Although ischemic changes may be apparent on the retina, maculopathy may be asymptomatic at first leaving visual acuity unchanged. Central retinal artery occlusion is a known feature of non-proliferative sickle cell retinopathy that has a low incidence in patients with non proliferative sickle cell retinopathy. Optic nerve sign is represented by dilated capillaries that can be visualized in the nerve using fluorescein angiography. Visual acuity often remains unchanged with this finding. Angioid streaks: Angioid streaks may be seen in up to 6% of cases. Proliferative sickle cell retinopathy (PSCR)
Proliferative sickle retinopathy is the most severe ocular complication of sickle cell disease. Even though PSCR begins in the first decade of life, the condition remains asymptomatic and unnoticed until visual symptoms occur due to vitreous hemorrhage or retinal detachment. Goldberg classification
Goldberg classified PSR into following 5 different self-explanatory stages:

Stage of peripheral arterial occlusion and ischemia: It is the earliest abnormality that can be visualized by fundus examination. The occluded arterioles can be seen as dark red lines. They eventually turn into white silver-wire vessels. Stage of peripheral arteriolar-venular anastomoses: Arteriolar-venular anastomoses develop as blood is diverted from blocked arteries to nearby venules. Stage of neovascularization and fibrous proliferation: Neovascularization starts from the arteriolar-venular anastomoses, and grow into the ischemic retina. Characteristic fan-shaped appearance due to neovasularization is known as sea fan neovascularization. Stage of vitreous hemorrhage. Peripheral neovascular tufts bleed and cause vitreous hemorrhage. Stage of vitreoretinal traction bands and tractional retinal detachment: Traction on the sea fan and adjacent retina causes traction retinal detachment.
In 1957 Black-Schaffer proposed a unitary explanation that stress on the ventricle, of any kind, may trigger the endocardial reaction, so that all EFE could be thought of as secondary.Evidence gradually accumulated as to the role of infection as one such type of stress. The studies of Fruhling and colleagues in 1962 were critical. They followed a series of epidemics of Coxsackie virus infection in their part of France. After each epidemic there were increased numbers of cases with EFE coming to autopsy. On closer study there were cases of pure acute myocarditis, cases of mixed myocarditis and EFE, and cases where myocarditis had healed, leaving just EFE. They were able to culture Coxsackie virus from the tissues of many of the cases at all stages  of this apparent progression. A similar progression from myocarditis to EFE was later observed at Johns Hopkins but no virology was done.Noren and colleagues at the University of Minnesota, acting on an idea floated at a pediatric meeting, were able to show a relation between exposure to maternal mumps in fetal life, EFE, and a positive skin test for mumps in infants. This brought on a large ongoing controversy and finally prompted a virologist colleague of theirs to inject embryonated eggs with mumps virus. The chicks at first showed the changes of myocarditis, about a year later, typical EFE, and transitional changes in between. Despite this, the controversy about the role of mumps continued as the actual incidence of EFE plummeted.