11.0 seconds). Monitoring of this patient while undergoing treatment disclosed the development of OCV on the optic nerve head and gradual decrease in the retinal hemorrhage. FA showed that the retinal circulation time was shortening and recovering to normal. IA verified an outflow through the OCV into choroidal veins. Later, ophthalmoscopy showed a narrowing of the diameter of the OCV. CONCLUSIONS: We suggest that the OCV developed to drain blood from the retinal veins into the vortex veins through choroidal veins to compensate for the slowing of retinal blood outflow. The reperfusion of the central retinal vein was accompanied by the narrowing of the OCV.