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Retinal vein occlusion is the second most common retinal vascular disease after diabetic retinopathy.1 Obstruction of any of the venous vessels within the retinal vascular system results in changes in both the appearance of the fundus and the function of the retina. Blockage of a retinal vein causes elevated venous and intracapillary pressures and subsequent slowing of the arterial blood flow in the region drained by the vein. The visual defects and retinal damage from the venous obstruction depend primarily on the rapidity of its development, the severity of the occlusion, and the availability of collateral pathways of venous outflow.


Venous occlusion is divided into three anatomical categories: central retinal vein occlusion (CRVO), hemiretinal vein occlusion (HRVO), and branch retinal vein occlusion (BRVO).

Central Retinal Vein Occlusion. CRVO is a relatively common cause of loss of vision, particularly the elderly individuals, with 90% of CRVO occurring in patients 50 years of age and older.1 CRVO develops when the circulation of the retina is compromised because of venous obstruction. CRVO is broadly divided into two main categories: ischemic and non-ischemic. The signs, symptoms, prognosis, and treatments differ between those groups.

Pathophysiology. Although the exact cause of CRVO is still unknown, both local and systemic factors appear to play a role. The central retinal vein and artery share a common sheath within the optic nerve head, and obstruction of the vein usually occurs near the narrowing at the lamina cribrosa.2 Arteriosclerosis may cause crowding and narrowing of the vein, which may ultimately lead to thrombus formation and occlusion. Various stages of thrombi at this location were identified by Green et al.2 Histopathology also identified inflammation at the region of the thrombus in and around the vein wall, endothelial cell proliferation, and arterial occlusive disease.2 Damage to the capillary bed of the retina may lead to chronic retinal edema with permanent damage to the macular retinal cells. Ischemia of the retina may cause the release of vascular endothelial growth factor (VEGF) and other angiogenic factors that promote the development of neovascularization, particularly of the iris, with subsequent angle closure and severe glaucoma.

Risk Factors. Ocular conditions may have a predisposing effect leading to development of CRVO, including open-angle glaucoma3 and drusen of the optic nerve head.2. As one might expect, systemic vascular diseases, including hypertension, cardiovascular disease, carotid artery disease, and diabetes, are also risk factors for CRVO.3,4 Blood dyscrasias, hypercoaguable states,5 systemic autoimmune diseases, systemic vasculitis, and oral contraceptive use in women have been associated with CRVO.

Symptoms. Patients with CRVO present with mild to severe visual loss occurring over days to weeks. Transient obscurations of vision may precede the actual loss of central acuity. If neovascular glaucoma develops, the eye will become inflamed, ...

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