Background
Much confusion exists in the literature because central retinal vein occlusions and branch retinal vein occlusions (BRVOs) often are grouped and studied together. The natural history and the complication rate for each entity differ. [1] The treatments and their results vary from one condition to the other. This article deals exclusively with BRVOs. Hemiretinal vein occlusions probably are variants of central retinal vein occlusions, and, as such, they are not included in this discussion.
Pathophysiology
Hypertensive, atherosclerotic, inflammatory, or thrombophilic conditions may lead to retinal endothelial vascular damage. [1] In eyes with an anatomic predisposition, intravascular thrombus formation may occur. Up to two thirds of BRVOs occur in the supertemporal quadrant. This rate may be related to the increased number of arteriovenous crossings in this quadrant with respect to the rest. In addition, nasal BRVOs often are asymptomatic; therefore, patients with this type of BRVO do not seek ophthalmic evaluation. Eyes with arteriovenous crossings appear to be at risk for BRVO. In these eyes, the artery is anterior to the vein in most cases. The artery and the vein share a common adventitial sheath. Increased arterial stiffness may be a mechanical factor in the pathogenesis of BRVO.
Arterial compression of the vein is believed to be the main cause of BRVO. [1] Compression of the vein may lead to turbulent flow in the vein. The turbulent flow in combination with the preexisting endothelial vascular damage from the different conditions creates a local environment favorable to intravascular thrombus formation. Once the venous flow is compromised or interrupted, retinal ischemia ensues downstream from the site of occlusion. Retinal ischemia is one of the most important up-regulators of vascular endothelial growth factor (VEGF) production. [2]
In a rat model, BRVO resulted in a rapid transient increase in the expression of VEGF and a delayed increase in the expression of pigment epithelial derived factor (PEDF), the most potent endogenous inhibitor of VEGF. [3, 4] VEGF has been shown to be a key molecular player in the pathogenesis of the major complications of a BRVO, macular edema and retinal neovascularization. [5] VEGF secretion causes breakdown of the blood-retinal barrier, contributing to the formation of macular edema. [1] The intraocular levels of VEGF are increased in eyes with macular edema secondary to BRVO. These elevated VEGF levels are correlated to the degree and severity of the areas of capillary nonperfusion and macular edema. [6] Undiluted vitreous samples from eyes with untreated acute BRVO demonstrate elevated levels of proinflammatory and proangiogenic cytokines. [7]
Rehak et al also have reported that there is down-regulation of potassium and water channels in Müller cells, which leads to intraretinal accumulation of fluid contributing to the formation of macular edema. [4]
Epidemiology
Frequency
United States
Retinal vein occlusions (branch and central) are the second most common retinal vascular diseases after diabetic retinopathy. [1] The Beaver Dam Study reported a prevalence of 0.6% in patients older than 43 years. The 15-year cumulative incidence of BRVO was 1.8% in the Beaver Dam Eye Study. [8] A cross-sectional study from 6 communities across the United States reported that the prevalence of BRVO was 0.9%. Furthermore, this same study showed that the prevalence of BRVO was similar across different ethnic and racial groups. [9]
International
In a population-based study from Australia, the Blue Mountains Eye Study, the prevalence of BRVO in the population older than 48 years was 1.1%. The Singapore Malay Eye Study reported a 0.6% prevalence of BRVO in the Malay population of persons aged 40-80 years living in Singapore. [10] The Beijing Eye Study reported that the prevalence of BRVO in a Chinese population of people aged 40 years and older was 1.3%. [11]
A recent study pooled data from population studies from the United States, Europe, and Australia. [12] This study reported that the age- and sex-standardized prevalence of BRVO was 4.42 cases per 1000 people. The prevalence increased with increasing age but did not differ by sex. Ethnic and racial background influenced the prevalence of BRVO. For instance, White patients had an age-adjusted prevalence of 3.7 cases per 1000 people, compared with 3.9 cases per 1000 people in African Americans, 5.7 cases per 1000 people in Asians, and 6.9 cases per 1000 people in Latinos.
Mortality/Morbidity
Given that BRVO often is associated with a concomitant systemic vascular condition, one has to wonder whether or not a BRVO is a marker for cardiovascular mortality or morbidity. There is conflicting evidence regarding the mortality in patients with BRVO.
A 9-year follow-up study in the United Kingdom suggested a relationship between cardiovascular mortality and all retinal vein occlusions (including branch, central, and hemiretinal).
In another study, the 10-year risk of developing cardiovascular complications was higher in patients with BRVO than in those with CRVO.
The Beaver Dam Eye Study reported that patients with BRVO at baseline did not have an increased 8-year risk of dying of ischemic heart disease. [13]
In a Danish study, the investigators did not find a significant difference in mortality between the patients with BRVO and the general population. [14]
Race
No racial predilection for the disease is apparent.
Sex
No predilection for either sex is apparent.
Age
The patients who are affected are usually in their fifth or sixth decade of life.
Prognosis
An analysis of several series indicates that 53% of eyes obtain 20/40 or better visual acuity, 25% have a visual acuity between 20/50 and 20/100, and 22% have a visual acuity of 20/200 or worse. [15]
The more distal the occlusion is from the optic disc, the better the visual prognosis.
According to Hayreh and Zimmerman, most eyes with macular edema secondary to BRVO improve to a certain degree without any intervention. The median time to macular edema resolution varied from 18-21 months. [16]
Patient Education
Instruct patients with BRVO to seek attention if further visual loss occurs during follow-up.
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Patient with an old branch retinal vein occlusion in which the hemorrhages have cleared. Note lipid exudation and evidence of cystoid macular edema.
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Patient with a branch retinal vein occlusion complicated by vitreous hemorrhage and tractional retinal detachment. The patient had undergone vitrectomy and endolaser treatment. Note the sclerotic supertemporal vein.
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This 42-year-old woman with hypertension noticed a sudden decrease in her vision. Visual acuity was 20/100. Note the intraretinal hemorrhages in just one segment of the retina.
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Arterial phase of an angiogram demonstrates the lack of filling in the first branch arteriole of the superior temporal artery.
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Late phase of an angiogram demonstrates late leakage in the macular area.
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Optical coherence tomography (OCT) of a patient with macular edema secondary to branch retinal vein occlusion (BRVO) prior to the initiation of anti-VEGF therapy. The visual acuity was 20/150.
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Optical coherence tomography (OCT) following 3 monthly intravitreal bevacizumab injections (1.25 mg). The visual acuity improved to 20/30.
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