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This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.
The Bottom Line
- CRVO causes painless monocular vision loss with “blood-and-thunder” retina
- Fundus: diffuse retinal hemorrhages in all quadrants, dilated tortuous veins, cotton-wool spots, and disc edema
- Major risk factors: age, hypertension, diabetes, hyperlipidemia, smoking, and glaucoma/ocular hypertension
- Vision loss is commonly due to macular edema; first-line treatment is intravitreal anti-VEGF therapy
- Ischemic CRVO can cause iris neovascularization and neovascular glaucoma — monitor closely
Overview
Central retinal vein occlusion (CRVO) results from thrombosis or compression of the central retinal vein, usually at or near the lamina cribrosa. Venous outflow obstruction causes retinal hemorrhage, edema, ischemia, and increased VEGF expression. CRVO is classified as nonischemic or ischemic. Ischemic CRVO has worse visual prognosis and higher risk of anterior segment neovascularization and neovascular glaucoma.
Epidemiology
CRVO typically occurs in older adults with systemic vascular risk factors. Hypertension is the most common systemic association. Other risks include diabetes mellitus, hyperlipidemia, smoking, glaucoma, ocular hypertension, sleep apnea, hyperviscosity, antiphospholipid syndrome, and inherited thrombophilias in younger patients. Open-angle glaucoma is a particularly important ocular risk factor because elevated IOP impairs venous outflow.
Clinical Features
Symptoms
Painless unilateral blurry vision or vision loss, often developing over hours to days
Central distortion or decreased reading vision from macular edema
Floaters may occur if vitreous hemorrhage develops
Pain is uncommon initially; painful red eye later suggests neovascular glaucoma
May be mild or incidental in nonischemic CRVO
Signs
Blood-and-thunder fundus: diffuse intraretinal hemorrhages in all quadrants
Dilated tortuous retinal veins
Cotton-wool spots, optic disc edema, and macular edema
Relative afferent pupillary defect suggests ischemic CRVO
Iris neovascularization or elevated IOP suggests neovascular glaucoma
Investigations
First-line
Dilated fundus examinationDiffuse hemorrhages, venous tortuosity, cotton-wool spots, disc edema, and macular edema support CRVO
Visual acuity and pupillary examPoor acuity and RAPD suggest ischemic CRVO and worse prognosis
Intraocular pressure measurementAssess for glaucoma/ocular hypertension and neovascular glaucoma
Second-line
Optical coherence tomography (OCT)Quantifies macular edema and guides anti-VEGF treatment response
Fluorescein angiographyAssesses capillary nonperfusion, macular ischemia, leakage, and neovascularization
Systemic risk evaluationBlood pressure, HbA1c/glucose, lipid panel, CBC; consider hypercoagulable testing in young patients or bilateral/recurrent disease
Specialist
Retina follow-upSerial OCT and surveillance for iris/angle neovascularization, particularly during the first 3-6 months
GonioscopyEvaluates angle neovascularization when ischemic CRVO or elevated IOP is present
1
Initial management
- Refer to ophthalmology/retina for classification as ischemic vs nonischemic and baseline OCT
- Optimize systemic risk factors: BP, diabetes, lipids, smoking, sleep apnea, and cardiovascular risk
- Check and treat elevated IOP or glaucoma
2
Macular edema
- Intravitreal anti-VEGF therapy is first-line for vision loss from macular edema
- Common agents: aflibercept, ranibizumab, or bevacizumab; treatment interval is guided by OCT and visual response
- Intravitreal corticosteroid implant may be considered second-line but increases cataract and glaucoma risk
3
Ischemic CRVO and neovascular complications
- Monitor closely for iris neovascularization and neovascular glaucoma
- Panretinal photocoagulation is indicated when neovascularization develops, not prophylactically for every CRVO
- Anti-VEGF may be used for rapid regression of neovascularization while definitive laser is arranged
4
What not to do
- Routine systemic anticoagulation does not treat typical CRVO unless another indication exists
- Do not confuse with CRAO: CRAO requires emergent stroke-center evaluation for arterial ischemia
Complications
- Chronic macular edema: Main cause of persistent visual impairment
- Macular ischemia: Poor visual recovery despite edema control
- Neovascular glaucoma: Painful red eye with high IOP after ischemic CRVO
- Vitreous hemorrhage: From retinal neovascularization
- Conversion: Nonischemic CRVO can convert to ischemic CRVO
USMLE Step 2 CK Exam Tips
- 1Blood-and-thunder retina = central retinal vein occlusion
- 2CRVO is diffuse hemorrhages in all quadrants; branch retinal vein occlusion is sectoral hemorrhage
- 3CRAO = pale retina with cherry-red spot; CRVO = hemorrhagic congested retina
- 4Most common systemic risk factor is hypertension; important ocular risk factor is glaucoma
- 5Macular edema from CRVO is treated with intravitreal anti-VEGF
- 6Painful red eye after CRVO suggests neovascular glaucoma
- 7Routine anticoagulation is not the Step 2 CK treatment for uncomplicated CRVO
- 8RAPD and very poor vision suggest ischemic CRVO
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