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Branch Retinal Vein Occlusion Clinical Presentation

  • Author: Lihteh Wu, MD; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: May 17, 2016
 

History

The Eye Disease Case-Control Study reported the following findings:[14]

  • Systemic hypertension is a risk factor for branch retinal vein occlusion (BRVO).
  • Diabetes mellitus and open-angle glaucoma are not risk factors for BRVO.
  • Moderate alcohol consumption reduces the risk of BRVO.

Patients often complain of a sudden painless decrease of vision in the affected eye.

Some patients may complain of a scotoma.

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Physical

In 1877, Leber first described the branch retinal vein occlusion ophthalmoscopically. During the acute phase, intraretinal hemorrhages (usually flame shaped), retinal edema, and cotton-wool spots are seen in the distribution of a retinal vessel. The horizontal raphe is respected. Intraretinal hemorrhages are shown in the image below.

This 42-year-old woman with hypertension noticed a 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.

During the chronic stage, hemorrhages may be absent. Macular edema may be the only sign present. Telangiectatic vessels that extend across the horizontal raphe usually can be demonstrated angiographically.

Exudative retinal detachment is an infrequent complication of a BRVO. It is characterized by layered subretinal blood in the inferior portion of the detachment, very few collateral vessels, and capillary nonperfusion.[15]

In certain eyes with large areas of nonperfusion, retinal neovascularization may be seen. Vitreous hemorrhage with tractional retinal detachments may ensue. Further traction may create retinal breaks, creating combined rhegmatogenous and tractional retinal detachments. Neovascular glaucoma and neovascularization at the disc are rare events with BRVO.

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Causes

Most cases of BRVO are due to idiopathic factors. Usually, patients have an anatomical predisposing factor, such as an arteriovenous crossing where the artery compresses the vein. This compression leads to clot formation and subsequent BRVO.

Inflammatory conditions that affect the retinal veins may cause local damage that predisposes the individual to intravascular clot formation with subsequent BRVO.

Some of the inflammatory conditions reported in the literature are the following:

  • Serpiginous choroiditis
  • Arterial hypertension and hypercholesterolemia, both of which contribute to atherogenesis, have been identified as risk factors for BRVO, as follows:
    • Atherosclerosis itself has recently been recognized as a chronic low-grade inflammatory disease with a distinct proinflammatory cytokine pattern. In addition to their role in atherogenesis, some cytokines have been shown to exert procoagulatory effects and may thus contribute to the development of BRVO by a second mechanism.
    • Gene polymorphisms affecting the expression of inflammation-related cytokines are candidates as potential risk factors for BRVO. Genotypes of the following functional single nucleotide polymorphisms were determined: interleukin 1 beta (IL-1B) -511C>T, interleukin 1 receptor antagonist (IL-1RN) 1018T>C, interleukin 4 (IL-4) -584C>T, interleukin 6 (IL-6) -174G>C, interleukin 8 (IL-8) -251A>T, interleukin 10 (IL-10) -592C>A, interleukin 18 (IL-18) 183A>G, tumor necrosis factor (TNF) -308G>A, monocyte chemoattractant protein 1. Neither genotype distributions nor allele frequencies of any of the investigated polymorphisms differed significantly between patients with BRVO and controls.[16]

Thrombophilic conditions, such as the following, may also be involved:

  • Protein S deficiency
  • Protein C deficiency
  • Resistance to activated protein C (factor V Leiden)
  • Antithrombin III deficiency
  • Antiphospholipid antibody syndrome
  • Lupus erythematosus
  • Gammopathies
  • Gene polymorphisms related to hemostasis might also contribute to the development of BRVO. Most studies, but not all, failed to detect an association between these genetic variants and BRVO.
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Contributor Information and Disclosures
Author

Lihteh Wu, MD Asociados de Macula Vitreo y Retina de Costa Rica

Lihteh Wu, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Club Jules Gonin, Macula Society, Pan-American Association of Ophthalmology, Retina Society

Disclosure: Received income in an amount equal to or greater than $250 from: Bayer Health; Quantel Medical; Heidelberg Engineering.

Coauthor(s)

Diana Monge-Lopez, MBBS Research Fellow, Instituto de Cirugía Ocular, Costa Rica

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Macula Society, Retina Society, Club Jules Gonin

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

V Al Pakalnis, MD, PhD Professor of Ophthalmology, University of South Carolina School of Medicine; Chief of Ophthalmology, Dorn Veterans Affairs Medical Center

V Al Pakalnis, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, South Carolina Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Teodoro Evans, MD Consulting Surgeon, Vitreo-Retinal Section, Clinica de Ojos, Costa Rica

Disclosure: Nothing to disclose.

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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.
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.
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.
Arterial phase of an angiogram demonstrates the lack of filling in the first branch arteriole of the superior temporal artery.
Late phase of an angiogram demonstrates late leakage in the macular area.
 
 
 
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