Acute retinal vascular occlusive disorders collectively constitute one of the major causes of blindness or seriously impaired vision, and yet there is marked controversy on their pathogeneses, clinical features and particularly their management. This is because the subject is plagued by multiple misconceptions. These include that: (i) various acute retinal vascular occlusions represent a single disease; (ii) estimation of visual acuity alone provides all the information necessary to evaluate visual function; (iii) retinal venous occlusions are a single clinical entity; (iv) retinal vein occlusion is essentially a disease of the elderly and is not seen in the young; (v) central retinal vein occlusion (CRVO) is one disease; (vi) fluorescein fundus angiography is the best test to differentiate ischemic from nonischemic CRVO; (vii) the site of occlusion in CRVO is invariably at the lamina cribrosa; (viii) clinical picture of CRVO is often due to compression or strangulation of the central retinal vein (CRV) in the lamina cribrosa and not its occlusion; (ix) an eye can develop both CRVO and central retinal artery occlusion (CRAO) simultaneously; (x) every eye with CRVO is at risk of developing neovascular glaucoma; (xi) lowering intraocular pressure (IOP) helps to improve retinal circulation in an eye with CRVO; (xii) every patient with retinal vein occlusion should have complete hematologic and coagulation evaluation; (xiii) the natural history of CRVO does not usually involve spontaneous visual improvement; (xiv) management of CRVO is similar to that of venous thrombosis anywhere else in the body, i.e. with aspirin and/or anti-coagulants; (xv) fibrinolytic agents can dissolve an organized thrombus in the CRV; (xvi) it is beneficial to lower blood pressure in patients with CRVO; (xvii) panretinal photocoagulation used in ischemic retinal venous occlusive disorders has no deleterious side-effects; (xviii) glaucoma or ocular hypertension can cause branch retinal vein occlusion; (xix) branch retinal vein occlusion can cause neovascular glaucoma; (xx) in eyes with CRAO, the artery is usually not completely occluded; (xxi) CRAO is always either embolic or thrombotic in origin; (xxii) amaurosis fugax is always due to retinal ischemia secondary to transient retinal arterial embolism; (xxiii) asymptomatic plaque(s) in retinal arteries do not require a detailed evaluation; (xxiv) retinal function can improve even when acute retinal ischemia due to CRAO has lasted for 20h or more; (xxv) CRAO, like ischemic CRVO, can result in development of ocular neovascularization; (xxvi) panretinal photocoagulation is needed for "disc neovascularization" in CRAO; (xxvii) fibrinolytic agents are the treatment of choice in CRAO; (xxviii) there is no chance of an eye with retinal arterial occlusion having spontaneous visual improvement; (xxix) absence of any abnormality on Doppler evaluation of the carotid artery or echography of the heart always rules out those sites as the source of embolism; and (xxx) absence of an embolus in the retinal artery means the occlusion was not caused by an embolus. The major cause of all these misconceptions is the lack of a proper understanding of basic scientific facts related to the various diseases. The objective of this paper is to discuss these misconceptions, based on these scientific facts, to clarify the understanding of these blinding disorders, and to place their management on a rational, scientific basis.