Ocular Vascular Occlusive Disorders

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In contrast to that, ischemic CRVO is a severely blinding disease, with a high incidence of anterior segment neovascularization, particularly, neovascular glaucoma. The major complication is chronic macular edema Figure 13 , leading on to cystoid macular degeneration, and permanent central scotoma; however, the peripheral visual field always remains normal. If an eye with non-ischemic CRVO has a cilioretinal artery, then that eye develops cilioretinal artery occlusion Figure 14 and an associated visual field defect and may produce sectoral optic atrophy.

The most important complication is the development of ocular neovascularization, with neovascular glaucoma as the most dreaded complication. Other complications of ischemic CRVO are vitreous hemorrhage, macular degeneration, optic atrophy, retinitis proliferans, phthisis bulbi or loss of eye.

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In ischemic CRVO the neovascularization is mainly of the anterior segment. Figure 15 is a graphic representation of cumulative chances of developing various types of neovascularization NV in ischemic CRVO. On the X axis for figure 15 are the days from the onset of ischemic CRVO, and on the Y axis is the cumulative chance or probability of developing neovascularization. The various graphs are, from above down, for iris neovascularization, angle neovascularization, neovascular glaucoma, disc neovascularization and retinal neovascularization.

These graphs provide very important information on a number of issues, including the following:. In my experience, the latter source of vitreous hemorrhage is much more common than the former, and can occur in non-ischemic as well as ischemic types of CRVO, usually during the early stages of the disease. Sometimes the vitreous hemorrhage can occur from intraretinal microvascular abnormalities secondary to CRVO or development of posterior vitreous detachment.

For proper management of a disease, understanding the natural history of the disease is absolutely essential, so that the natural history may not be interpreted as a beneficial effect of the treatment being advocated. I have discussed elsewhere the following aspects of natural history of CRVO. In , I analyzed the final visual acuity in consecutive non-ischemic CRVO eyes with completely resolved retinopathy who were followed in my clinic up till Table 2 gives the final visual acuity achieved in these eyes.

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Management of CRVO still remains uncertain and highly controversial. Over the years many treatments have been advocated enthusiastically and success claimed but none has stood the test of time. These include anticoagulants, hemodilution, corticosteroids, acetazolamide, fibrinolytic agents, low molecular weight dextran infusion, carbon dioxide inhalation, vasodilators, hyperbaric oxygen, ocular hypotensive therapy, surgical decompression of CRVO, laser-induced chorioretinal anastomoses, photocoagulation, and a host of others.

The most important consideration when evaluating a therapy for any disease is to determine whether the therapy is based on incontrovertible scientific facts. Treatments without such a logical foundation prove not only useless but also sometimes harmful. Recently I have reviewed the various advocated modes of treatment in CRVO and their scientific validity [ 6] This review revealed that, unfortunately, most of the advocated treatments lack an incontrovertible scientific basis. Successes and beneficial effects claimed for many therapies in most cases simply represent the natural history of the disease, and that basic fact has been ignored in almost all the studies.

Ocular Vascular Occlusive Disorders

The fact that I would like to stress at the outset is that ischemic CRVO is a different, far more serious and potentially blinding disease than non-ischemic CRVO, and it requires wholly different management. Following is a brief account of the major therapies advocated and tried from time to time. The main treatments can be divided into three categories: A medical, B surgical and C photocoagulation. Complications : Various studies have reported a number of complications which can be divided into immediate and late complications.

When evaluating the validity of claims of improved visual acuity in any study in the literature, one has to be aware of the possibility that apparent "improvement" in visual acuity can simply be the result of multiple artifacts in visual acuity testing which is often done by technicians. In my experience of repeated testing of visual acuity, myself, in about three thousand patients with various circulatory disorders of the eye e.

This applies particularly to an eye which has a visual field defect or a scotoma passing through or just involving the central fixation spot. Eyes with nonischemic CRVO invariably have poor visual acuity due to central scotoma. That is why reports of improved visual acuity without corresponding improvement of central visual field defects can be misleading. It is therefore evident from the available data that the visual outcome apparently achieved in eyes with nonischemic CRVO by laser-induced chorioretinal venous anastomosis seems no better, if not worse, than the natural history of the disease.

