Retinal Venous Occlusion (RVO)

• Retinal Venous Occlusion (RVO) involves decreased venous outflow, leading to retinal vascular leakage, macular edema, and intraretinal hemorrhages.
• Vision loss in RVO is associated with macular ischemia/edema, retinal hemorrhages, vitreous hemorrhage, epiretinal membrane formation, rubeosis iridis, and neovascular glaucoma.
• Additional findings include retinal arterial macroaneurysm formation and cilioretinal artery occlusions.

RVO Risk Factors

• Older age is the main risk factor for both CRVO and BRVO, with 50% of patients being over 65 years old.
• A prior RVO in one eye increases the risk of RVO in the fellow eye.
• Patients with a BRVO in one eye have a 10% risk of developing an RVO in the fellow eye over 3 years.
• Arteriovenous crossing changes and high IOP are the primary risks for BRVO.
• Systemic conditions like HBP, hyperlipidemia, diabetes, and coronary artery disease are also risk factors for BRVO.

Classification

• RVO can be classified by the extent of retinal ischemia.

Signs and Symptoms

• Sudden onset unilateral painless vision loss occurs, with the degree of loss depending on whether the RVO is ischemic or non-ischemic.
• Vision worse than 20/200 is associated with non-perfusion (ischemic RVO).

Testing

• FA helps evaluate the degree of ischemia, defined as eyes with >10 disc areas of capillary nonperfusion and extensive retinal hemorrhages.
• OCT is used for detecting macular edema.
• OCTA accurately evaluates changes in microvasculature, differentiating between ischemic and non-ischemic RVO.
• VF testing is part of testing.

Evaluation

• Complete medical and ocular history, retinal imaging, and lab work are needed.
• Lab work consists of CBC, glucose tolerance test, lipid profile, serum protein electrophoresis, chemistry profile, hematologic tests, syphilis serology, and thrombophilic screening.

Retinal Imaging

• FA is essential to detect non-perfused capillary areas and the extent of macular ischemia.
• OCT quantifies the presence and extent of macular edema.
• OCTA accurately evaluates changes in microvasculature.

Differentials

• Ocular Ischemic Syndrome & retinopathy of carotid occlusive disease
• Diabetic Retinopathy DOES NOT respect horizontal
• Papilledema, papillophlebitis
• Radiation therapy

RVO Treatment

• Treat underlying medical conditions, discontinue oral contraceptives, ensure hydration, and consider alternative diuretics.
• Reduce IOP, if elevated.
• Anti-VEGF injections treat macular edema and neovascularization.
• PRP is indicated if NVD or retinal neovascularization is present.
• Aspirin is often recommended, though its efficacy hasn't been proven.

Anti-VEGF

• Vabysmo is a bispecific antibody approved for ME following RVO, with inhibitory effects on both VEGF-A and Ang-2.

Steroids

• Steroids can treat macular edema associated with RVO, but carry risks of cataracts and glaucoma.

Macular Edema Treatment

• First-line treatment involves anti-VEGF therapy with intravitreal bevacizumab, ranibizumab, aflibercept, or faricimab-svoa.
• Second-line treatments include intravitreal triamcinolone and dexamethasone implant.

Neovascularization Treatment

• Peripheral PRP is recommended for patients with NVI and NVA angle.

Laser Photocoagulation

• BVOS demonstrated the efficacy of grid laser photocoagulation surgery for macular edema due to BRVO.
• CVOS did not show any value of focal photocoagulation for macular edema in patients with CRVO.

Follow Up

• Educate patients on the 8-10% risk of an RVO in the other eye.
• Follow-up intervals vary based on VA, with frequent monitoring for neovascularization.

Central Retinal Vein Occlusion (CRVO)

• CRVO: occlusion of the central retinal vein at or posterior to the lamina cribosa.
• Most patients with CRVO are over 50 and men get this slightly more than women.
• Younger patients often have an inflammatory cause and a more benign course.
• Systemic HTN, DM, and open-angle glaucoma are risk factors.

Etiology

• A/V mechanical compression occurs.
• Occlusion at the lamina cribosa occurs.
• Blood disorders & inflammation are causes.

