Triamcinolone (Aristospan, Kenalog)

Intraocular steroid injection has been shown to be effective in decreasing macular edema. Although the exact mechanism of action is unknown, steroids work by targeting various inflammatory pathways and decreasing expression of VEGF, reducing vascular permeability, stabilizing endothelial tight junctions, and decreasing macular edema.

Dexamethasone intravitreal implant (Ozurdex)

Intraocular steroid injection has been shown to be effective in decreasing macular edema. Although the exact mechanism of action is unknown, steroids work by targeting various inflammatory pathways and decreasing expression of VEGF, reducing vascular permeability, stabilizing endothelial tight junctions, and decreasing macular edema.

 

Follow-up

Further Outpatient Care

 

Since neovascular complications and development of second venous occlusions can develop after central retinal vein occlusion (CRVO), all of these patients need follow-up care for long periods of time.

 

CVOS recommended careful observation with frequent follow-up examinations in the early months for detection of iris neovascularization and prompt treatment.

 

Patients with poor initial visual acuity should be monitored every month during the first few months and spaced thereafter, depending on the course of the disease. These criteria apply more for patients with ischemic CRVO than with patients with nonischemic CRVO.

 

With any associated complications, follow-up care should be individualized.

Deterrence/Prevention

 

Optimal control of associated systemic diseases may reduce the incidence of similar occlusions in the fellow eye.

 

Even though controversial, good control of intraocular pressure in patients known to have glaucoma may prevent CRVO.

Complications

Ocular neovascularization is a potential complication. ^[33] Anterior segment neovascularization can lead to neovascular glaucoma. Posterior segment neovascularization can lead to vitreous hemorrhage.

 

Macular edema is another potential complication. ^{[51, 38, 52]} Macular edema is the common cause of decreased vision in CRVO, more so in the nonischemic type. It may resolve with good visual return. The patient may develop permanent degenerative changes with poor visual prognosis and may develop cystoid macular edema leading to lamellar or full-thickness macular hole.

 

Other potential complications include cellophane maculopathy and macular pucker, as well as optic atrophy.

 

Reported complications due to treatment with intravitreal injections include endophthalmitis, vitreous hemorrhage, and retinal detachment.

 

Prognosis

For nonischemic CRVO, complete recovery with good visual recovery occurs only in about 10% of cases. Fifty percent of patients will have 20/200 or worse vision. About one third of patients convert to ischemic CRVO. CVOS noted that, of 547 eyes initially diagnosed to have nonischemic central retinal vein obstructions, 185 (34%) progressed to become ischemic central retinal vein obstructions within 3 years; 15% converted within the first 4 months.

 

For ischemic CRVO, more than 90% of patients will have 20/200 or worse vision. About 60% of patients develop ocular neovascularization with associated complications. About 10% of patients can develop CRVO or other type of vein occlusions within either the same eye or the contralateral eye within 2 years.

 

The long-term prognosis of CRVO has significantly improved with new anti-VEGF agents and steroids, maintaining good visual acuity for a long duration in most patients, except those with severe ischemic maculopathy. Development of neovascular complications has also decreased with continued monitoring and anti–VEGF treatment.

 

Patient Education

Good control of systemic medical problems is important, as are regular medical and ophthalmologic checkups.

 

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