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Branch retinal vein occlusion

AI overview

Branch retinal vein occlusion is a common retinal vascular disease of the elderly caused by the occlusion of one of the branches of central retinal vein.

Key points
  • It is a common retinal vascular disease of the elderly.
    source quote
    Branch retinal vein occlusion is a common retinal vascular disease of the elderly.
  • It is four times more common than central retinal vein occlusion.
    source quote
    Branch retinal vein occlusion is four times more common than central retinal vein occlusion.
  • Usual age of onset is 60-70 years.
    source quote
    Usual age of onset is 60–70 years.
  • Approximately 16 million people worldwide may have retinal vein occlusion.
    source quote
    approximately 16 million people worldwide may have retinal vein occlusion
Symptoms
  • Patients usually have sudden onset of blurred vision or central visual field defect.
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    Patients with branch retinal vein occlusion usually have a sudden onset of blurred vision or a central visual field defect.
  • Acute findings include superficial hemorrhages, retinal edema, and cotton-wool spots in affected sector.
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    The eye examination findings of acute branch retinal vein occlusion include superficial hemorrhages, retinal edema, and often cotton-wool spots in a sector of retina drained by the affected vein.
  • The obstructed vein is dilated and tortuous.
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    The obstructed vein is dilated and tortuous.
  • The superotemporal quadrant is most commonly affected (63%).
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    The quadrant most commonly affected is the superotemporal (63%).
  • Retinal neovascularization occurs in 20% of cases within the first 6-12 months.
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    Retinal neovascularization occurs in 20% of cases within the first 6–12 months of occlusion
  • Vitreous hemorrhage can ensue from neovascularization.
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    vitreous hemorrhage can ensue
Diagnosis
  • Diagnosis is made clinically by finding retinal hemorrhages in the distribution of an obstructed retinal vein.
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    The diagnosis of branch retinal vein occlusion is made clinically by finding retinal hemorrhages in the distribution of an obstructed retinal vein.
  • Fluorescein angiography is a helpful adjunct showing delayed venous filling, hypofluorescence, and capillary nonperfusion.
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    Fluorescein angiography is a helpful adjunct. Findings include delayed venous filling, hypofluorescence caused by hemorrhage and capillary nonperfusion
  • Optical coherence tomography is an adjunctive test used to monitor macular edema.
    source quote
    Optical coherence tomography is an adjunctive test in branch retinal vein occlusion. Macular edema is commonly seen on optical coherence tomography exams.
Treatment
  • Systemic treatment with aspirin, heparin, or thrombolysis has not been shown to be effective.
    source quote
    Systemic treatment with oral aspirin, subcutaneous Heparin, or intravenous thrombolysis have not been shown to be effective treatments
  • Laser treatment for macular edema is indicated in patients with 20/40 or worse vision after at least 3 months.
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    Laser treatment of the macular area to reduce macular edema is indicated in patients who have 20/40 or worse vision and did not spontaneously improve for at least 3 months
  • Grid laser was found to be preferable to no laser in a Cochrane Review.
    source quote
    grid laser was found to be preferable to no laser
  • Retinal photocoagulation is applied for neovascularization.
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    The second indication of laser treatment is in case of neovascularization. Retinal photocoagulation is applied to the involved retina
  • Triamcinolone acetonide injection has similar effect to laser but higher rates of elevated intraocular pressure and cataract formation.
    source quote
    Triamcinolone injection is shown to have similar effect on visual acuity when compared with standard care (laser therapy). However, the rates of elevated intraocular pressure and cataract formation is much higher with the triamcinolone injection
  • Anti-VEGF drugs are the treatment of choice for macular edema or neovascularization with good evidence of improved outcomes.
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    Anti- vascular endothelial growth factor (VEGF) drugs such as bevacizumab (Avastin; 1.25–2.5 mg in 0.05 ml) and ranibizumab (Lucentis) injections are widely used and there is good evidence of improved visual and anatomic outcomes with these agents.
  • Anti-VEGF drugs have low incidence of adverse side effects but often require repeated injections.
    source quote
    Intravitreal anti-VEGF drugs have a low incidence of adverse side effects compared with intravitreal steroids, but are often requiring repeated injections.
Red flags
  • Neovascularization is more likely if more than five disc diameters of nonperfusion are present.
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    Neovascularization is more likely to occur if more than five disc diameters of nonperfusion are present
  • Vitreous hemorrhage can ensue from neovascularization.
    source quote
    vitreous hemorrhage can ensue
  • Triamcinolone injection complications include elevated intraocular pressure and cataract development.
    source quote
    has complications including elevated intraocular pressure and development of cataract
  • Ischemia alone is not an indication for treatment provided follow-up could be maintained.
    source quote
    Ischemia alone is not an indication for treatment provided that follow-up could be maintained.
Prognosis

Branch retinal vein occlusion has a good prognosis: after 1 year 50-60% of eyes have been reported to have a final visual acuity of 20/40 or better even without any treatment.

