In conclusion, (i) the initial and final visual acuities and visual field defects differ significantly ( P < 0.001) among the four types of CRAO, (ii) significant improvement can occur in visual acuity and visual field without treatment, and (iii) classification of CRAO is crucial for understanding differences in visual outcome.ĭuration of acute retinal ischemia: This is by far the most important factor. Unfortunately, the common use of automated static threshold perimetry nowadays, rather than manual kinetic perimetry performed with a Goldmann perimeter, does not provide full information about the peripheral visual fields, because automated perimetry does not provide information beyond the central 30° or less of the field, whereas kinetic perimetry covers the peripheral visual field up to about 90°. Importance of peripheral visual fields for visual functionĬentral visual field loss results in impaired central vision, while the peripheral visual field is essential for day-to-day living and navigation therefore, a person with central visual loss but with good peripheral visual fields, as in age-related macular degeneration, can lead a reasonably satisfactory functional life although unable to read or do fine work. Simultaneous onset of CRAO in both eyes does not normally occur it happens rarely, when there is compression of both eyes during a prolonged surgical procedure or during hemodialysis. Hallucinations have been reported with severe vision loss associated with CRAO. Some patients complain of a purplish hue to the blur, which is highly suggestive of retinal ischemia. In patients aged 50 years or older with a history of amaurosis fugax, the first essential is to rule out giant cell arteritis, which is an ophthalmic emergency, because if it is not treated immediately, it can result in massive visual loss which can involve both eyes. I found a history of amaurosis fugax before development of CRAO in 12% in NA-CRAO, in 20% in NA-CRAO with cilioretinal artery sparing, in 30% in arteritic CRAO, and in 13% in transient CRAO. The visual loss may be preceded by history of amaurosis fugax, caused by transient migrating embolism or giant cell arteritis. When the visual loss is discovered on waking up in the morning, it may be due to embolism, thrombosis, or due to transient CRAO from a fall of perfusion pressure during sleep caused by nocturnal arterial hypotension. In my study of 260 eyes with CRAO, visual loss was discovered on waking up in the morning in 35% in NA-CRAO, in 29% in NA-CRAO with cilioretinal artery sparing, in 39% in transient CRAO, and in 30% in arteritic CRAO. Typically, there is a sudden, massive loss of vision in the involved eye. Prevalent multiple misconceptions on CRAO are discussed. Investigations to find the cause and to prevent or reduce the risk of any further visual problems are discussed. Recent studies have shown that administration of local intra-arterial thrombolytic agent not only has no beneficial effect but also can be harmful. The incidence of spontaneous visual acuity improvement during the first 7 days differs significantly ( P < 0.001) among the four types of CRAO among them, in eyes with initial visual acuity of counting finger or worse, visual acuity improved, remained stable, or deteriorated in NA-CRAO in 22%, 66%, and 12%, respectively in NA-CRAO with cilioretinal artery sparing in 67%, 33%, and none, respectively and in transient NA-CRAO in 82%, 18%, and none, respectively. Contrary to the prevalent belief, spontaneous improvement in both visual acuity and visual fields does occur, mainly during the first 7 days. Clinical characteristics, visual outcome, and management very much depend upon the type of CRAO. CRAO consists of the following four distinct clinical entities: non-arteritic CRAO (NA-CRAO), transient NA-CRAO, NA-CRAO with cilioretinal artery sparing, and arteritic CRAO. The pathogeneses, clinical features, and management of central retinal artery occlusion (CRAO) are discussed.
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