Etiology of Branch Retinal Vein Occlusion (BRVO)
Branch retinal vein occlusion primarily occurs at arteriovenous crossing points where the artery passes over the vein, causing compression and narrowing of the venous lumen, with systemic arterial hypertension, arteriosclerosis, and diabetes being the major risk factors. 1
Pathophysiological Mechanism
Branch retinal vein occlusions typically involve:
Anatomical factors:
- Occur at arteriovenous crossing points where arteries and veins share a common adventitial sheath 1, 2
- Most commonly detected in the superior temporal quadrant of the retina 1, 2
- Compression of the vein by the overlying artery leads to turbulent blood flow, endothelial damage, and thrombus formation 1
Hemodynamic changes:
Major Risk Factors
Systemic Risk Factors:
Hypertension: The most significant risk factor, causing arterial wall thickening and increased compression at arteriovenous crossings 1, 3
Arteriosclerosis: Contributes to vessel wall rigidity and narrowing 1
Diabetes mellitus: Associated with microvascular damage and endothelial dysfunction 1, 3
Hyperlipidemia: Promotes atherosclerotic changes in vessels 3
Metabolic syndrome: The combination of hypertension, diabetes, and hyperlipidemia significantly increases risk 3
Age: Most common in people over 40 years, with peak incidence in the 6th to 7th decade 1
Thrombophilia and hypercoagulable states: May contribute to thrombus formation 3
Ocular Risk Factors:
Glaucoma and ocular hypertension: Associated with increased risk of BRVO 3
Higher ocular perfusion pressure: May contribute to vessel damage 3
Retinal arterial changes: Arterial wall changes can exacerbate compression at crossings 3
Epidemiology
- BRVO is the second most common retinal vascular disorder after diabetic retinopathy 1
- Six to seven times more common than central retinal vein occlusion (CRVO) 1
- Prevalence of approximately 0.5% to 1.2% in the general population 4
- More common in individuals over 40 years of age 1
Clinical Consequences
BRVO can lead to vision loss through several mechanisms:
- Macular edema (most common complication) 1, 4
- Retinal ischemia and capillary non-perfusion 4
- Retinal neovascularization 1, 4
- Vitreous hemorrhage 4
- Epiretinal membrane formation 1
- Tractional retinal detachment 5
Clinical Implications
Understanding the etiology of BRVO is crucial for:
Risk factor management: Optimizing control of systemic hypertension, diabetes, and serum lipid levels is essential 1
Early detection: Identifying patients at risk and monitoring arteriovenous crossings, especially in the superior temporal quadrant 2
Communication with primary care: Informing primary care providers about end-organ damage and coordinating care for systemic risk factors 1
Prevention strategies: Addressing modifiable risk factors to prevent BRVO occurrence and recurrence 3
The pathogenesis of BRVO is multifactorial, with arteriovenous crossing compression being the primary anatomical factor, exacerbated by systemic vascular diseases that affect vessel walls and blood flow. Management should focus on both treating the ocular complications and addressing the underlying systemic risk factors.