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Branch retinal vein occlusion
Branch retinal vein occlusion
SpecialtyNeurology 

Branch retinal vein occlusion is a common retinal vascular disease of the elderly. It is caused by the occlusion of one of the branches of central retinal vein.[1]

Patients with branch retinal vein occlusion usually have a sudden onset of blurred vision or a central visual field defect. The eye examination findings of acute branch retinal vein occlusion include superficial hemorrhages, retinal edema, and often cotton-wool spots in a sector of retina drained by the affected vein. The obstructed vein is dilated and tortuous.

The quadrant most commonly affected is the superotemporal (63%).

Retinal neovascularization occurs in 20% of cases within the first 6–12 months of occlusion and depends on the area of retinal nonperfusion. Neovascularization is more likely to occur if more than five disc diameters of nonperfusion are present and vitreous hemorrhage can ensue.[2]

Branch retinal vein occlusion revealed by laser Doppler imaging through flow alteration in the upper right branch artery.

The diagnosis of branch retinal vein occlusion is made clinically by finding retinal hemorrhages in the distribution of an obstructed retinal vein.

  • Fluorescein angiography is a helpful adjunct. Findings include delayed venous filling, hypofluorescence caused by hemorrhage and capillary nonperfusion, dilation and tortuosity of veins, leakage due to neovascularization and macular edema.
  • Optical coherence tomography is an adjunctive test in branch retinal vein occlusion. Macular edema is commonly seen on optical coherence tomography exams. Serial optical coherence tomograph is used as a rapid and noninvasive way of monitoring the macular edema.
  • Laser Doppler imaging[3] reveals dynamic hemodynamics discrepancies between branch arteries and veins, from local vascular resistance increase by the venous occlusion.

Several options exist for the treatment of branch retinal vein occlusion. These treatments aim for two of the most significant complications, namely macular edema and neovascularization.[1]

  • Systemic treatment with oral aspirin, subcutaneous Heparin, or intravenous thrombolysis have not been shown to be effective treatments for central retinal vein occlusion and for branch retinal vein occlusion no reliable clinical trial has been published.
  • Laser treatment of the macular area to reduce macular edema is indicated in patients who have 20/40 or worse vision and did not spontaneously improve for at least 3 months (to permit the maximum spontaneous resolution) after the development of the vein occlusion. It is typically administered with the argon laser and is focused on edematous retina within the arcades drained by the obstructed vein and avoiding the foveal avascular zone. Leaking microvascular abnormalities may be treated directly, but prominent collateral vessels should be avoided. In a Cochrane Review comparing laser treatment to other treatments, grid laser was found to be preferable to no laser.[4] Due to quality of evidence it is uncertain whether bevacizumab injections or subthreshold diode were preferable to grid laser treatments.
  • The second indication of laser treatment is in case of neovascularization. Retinal photocoagulation is applied to the involved retina to cover the entire involved segment, extending from the arcade out to the periphery. Ischemia alone is not an indication for treatment provided that follow-up could be maintained.
  • Preservative-free, nondispersive Triamcinolone acetonide in 1 or 4 mg dosage may be injected into the vitreous to treat macular edema but has complications including elevated intraocular pressure and development of cataract. Triamcinolone injection is shown to have similar effect on visual acuity when compared with standard care (laser therapy). However, the rates of elevated intraocular pressure and cataract formation is much higher with the triamcinolone injection, especially the higher dosage.[5] Intravitreal injection of Dexamethasone implant (Ozurdex; 700.350 μg) is being studied, its effect may last for 180 days. The injection may be repeated however with less pronounced effect. Although the implant was designed to cause less complications, pressure rise and cataract formation is noted with this treatment too.[6]
  • Anti-vascular endothelial growth factor (VEGF) drugs such as bevacizumab (Avastin; 1.25–2.5 mg in 0.05 ml) and ranibizumab (Lucentis) injections are widely used and there is good evidence of improved visual and anatomic outcomes with these agents.[7] Intravitreal anti-VEGF drugs have a low incidence of adverse side effects compared with intravitreal steroids, but are often requiring repeated injections. They are the treatment of choice for macular edema or neovascularization. The mechanism of action and duration of anti-VEGF effect on macular edema is currently unknown. The intraocular levels of VEGF are increased in eyes with macular edema secondary to branch retinal vein occlusion and the elevated VEGF levels are correlated to the degree and severity of the areas of capillary nonperfusion and macular edema.[8]
  • Surgery is employed occasionally for longstanding vitreous hemorrhage and other serious complications such as epiretinal membrane and retinal detachment.
  • Arteriovenous sheathotomy has been reported in small, uncontrolled series of patients with branch retinal vein occlusion. Branch retinal vein occlusiontypically occurs at arteriovenous crossings, where the artery and vein share a common adventitial sheath. In arteriovenous sheathotomy an incision is made in the adventitial sheath adjacent to the arteriovenous crossing and is extended along the membrane that holds the blood vessels in position to the point where they cross, the overlying artery is then separated from the vein.

