Very little progress has been made in the past two decades in elucidating the precise pathogenesis of central retinal vein occlusion (CRVO); controversy still exists about the mechanism of arterial compression of the vein as well as the role of thrombosis. There is less controversy about the pathogenesis of branch retinal vein occlusion (BRVO); compression of the vein by a branch artery is widely accepted, but again the role of thrombosis is unclear.

Although many physicians order a battery of lab tests, only homocysteine and anticardiolipin antibodies have been shown in meta-analysis to be associated with retinal vein occlusion (RVO) (1). Systemic hypertension, atherosclerotic cardiovascular disease, and associated risk factors are risk factors for RVO as well. The role of systemic disease does not lead to a systemic treatment for RVO, although it emphasizes the role of wellness-based approaches to prevention.

Systemic anticoagulation does not prevent RVO; many patients presenting with vein occlusions are adequately anticoagulated (2). Similarly, there is no randomized clinical trial evidence that systemic anticoagulation is effective in the treatment of RVOs.

PHARMACOTHERAPY

Historical treatments of interest include topical administration of potassium iodide and pilocarpine, antihyperlipidemic agents, anticoagulants, fibrinolytic agents, hyperosmotic agents, carbogen inhalation, and isovolemic hemodilution. These treatments have been demonstrated to be largely ineffective and therefore abandoned.

The modern era of pharmacotherapy for RVO began in the 1990s with intravitreal triamcinolone acetonide (Kenalog, Bristol Myers Squibb) injections to treat macular edema. Many observers noted marked decrease in retinal thickness by optical coherence tomography but modest increase in best corrected visual acuity presumably because of ischemia-induced neuronal loss and permanent macular structural changes. Prior to the widespread use of intravitreal triamcinolone, it was thought that steroid glaucoma only occurred in about 6% of the population referred to as steroid responders. This notion was based on studies using topical 1.0% prednisolone acetate. Steroid glaucoma has been shown to occur in approximately 30% of patients receiving intravitreal triamcinolone (3); unfortunately, efficacy is proportional to the steroid glaucoma and cataract side effects. Prior to the use of intravitreal triamcinolone, it was thought that steroid glaucoma was reversible after the drug was withdrawn, but many patients receiving intravitreal triamcinolone develop permanent glaucoma. Steroid cataracts occur in at least 50% of the patients receiving intravitreal triamcinolone (4). The authors do not use intravitreal triamcinolone for RVO patients, but controversy exists among physicians still using this therapy about whether the drug should be used in patients with a personal or family history of glaucoma. Kenalog use is off-label in the United States; the manufacturer sent a warning letter to the retinal community in 2007. Some surgeons filter and resuspend Kenalog, while others decant the diluent to reduce the adverse effects related to preservatives. Triesence (Alcon Laboratories, Ft. Worth, Texas), a preservative-free triamcinolone, received FDA approval in 2007 and addresses the preservative toxicity issue.

Dexamethasone (Decadron) can be used to treat macular edema secondary to RVO but has a very short duration of action, with an approximate half-life of 4 hours (5). Short duration of action reduces the chances of cataract and steroid glaucoma, but the only potential clinical benefit is to reduce retinal thickness a few days prior to laser treatment. Sustained-release dexamethasone (Ozurdex, Allergan), was recently introduced into the US market.The duration of action is longer than intravitreal triamcinolone, with a single treatment producing statistically significant best corrected visual acuity improvements 90 days after treatment. Kuppermann et al. (6) have shown that the dexamethasone molecule is less toxic than triamcinolone without preservative when tested against human retinal neuronal cells, glial cells, and retinal pigment epithelial cells in tissue culture (7,8).

An intravitreal fluocinolone 0.59 mg sustained-release device (Retisert, Bausch & Lomb, St. Louis, Missouri) is FDA approved for posterior uveitis and has been used for the treatment of macular edema by some surgeons. Unfortunately, the Retisert produces a 90% glaucoma incidence, and at least 30% of the patients ultimately require a glaucoma filtering procedure (9). This level of adverse effects is simply not justifiable when treating macular edema secondary to RVO.

Nonsteroidals are effective when used topically for macular edema after cataract surgery. Postoperative macular edema (Irvine-Gass syndrome) is inflammatory in nature, while macular edema in RVO patients is primarily driven by vascular endothelial growth factor (VEGF) and increased hydrostatic pressure. There is little direct evidence that inflammation is a significant factor in macular edema, but the observation that intravitreal steroids reduce macular edema in RVO suggests a role for inflammatory mediators. Ketorolac tromethamine 0.5% (Acular, Allergan, Irvine, California) and diclofenac 0.1% (Voltaren, Novartis Ophthalmics) suppress the anterior segment inflammation that causes postoperative macular edema but have minimal direct effect on the macula. Bromfenac 0.09% (Xibrom, Ista Pharmaceuticals, Irvine, California) and nepafenac (Nevanac, Alcon Laboratories, Ft. Worth, Texas) have been shown to reduce macular edema secondary to retinal vascular disease in several observational series as well as to be effective for postcataract surgery of macular edema (10,11). Nepafenac is a prodrug that has been shown to produce significant drug levels at the macula in phakic and pseudophakic eyes (12).

Proliferative diabetic retinopathy, RVOs, and retinopathy of prematurity all produce high levels of intravitreal VEGF (Lloyd Paul Aiello), which is not the case for retinal detachments or proliferative vitreoretinopathy (PVR) (13

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