branch retinal vein occlusion
Branch retinal vein occlusion (BRVO) is the second most commonly occurring retinal vascular abnormality after diabetic retinopathy (1)
- BRVO is an occlusion of either a major branch retinal vein draining one quadrant of the retina, a macular branch vein draining the macula, or a peripheral branch vein draining a portion of the retinal periphery
- is more common than central retinal vein occlusion, most frequently resulting from occlusion at the first major arteriovenous crossing from the optic disc
- pathogenesis of BRVO is thought to involve both retinal vein compression and damage to the vessel wall, possibly leading to thrombus formation
- BRVOs are hypothesised to occur at sites where retinal arterioles cross retinal veins
- the vein is engorged and tortuous distal to the obstruction. The retina is oedematous and there are haemorrhages with occasionally, cotton wool exudates. Visual loss is related to the degree of macular involvement
- BRVO may be classified on a spectrum of ischaemic or nonischaemic designated by the disc areas (DA) of hypoperfusion on fluorescein angiography
- the prognosis for recovery is good when less than 25% of the macula is oedematous. Neovascularisation occurs in many patients. The new vessels may bleed behind the vitreous and initiate vitreous detachment
- age and gender standardised prevalence for BRVO of 4.42 per 1000 (confidence interval (CI) 3.65 to 5.19) (2)
- risk factors for BRVO include hypertension, atherosclerosis, hyperlipidaemia, diabetes mellitus, thrombophilia and other inflammatory and myeloproliferative disorders
Visual loss in BRVO:
- most common cause of visual loss in BRVO patients is macular oedema (MO) - occurs in 5% to 15% of patients within the first year (2)
- other causes of visual loss include macular ischaemia, glaucoma and neovascularisation
- MO and neovascularisation of the retina or disc are the two major complications that require therapy (2)
Treatment is determined after specialist review:
- treatment may not be necessary
- medical therapy options include grid laser photocoagulation (GLP), sector panretinal photocoagulation, intravitreal steroids (triamcinolone, dexamethasone) and intravitreal vascular endothelial growth factor inhibitors
- surgical treatment options include include vitrectomy with internal limiting membrane peeling and vitrectomy with arteriovenous sheathotomy
Dexamethasone intravitreal implant is recommended as an option for the treatment of macular oedema following branch retinal vein occlusion when (3):
- treatment with laser photocoagulation has not been beneficial, or
- treatment with laser photocoagulation is not considered suitable because of the extent of macular haemorrhage.
Ranibizumab is recommended as an option for treating visual impairment following branch retinal vein occlusion only if treatment with laser photocoagulation has not been beneficial, or when laser photocoagulation is not suitable because of the extent of macular haemorrhage (4)
- evidence suggests that treatment of MO secondary to BRVO with anti-vascular endothelial growth factor (anti-VEGF) improves visual and anatomical outcomes at six and 12 months (5)
- ranibizumab belongs to a class of drugs that block the action of vascular
endothelial growth factor (VEGF)-A
- retinal vein occlusion (RVO) is a common cause of reduced vision as
a result of retinal vascular disease. Thrombosis in the retinal veins
causes an increase in retinal capillary pressure, resulting in increased
capillary permeability and the discharge of blood and plasma into the
retina. This leads to macular oedema and varying levels of ischaemia through
reduced perfusion of capillaries. These changes trigger an increase in
VEGF, which increases vascular permeability and new vessel proliferation
- by inhibiting the action of VEGF-A, ranibizumab reduces oedema and limits visual loss or improves vision.
- retinal vein occlusion (RVO) is a common cause of reduced vision as a result of retinal vascular disease. Thrombosis in the retinal veins causes an increase in retinal capillary pressure, resulting in increased capillary permeability and the discharge of blood and plasma into the retina. This leads to macular oedema and varying levels of ischaemia through reduced perfusion of capillaries. These changes trigger an increase in VEGF, which increases vascular permeability and new vessel proliferation
- Mitchell P et al. Prevalence and associations of retinal vein occlusion in Australia. The Blue Mountains Eye Study. Archives of Ophthalmology 1996;114(10):1243-7.
- Rogers S et al. The prevalence of retinal vein occlusion: pooled data from population studies from the United States, Europe, Asia, and Australia. Ophthalmology 2010;117(2):313-9.
- NICE (July 2011). Dexamethasone intravitreal implant for the treatment of macular oedema secondary to retinal vein occlusion
- NICE (May 2013). Ranibizumab for treating visual impairment caused by macular oedema secondary to retinal vein occlusion
- Shalchi Z et al. Anti-vascular endothelial growth factor for macular oedema secondary to branch retinal vein occlusion (Review). Cochrane Database of Systematic Reviews 2020, Issue 7. Art. No.: CD009510. DOI: 10.1002/14651858.CD009510.pub3.
Last edited 10/2020 and last reviewed 07/2021