In general, branch retinal vein occlusion has a good prognosis: after 1 year 50–60% of eyes have been reported to have a final visual acuity of 20/40 or better even without any treatment. With time the dramatic picture of an acute branch retinal vein occlusion becomes more subtle, hemorrhages fade so that the retina can look almost normal. Collateral vessels develop to help drain the affected area.

  • Branch retinal vein occlusion is four times more common than central retinal vein occlusion.
  • Usual age of onset is 60–70 years.
  • An analysis of population from several countries estimates that approximately 16 million people worldwide may have retinal vein occlusion.[9]

  1. 1 2 "Retina and vitreous". Basic and clinical science course. American Academy of Ophthalmology. 2011–2012. pp. 150–154. ISBN 978-1-61525-119-3.
  2. ↑ Yanoff M, Duker JS (2009). Ophthalmology (3rd ed.). Mosby Elsevier. ISBN 978-0-323-04332-8.
  3. ↑ Puyo, L., M. Paques, M. Fink, J-A. Sahel, and M. Atlan. "In vivo laser Doppler holography of the human retina." Biomedical optics express 9, no. 9 (2018): 4113–4129.
  4. ↑ Lam FC, Chia SN, Lee RM (May 2015). "Macular grid laser photocoagulation for branch retinal vein occlusion". The Cochrane Database of Systematic Reviews (5) CD008732. doi:10.1002/14651858.cd008732.pub2. PMC 10879914. PMID 25961835.
  5. ↑ Scott IU, Ip MS, VanVeldhuisen PC, Oden NL, Blodi BA, Fisher M, et al. (September 2009). "A randomized trial comparing the efficacy and safety of intravitreal triamcinolone with standard care to treat vision loss associated with macular Edema secondary to branch retinal vein occlusion: the Standard Care vs Corticosteroid for Retinal Vein Occlusion (SCORE) study report 6". Archives of Ophthalmology. 127 (9): 1115–28. doi:10.1001/archophthalmol.2009.233. PMC 2806600. PMID 19752420.
  6. ↑ Haller JA, Bandello F, Belfort R, Blumenkranz MS, Gillies M, Heier J, et al. (December 2011). "Dexamethasone intravitreal implant in patients with macular edema related to branch or central retinal vein occlusion twelve-month study results". Ophthalmology. 118 (12): 2453–60. doi:10.1016/j.ophtha.2011.05.014. PMID 21764136.
  7. ↑ Shalchi Z, Mahroo O, Bunce C, Mitry D (July 2020). "Anti-vascular endothelial growth factor for macular oedema secondary to branch retinal vein occlusion". The Cochrane Database of Systematic Reviews. 2020 (7) CD009510. doi:10.1002/14651858.cd009510.pub3. PMC 7388176. PMID 32633861.
  8. ↑ Karia N (July 2010). "Retinal vein occlusion: pathophysiology and treatment options". Clinical Ophthalmology. 4: 809–16. doi:10.2147/opth.s7631. PMC 2915868. PMID 20689798.
  9. ↑ Rogers S, McIntosh RL, Cheung N, Lim L, Wang JJ, Mitchell P, et al. (February 2010). "The prevalence of retinal vein occlusion: pooled data from population studies from the United States, Europe, Asia, and Australia". Ophthalmology. 117 (2): 313–9.e1. doi:10.1016/j.ophtha.2009.07.017. PMC 2945292. PMID 20022117.