Central retinal vein occlusion is generally categorized into two forms: non–ischemic and ischemic. This means that some central retinal vein occlusions are associated with significant obstruction of capillaries or non–perfusion. This predisposes to a peculiar type of neovascularization that occurs in front of the eye on the iris (rubeosis irides). These eyes may develop a very high pressure known as neovascular glaucoma due to obstruction of the fluid outflow channels. This is a very serious complication which is associated with severe vision loss and may cause pain and loss of the eye itself. Laser photocoagulation treatment is very useful in managing rubeosis irides. If performed early in the course (when iris neovascularization is first detected), it may help prevent these complications. Patients with recent central retinal vein occlusions must be followed frequently in order to detect this complication in a timely manner.

Less frequently than in branch vein occlusion, patients with central retinal vein occlusion may also develop neovascularization in the back of the eye, causing vitreous hemorrhage and retinal detachment. Laser treatment may be useful in managing these complications.

This is a color photograph showing diffuse intraretinal hemorrhage of a central retinal vein occlusion.

As with branch retinal vein occlusion, macular edema, and non–perfusion is also frequently seen with central retinal vein occlusion. Macular edema, even without significant macular ischemia, is not treated routinely with laser photocoagulation. This is because a recent study failed to show a benefit for patients with central retinal vein occlusion, particularly for those who are elderly. (In contrast, laser treatment has been shown to be effective for patients with branch retinal vein occlusion). It is possible, but not proven, that some young patients with central vein occlusion of the non–ischemic type may benefit from localized laser treatment for macular edema.

Optical Coherence Tomography showing macular edema from a central vein occlusion.

Some patients with macular edema from central vein occlusions may respond to the off-label intraocular injection of steroids (triamcinolone) or anti–vasogenic drugs (Avastin). These pharmacologic agents wear off over a period of approximately two months and may need to be re-injected if the edema returns. Optical Coherence Tomography (OCT) is a useful test for the detection of macular edema in CRVO and for following the response to treatment.

If the fluorescein angiogram indicates that capillary non–perfusion is the cause of the vision loss, it is unlikely that the vision will improve significantly over time regardless of any treatment.

If a patient develops an occlusion of the central vein in both eyes, there is a greater possibility of an underlying systemic cause. It is recommended (by our group) that such patients have a thorough medical workup as outlined previously.

Sometimes in venous occlusive disease, scar tissue can form on the surface of the retina. This condition, which is called a macular pucker or an epiretinal membrane, may result in distorted vision (metamorphopsia) which is not improved with laser or pharmacologic treatment. Vitrectomy surgery may be indicated for the removal of a macular pucker.

The most devastating potential problem in a vein occlusion is that of neovascularization. The neovascularization may develop in 40% of those cases where branch vein occlusions produce large areas of capillary non–perfusion. This retinal neovascularization generally develops in the first 6 to 12 months after the occlusion. Unless laser treatment is performed, at least 60% of the patients with neovascularization will experience episodes of vitreous hemorrhage. In severe cases of neovascularization, retinal detachment can occur from pulling by these vessels and associated scar tissue on the retina (traction detachment).