Central Retinal Vein Occlusion

Our Management Regimen for Ischemic CRVO

Since neovascular glaucoma is the most dreaded complication of ischemic CRVO, naturally the question arises how to manage ischemic CRVO. For a logical management of any disease, first one has to understand the basic issues involved and the information available which should act as guidelines. In ischemic CRVO, we have currently the following information available:

Figure 15 (click on image to enlarge)

• A maximum of about 45% of ischemic CRVO patients are likely to develop neovascular glaucoma (Figure 15), (contradicting the common impression among ophthalmologists that a vast majority of these eyes develop neovascular glaucoma); 55% are never going to develop it.⁵
• The risk of developing neovascular glaucoma is mainly during the first 7-8 months of the disease (about 40%)⁵ (Figure 15). After that the risk falls dramatically to 5% or less. So the most crucial period to monitor these patients closely is first 7-8 months.
• The multi-center CRVO study Group showed that prophylactic panretinal photocoagulation in ischemic CRVO does not prevent iris and angle neovascularization.⁴
• Our panretinal photocoagulation study showed that eyes subjected to panretinal photocoagulation usually suffer marked loss of peripheral visual fields²³ (Figures 16,17). Combined with the large central scotoma in these eyes, that peripheral visual fields loss can make these eyes almost blind.

Figure 16

Figure 17.
Visual Field Examples before and after Pan Retinal Photocoagulation

• I find no convincing scientific evidence that panretinal photocoagulation usually helps prevent development of neovascular glaucoma, in spite of claims made to that effect.⁴
• Understanding the natural history of a disease is paramount to its management, so that natural history is not interpreted as beneficial effect of the treatment being advocated. Our natural history studies on the course of ischemic CRVO have revealed that the retinopathy runs a self-limited course, and after a variable length of time it usually burns itself out and resolves spontaneously. Once the retinopathy burns itself out, the stimulus for neovascularization disappears and consequently the anterior segment neovascularization spontaneously starts to regress - a fact usually not appreciated in the management of these eyes. An understanding of this important fact must change our approach to the management of ischemic CRVO and associated anterior segment neovascularization. We need to, so to say, "babysit" for these eyes during that period when they are at maximum risk of developing neovascular glaucoma, i.e. first 7-8 months (Figure 15).

In the light of these facts, I follow the following regimen of management of these patients:

• I follow these patients every 2-3 weeks in my clinic for the first 7-8 months to look for any evidence of anterior segment neovascularization and rise of intraocular pressure. Every 1-2 months I do a complete ophthalmic evaluation.
• If an eye develops moderate to marked anterior segment neovascularization, I start topical steroid therapy because we have the evidence that they have anti-angiogenic properties. (Warning: Topical steroids in steroid responders may cause the intraocular pressure to go high and that may be misdiagnosed as neovascular glaucoma.)
• If the intraocular pressure goes above 21 mmHg, I start topical ocular hypotensive therapy to lower the intraocular pressure. If need be, I may add oral carbonic anhydrase inhibitors also. Most of the time, this medical treatment regimen is enough to keep the intraocular pressure under satisfactory control.
• If the intraocular pressure goes very high and is not controlled by the above medical regimen, then we add graduated cyclocryotherapy (or other graduated cycloablation procedures). In this we first do cyclocryotherapy to 90^o of the ciliary body, and if after a week the intraocular pressure is still high then we do cyclocryotherapy to the adjacent 90^o, i.e. a total of 180^o. In my experience this, combined with medical therapy, can control the intraocular pressure in the vast majority of the eyes. Some of the eyes require repeated cyclocryotherapy to keep the intraocular pressure under control. The universal impression that cyclocryotherapy invariably results in phthisis bulbi is based on aggressive 360^o application at one sitting. Our study showed that a graduated cyclocryotherapy over a period of time, titrated according to the intraocular pressure, is generally not associated with phthisis bulbi.

With this treatment regimen, I have been able to tide many of these eyes over through the first 7-8 months, or until the retinopathy starts to resolve and the stimulus for anterior segment neovascularization starts to subside. After that these eyes start to settle down. So long as the intraocular pressure is maintained within reasonable limits, the eyes maintain the residual peripheral vision. However, a few eyes very rapidly go into fulminant neovascular glaucoma and no amount of any treatment can control the intraocular pressure. In our studies on panretinal photocoagulation, we saw some eyes develop fulminant neovascular glaucoma in spite of early and extensive panretinal photocoagulation of up to about 3,500 burns and finally become totally blind and even developed phthisis bulbi.

Thus, the prevailing impression among ophthalmologists that ischemic CRVO always has a very bleak prognosis and is always associated with neovascular glaucoma and total blindness is shown to be not true for a majority of the eyes in our studies. With proper management and perseverance, many of these patients can maintain a good peripheral vision which is very helpful in steering themselves in this world. In contrast to that, if panretinal photocoagulation is done in every eye with acute ischemic CRVO with the hope of preventing neovascular glaucoma, as is often advocated, then a vast majority of the eyes are going to lose their peripheral vision and that combined with a large central scotoma is going to convert most of the eyes practically blind which otherwise would have had good peripheral vision - that is not a good medicine. Of course, I have seen eyes which became totally blind and even developed phthisis bulbi no matter what treatment was given but those are in a small minority.

Retinal and optic disc neovascularization without neovascular glaucoma tend to develop late (Figure 15), usually when the retinal edema and hemorrhages have largely resolved. In those cases, I do advocate doing panretinal photocoagulation at this late stage in the evolution of the retinopathy; this is because the risk of panretinal photocoagulation causing severe peripheral visual loss is much less at this late stage than during the acute phase, when there is marked retinal edema and hemorrhages. The reason is that much higher laser intensity is required to produce a satisfactory laser burn when the retina has marked edema than when retina has little or no edema. Also, marked retinal hemorrhages during the acute phase of retinopathy absorb the heat. Thus, a combination of these two factors during the acute stages of retinopathy produces marked retinal damage and marked loss of peripheral visual field due to panretinal photocoagulation.