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Vascular occlusion results from thrombosis, embolism, stenosis, (as in atherosclerosis), vascular compression, intravascular sludging or coagulation, and vasoconstriction ( for instance in hypertensive retinopathy and migraine).

Prevalent misconceptions about acute retinal vascular occlusive disorders. Prog Retin Eye Res. 2005 Jul;24(4):493-519.

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.

Visit: Normal histology and diseases of the retina ; Central Retinal Vein Occlusion ; Central Retinal Artery Occlusion ; Comparison between central retinal vein and central retinal artery occlusions ;Hypertensive Retinopathy.

Thrombosis of the ocular vessels may accompany disease of these vessels, as in giant cell arteritis.

Certain disorders of the heart, and of major vessels such as the carotid arteries, predispose to emboli that lodge in the retina and are evident on funduscopic examination at points of vascular bifurcation.

The detection of fat, air, and other emboli within the retina may aid in the clinical diagnosis of embolization.

A frequent site of embolic obstruction of the central retinal artery is that portion of the sclera which is perforated for the passage of the optic nerve (lamina cribrosa), where the arterial lumen is narrower than in the orbital portion of the artery.

The effects of vascular obstruction depends upon the size of the vessel involved, the degree of resultant ischemia, and the nature of the embolus.

Small emboli often do not interfere with retinal function, while septic emboli may cause foci of ocular infection.

Ischemia of any cause deprives the retina of oxygen and other essential metabolites and frequently results in the appearance of white fluffy patches that resemble cotton (“cotton-wool patches”) on opthalmoscopic examination.

These spots, which are generally round and seldom wider than the optic disc, consist of aggregates of various swollen axons in the nerve fiber layer of the retina.

The affected axons contain numerous degenerated mitochondria and other dense bodies related to the lysosomal system that accumulate because of impaired axoplasmic flow.

Histologically, cross sections of the individual swollen axons resemble cells (“cytoid bodies”).

Cotton-wool spots are reversible if the circulation is restored in time.

Combined occlusion of the central retinal artery and vein.Jpn J Ophthalmol. 1994;38(2):202-7.

A 56-year-old man, complaining of sudden visual loss in his left eye, demonstrated cream-colored retinal edema along a macular branch of the central retinal artery, overall delay of fluorescence in angiography and general depression of the central visual field, which were interpreted as the incomplete form of central retinal artery occlusion (CRAO) mimicking cilioretinal or branch retinal artery occlusion. After receiving paracentesis and fibrinolytic agents, the patient recovered his vision gradually, while the ophthalmoscopic findings progressed to show central retinal vein occlusion (CRVO) changes consisting of dilated and tortuous retinal veins and scattered intraretinal hemorrhages. The condition associated with the retinal edema indicated combined obstruction of the central retinal artery and the central retinal vein (combined CRAO/CRVO). Six months later, both the ocular fundus and the vision returned to normal. The similar cases in Japanese literature in which ophthalmoscopic findings of combined CRAO/CRVO was followed by aggravation of CRVO changes with or without recovery of vision were reviewed.

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