Non-Ischemic CRVO

• VA is better than 20/400.
• Has no/mild RAPD.
• Signs: tortuous and dilated veins, dot & blot & flame-shaped hemorrhages, some cotton wool spots, disc edema, macular edema.
• Often converts to ischemic form.

Ischemic CRVO

• VA is worse than 20/400.
• RAPD is present.
• ERG shows decreased b wave amplitude.
• VF shows constriction.
• Signs: retinal hemorrhages (4 quadrants), dilated & tortuous retinal veins, superficial hemorrhages, CWS, and macular edema.
• Neovascularization (anterior > posterior) occurs.
• Can have a vitreous hemorrhage.
• Neovascular glaucoma occurs in 60% of patients.

Impending CRVO

• Mild blurring, worse on awakening and improves during the day are symptoms.
• Mild dilation and tortuosity of veins and scattered flame-shaped hemorrhages are signs.

Hemiretinal Vein Occlusion (HRVO)

• HRVO is an occlusion at the disc involving half of the retinal venous drainage.
• Vascular tortuosity and dilation, retinal and macular edema & retinal hemorrhages noted.
• Late findings: collaterals, disc edema, neovascularization, vitreous hemorrhage, neovascular glaucoma.

Branch Retinal Vein Occlusions (BRVO)

• BRVOs occur at arteriovenous crossing points.
• Vein compression causes endothelial cell loss, thrombus formation and potential occlusion.
• Complete or partial obstruction at a branch of the CRV.
• Have sudden, onset, unilateral painless decreased vision loss w/ a VF defect.

Signs of BRVO

• Vein dilated & tortuous
• Occlusion site at AV cross point
• Flame shape, dot/blot heme
• Retinal edema
• May have CWS in area

BRVO Late Clinical Findings:

• Collaterals
• Sclerosed vessels, exudate
• Neovascularization: posterior segment > anterior segment that may lead to recurrent vitreous heme or pre-retinal heme, and occasionally tractional retinal detachment.
• Macular edema; chronic macular edema most common cause of persistent poor VA.

Retinal Arterial Occlusions (RAO)

• RAO is a blockage of one or more arteries of the retina.
• Treated as a brain stroke.
• GCA should be suspected in patients over 50 years of age, consider urgent systemic corticosteroid therapy when GCA is diagnosed.
• Partial or complete obstruction of any of the branch tributaries of the CRA.

Pathophysiology

• Emboli are the MOST COMMON CAUSE!
• Non-embolic: Thrombosis, Atherosclerosis, Vasculitis

Risk Factors

• Common ones: HTN, Hyperlipidemia, Carotid occlusive disease, Cardiac disease, Diabetes

Central Retinal Artery Occlusion

• Impending stroke = patient needs to be sent to hospital immediately
• Causes sudden, unilateral painless decrease in vision and field of vision.
• Preceded by amaurosis fugax.
• Early signs: RAPD, emboli, whitening of the posterior pole of retina, cherry red spot in the macula & box-carring or segmentation of arterioles.
• OCt shows thickening & increased inner retinal reflectivity may be present, followed by inner retinal thinning in chronic RAO
• FA shows a delayed arm to retina time period.

Branch Retinal Artery Occlusion

• Causes Unilateral, painless, sudden partial VF loss

Management

• Acute, symptomatic artery occlusions with visible emboli should prompt an immediate referral to the nearest stroke referral center!
• Occlusion beyond the 240 minutes results in catastrophic, irreversible retinal damage.
• Digital ocular massage as well as topical pressure lowering therapies is proposed as an intervention.

Ophthalmic Artery Occlusion

• Causes a Diffusely pale retina with No cherry red spot and LP/NLP in vision.
• GCA is likely!

Susac Syndrome

• Usually affects young women and involves BRAO, hearing loss & headaches with focal neurologic signs. AWH = Arterial Wall Hyperflourescence and Gass plaques can be seen

Ocular Ischemic Syndrome

• Severe blood restriction to the anterior and posterior ocular segments.
• Usually monocular in 80% of cases.
• Causes vision loss and ocular angina.
• Retinal arteries narrowing and dilated veins with no signs of tortuosity.
• Retinopathy of occlusion, Hypoperfusion retinopathy/venous stasis retinopathy veins are dilated and not tortuous & in the mid-periphery