Branch Retinal Vein Occlusion

Updated: May 17, 2016
  • Author: Lihteh Wu, MD; Chief Editor: Hampton Roy, Sr, MD  more...
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Much confusion exists in the literature because central retinal vein occlusions and branch retinal vein occlusions (BRVOs) are often grouped and studied together. The natural history and the complication rate for each entity differ. The treatments and their results vary from one condition to the other. This article deals exclusively with BRVOs. Hemiretinal vein occlusions are probably variants of central retinal vein occlusions, and, as such, they are not included in this discussion.



Hypertensive, atherosclerotic, inflammatory, or thrombophilic conditions may lead to retinal endothelial vascular damage. In eyes with an anatomical 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. 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. [1]

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. [2, 3] 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. [4] VEGF secretion causes breakdown of the blood-retinal barrier, contributing to the formation of macular edema. 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. [5] Undiluted vitreous samples from eyes with untreated acute BRVO demonstrate elevated levels of proinflammatory and proangiogenic cytokines. [6]

Rehak et al have also 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. [3]




United States

Retinal vein occlusions (branch and central) are the second most common retinal vascular diseases after diabetic retinopathy. 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. [7] 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. [8]


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. [9] The Beijing Eye Study reported that the prevalence of BRVO in a Chinese population of people aged 40 years and older was 1.3%. [10]

A recent study pooled data from population studies from the United States, Europe, and Australia. [11] 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.


Given that BRVO is often 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. [12]

In a Danish study, the investigators did not find a significant difference in mortality between the patients with BRVO and the general population. [13]


No racial predilection for the disease is apparent.


No predilection for either sex is apparent.


The patients who are affected are usually in their fifth or sixth decade of life.