20/200, depending on the disease severity. Patients with ischemic CRVO have severe visual impairment, and the VA usually decreases to 20/200 or less and even to hand motions in some cases. The VA of patients with nonischemic CRVO is better than that in ischemic CRVO and is usually better than 20/200; VA better than 20/40 is not rare. Patients rarely report ocular pain unless rubeotic glaucoma develops.

The symptoms associated with BRVO depend on the amounts and location of damage compromised by the occlusion. Patients with macular involvement report blurred vision and a relative visual field defect. Patients with peripheral occlusions are usually asymptomatic.

Patients with RVO are systemically asymptomatic; however, they may have systemic symptoms due to systemic diseases associated with CRVO, including hypertension and cardiovascular diseases.

TREATMENT OPTIONS

CENTRAL RETINAL VEIN OCCLUSION

Medications for CRVO include tissue plasminogen activator (tPA), corticosteroids, and bevacizumab (Avastin). Other medications of coumadin (warfarin), urokinase, troxerutin, ticlodipine, and pentoxifylline were also reported. Other treatments are hemodilution, laser treatment (including panretinal photocoagulation, grid macular photocoagulation, and chorioretinal venous anastomosis). Radial optic neurotomy (RON) is a surgical option.

BRANCH RETINAL VEIN OCCLUSION

Treatments for BRVO include corticosteroids and bevacizumab (Avastin), laser treatment using grid macular laser photocoagulation, and arteriovenous crossing sheathotomy.

TREATMENT OUTCOMES AND PROGNOSIS

CENTRAL RETINAL VEIN OCCLUSION

clinical trial of 728 eyes with CRVO, the VA outcomes largely depend on the initial VA. The baseline VA was 20/40 or better (good VA) in 29%, 20/50–20/200 (intermediate VA) in 43%, and 20/250 or worse (poor VA) in 28%, with a median baseline VA of 20/80. Sixty-five percent of patients who had an initially good VA (20/40 or better) maintained good VA at the end of the study. The visual outcomes in eyes with intermediate VA (20/50–20/200) varied: 21% improved to better than 20/50, 41% stayed in the intermediate range, and 38% had worse than 20/200. Patients with poor VA (<20/200) at the first visit had an 80% chance of having VA less than 20/200 at the final visit.23

TISSUE PLASMINOGEN ACTIVATOR (tPA)

tPA converts plasminogen to plasmin and destabilizes intravascular thrombi. tPA reduces clot size in occlusive vessels, resulting in dislodgment of the entire thrombus or recanalization of the occluded retinal vein. When used to treat CRVO, tPA has been administered by several routes: systemic, intravitreal, and by endovascular cannulation of retinal vessels. Systemic administration of low-dose (50 mg) tPA resulted in a VA increase of one line or more in 10 (7 CRVO, 3 BRVO) of 14 patients (8 CRVO, 6 BRVO) with RVO.24 The VA improved 2 lines or more in 10 of 23 patients with CRVO.25 However, one patient died of an intracranial hemorrhage following tPA administration.26 Intravitreal administration of tPAis associated with less risk of systemic complications. tPAinjected into the vitreous cavity subsequently reaches the retinal vessels. tPA (65–110 g) was injected intravitreally in 23 patients with CRVO with recent onset of visual symptoms and the VA improved or stabilized in 16 eyes (70%).27 Another study reported that 4 of 9 patients with CRVO treated with 100 g of tPA intravitreally had 3 lines or more of VA improvement.28 However, tPA is associated with retinal toxicity.29 Endovascular delivery of tPA involved cannulation of retinal vessels and tPA was injected directly into the occluded retinal vein, resulting in release of the suspected thrombus. Pars plana vitrectomy followed by cannulation of a branch vein and, with the help of a stabilization arm, injection of a bolus of 200 g/ml of tPA toward the optic nerve head improved the VAmore than 3 lines in 50% of 28 eyes after a mean followup of 12 months. Complications included vitreous hemorrhage in 7 eyes and retinal detachment in 1 eye.30

CORTICOSTEROIDS