On the top of that, the procedure is associated with a fairly high risk of serious vision threatening complications, not seen in non-ischemic CRVO. Conclusion : It is evident that the complications of laser-induced chorioretinal venous anastomosis for treatment of non-ischemic CRVO heavily outweigh any dubious benefits, and that this is not a safe and effective mode of treatment for a condition which has a fairly good outcome if simply left alone see "Natural history of CRVO" above.

In the management of CRVO, panretinal photocoagulation has been widely advocated as the treatment of choice. The presumed role of panretinal photocoagulation in retinal diseases is to prevent development of neovascularization in eyes with retinal ischemia. Moreover, panretinal photocoagulation is not a harmless procedure; it can produce loss of peripheral visual fields in CRVO see below - Figures 16,17 and may cause defective vision in the dark. Some ophthalmologists advocate the use of macular grid photocoagulation for microcystic macular edema; however, a recent multicenter CRVO photocoagulation study revealed that it has no beneficial effects in these eyes and does not improve visual acuity[ 22].

In my experience, some patients may land up with much worse central scotoma from such a treatment. Thus, photocoagulation has no role whatsoever in the management of non-ischemic CRVO. Ischemic CRVO : It has been almost universally accepted that prophylactic panretinal photocoagulation is the treatment of choice to prevent neovascular glaucoma or treat neovascular glaucoma itself. I have found little definite scientific proof in support of this assumption[ 23].

Therefore, we investigated this in a year prospective study, to find out its effect on ocular neovascularization, particularly neovascular glaucoma associated with ischemic CRVO.


The results, which were very surprising, were published in [ 23]. Thus, contrary to the prevalent impression, our study showed that panretinal photocoagulation has no statistically significant beneficial effect in reducing neovascular glaucoma. On the other hand, it markedly damages the peripheral visual field, and may convert an eye with normal peripheral vision into almost a blind eye. The most important feature of any study is its design, because that can determine its conclusions and their validity.

Based on my clinical and experimental study on CRVO during the past 30 years, I have some important concerns about the baseline design of the study[ 25].

Central Retinal Artery Occlusion | Johns Hopkins Medicine

For a study claiming beneficial effects of panretinal photocoagulation on anterior segment neovascularization in ischemic CRVO, it is imperative to ask at least the following three very basic questions:. When all these facts are put together, a very different perspective on ischemic CRVO emerges - and, consequently, a different perspective on its management. Central Retinal Artery Occlusion. Hemicentral Retinal Artery Occlusion.

Branch Retinal Arteriolar Occlusion.

tailacbuchef.ga Cilioretinal Artery Occlusion. Ischemic Optic Neuropathies. Anterior Segment Ischemia. Ocular Ischemic Syndrome. Ophthalmic Manifestations of Carotid Artery Disease.

Arterial Hypertension and the Eye. Central Retinal Vein Occlusion. Hemicentral Retinal Vein Occlusion. Branch Retinal Vein Occlusion. Vortex Vein Occlusion.

Vision loss due to Retinal Vein Occlusion (RVO)

However, other factors that affect blood flow can put you at a higher risk of having retinal vascular occlusion. These risk factors include:.

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The primary symptom of retinal vascular occlusion is a sudden change in vision. This could include blurry vision, or a partial or complete loss of vision. The vision symptoms usually only occur in one eye. Physical pain is not a symptom of retinal vascular occlusion.


The changes in eyesight could be short term or permanent, depending on how quickly you seek treatment and if you have other health conditions. You should make an appointment with your ophthalmologist, or eye doctor, right away if you experience any changes in your vision. Definitely go to the emergency room immediately if you suddenly lose your vision in one eye. The condition can occasionally lead to complications and more serious symptoms. Vision may be severely and permanently affected if any of the following complications occur:. Macular edema is a swelling in the macula, or the central part of your retina, due to a buildup of blood.

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  • Neovascularization is an abnormal growth of blood vessels caused by poor blood flow and a lack of oxygen to your retina. Neovascular glaucoma involves fluid buildup and high pressure in your eye.