Central Retinal Vein Occlusion
A 'stroke' of the main vein leaving the eye, causing severe retinal bleeding, swelling, and sudden painless loss of vision.
Emergency Management: Neovascular glaucoma with intraocular pressure >40 mmHg. Requires emergent topical hypotensive drops, systemic Diamox, and urgent Anti-VEGF injection and PRP laser.
A vascular disorder of the eye caused by occlusion of the central retinal vein at the level of the optic nerve head, leading to backup of venous blood, elevated retinal venous pressure, severe retinal hemorrhage, and potentially severe painless vision loss.
Detailed Overview
The central retinal artery and vein share a common adventitial sheath as they exit the optic nerve at the lamina cribrosa. Atherosclerosis of the artery can compress the adjacent vein, causing turbulent flow, endothelial damage, and thrombus formation. The blockage causes extensive intraretinal hemorrhages ('blood') and severe macular edema ('thunder'). It is classified as ischemic (worse prognosis, high risk of neovascularization) or non-ischemic.
Epidemiology & Demographics
One of the most common retinal vascular diseases after diabetic retinopathy. Usually occurs in patients over 50 years old. Affects roughly 0.1-0.4% of the population.
Etiological Mechanism
Thrombus formation in the central retinal vein at the lamina cribrosa, driven by Virchow's triad (stasis, endothelial damage from adjacent rigid arterial compression, and hypercoagulability).
Primary Causes
["Arteriosclerosis of the adjacent central retinal artery", "Glaucoma (increased intraocular pressure compressing the vein)", "Hypercoagulable states (Factor V Leiden, polycythemia, multiple myeloma)"]
Occlusion blocks venous drainage. Blood backs up into the retinal capillary bed, increasing hydrostatic pressure. Capillaries rupture, causing flame-shaped and dot-blot hemorrhages throughout all four quadrants of the retina. Increased pressure also causes fluid extravasation, leading to massive macular edema (the primary cause of vision loss). In the ischemic variant, severe capillary non-perfusion leads to profound retinal hypoxia, triggering VEGF release and subsequent devastating neovascularization.
Diagnostic Criteria & Guidelines
Clinical diagnosis based on dilated fundus examination showing characteristic 4-quadrant hemorrhages and tortuous veins. Fluorescein angiography distinguishes ischemic vs non-ischemic by quantifying capillary non-perfusion.
Intravitreal Anti-VEGF injections (e.g., Aflibercept 2 mg, Ranibizumab 0.5 mg, or Bevacizumab 1.25 mg) injected directly into the eye every 4 weeks. This drastically reduces macular edema and improves vision. Immediate systemic management of hypertension and glaucoma.
Second-Line & Adjunctive Therapy
Intravitreal Corticosteroids (e.g., Dexamethasone 0.7 mg implant [Ozurdex]) for patients who fail anti-VEGF therapy, noting the risk of inducing cataracts and raising intraocular pressure.
Surgical & Procedural Management
Panretinal Photocoagulation (PRP) laser surgery is absolutely indicated if anterior segment neovascularization (rubeosis iridis) or neovascular glaucoma develops. PRP destroys ischemic peripheral retina to halt VEGF production.
Patient Counseling & Advice
Warn the patient that they require long-term, frequent eye injections to maintain vision. Emphasize that severe eye pain in the affected eye could signal neovascular glaucoma and requires an immediate emergency visit.
Follow-Up & Monitoring Schedule
Monthly visits for OCT and Anti-VEGF injections. Gonioscopy and undilated iris exam at every visit to check for neovascularization, particularly during the first 3-6 months.
Preventive Strategies
Optimization of systemic cardiovascular risk factors and routine glaucoma screening.
Non-ischemic CRVO: about 50% regain 20/40 or better vision with treatment. Ischemic CRVO: very poor visual prognosis, with high risk of blindness and loss of the eye if neovascular glaucoma is not prevented.