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In This Topic
Eye Disorders
Retinal Disorders
Central and Branch Retinal Vein Occlusion
Etiology
Symptoms and Signs
Diagnosis
Prognosis
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    Central and Branch Retinal Vein Occlusion(Retinal Vein Occlusion)

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    Central retinal vein occlusion is a blockage of the central retinal vein by a thrombus. It causes painless vision loss, ranging from mild to severe, and usually occurs suddenly. Diagnosis is by funduscopy. Treatments can include antivascular endothelial growth factor drugs (eg, ranibizumab, pegaptanib, bevacizumab), intraocular injection of a dexamethasone implant or triamcinolone, and laser photocoagulation.

    Etiology

    Major risk factors include

    • Hypertension
    • Age

    Other risk factors include

    • Glaucoma
    • Diabetes
    • Increased blood viscosity

    Occlusion may also be idiopathic. The condition is uncommon among young people. Occlusion may affect a branch of the retinal vein or the central retinal vein.

    Neovascularization (abnormal new vessel formation) of the retina or iris (rubeosis iridis) occurs in about 16% of patients with central retinal vein occlusion and can result in secondary (neovascular) glaucoma, which can occur weeks to months after occlusion. Vitreous hemorrhage may result from retinal neovascularization.

    Symptoms and Signs

    Painless vision loss is usually sudden but it can also occur gradually over a period of days to weeks. Funduscopy reveals hemorrhages throughout the retina, engorged (dilated) and tortuous retinal veins, and, usually, significant retinal edema. These changes are typically diffuse if obstruction involves the central retinal vein and are limited to one quadrant if obstruction involves only a branch of the central retinal vein.

    Photographs

    Central Retinal Vein Occlusion

    Central Retinal Vein Occlusion

    Diagnosis

    • Funduscopy
    • Color fundus photography
    • Fluorescein angiography

    The diagnosis is suspected in patients with painless vision loss, particularly those with risk factors. Funduscopy, color photography, and fluorescein angiography confirm the diagnosis. Patients with a central retinal vein occlusion are evaluated for hypertension and glaucoma and tested for diabetes. Young patients are tested for increased blood viscosity (with a CBC and other coagulable factors as deemed necessary).

    Prognosis

    Most patients have some visual deficit. In mild cases, there can be spontaneous improvement to near-normal vision over a variable period of time. Visual acuity at presentation is a good indicator of final vision. If visual acuity is at least 20/40, visual acuity will likely remain good, occasionally near normal. If visual acuity is worse than 20/200, it will remain at that level or worsen in 80% of patients. Central retinal vein occlusions rarely recur.

    Treatment

    • For macular edema, intraocular injection of antivascular endothelial growth factor (anti-VEGF) drugs, dexamethasoneSome Trade Names
      DECADRON
      DEXASONE
      HEXADROL
      Click for Drug Monograph
      implant, and/or triamcinoloneSome Trade Names
      ARISTOCORT
      KENACORT
      KENALOG
      NASACORT
      Click for Drug Monograph
      acetonide
    • For some cases of macular edema with branch retinal vein occlusion, focal laser photocoagulation
    • Panretinal laser photocoagulation if neovascularization develops

    Treatment for branch retinal vein occlusion in patients with macular edema that involves the fovea is usually intraocular injection of an anti-VEGF drug (eg, ranibizumab, pegaptanib, bevacizumabSome Trade Names
    AVASTIN
    Click for Drug Monograph
    ) or intraocular injection of a dexamethasoneSome Trade Names
    DECADRON
    DEXASONE
    HEXADROL
    Click for Drug Monograph
    implant. These treatments, in addition to another anti-VEGF drug called aflibercept, can also be used to treat central retinal vein occlusion in patients with macular edema whose premorbid visual acuity was better than 20/400. Patients with central retinal vein occlusion whose premorbid visual acuity was better than 20/400 can also be treated with intraocular triamcinoloneSome Trade Names
    ARISTOCORT
    KENACORT
    KENALOG
    NASACORT
    Click for Drug Monograph
    injection. With these treatments, vision improves significantly in 30 to 40% of patients.

    Focal laser photocoagulation can be used for branch retinal vein occlusion with macular edema but is less effective than intraocular injection of an anti-VEGF drug or a dexamethasoneSome Trade Names
    DECADRON
    DEXASONE
    HEXADROL
    Click for Drug Monograph
    implant. Focal laser photocoagulation is typically not effective for the treatment of macular edema due to a central retinal vein occlusion.

    If retinal or anterior segment neovascularization develops secondary to central or branch retinal vein occlusion, panretinal laser photocoagulation should be done promptly to decrease vitreous hemorrhage and prevent neovascular glaucoma.

    Key Points

    • Retinal vein occlusion involves blockage by a thrombus.
    • Patients have painless loss of vision that is typically sudden and may have risk factors (eg, older age, hypertension).
    • Diagnose patients if funduscopy shows edema with dilated veins and hemorrhages and do color fundus photography and fluorescein angiography.
    • Treat patients who have macular edema with an intraocular injection of an anti-VEGF drug (ranibizumab, pegaptanib, bevacizumabSome Trade Names
      AVASTIN
      Click for Drug Monograph
      , or, for central retinal vein occlusion, aflibercept) or intraocular injection of a dexamethasoneSome Trade Names
      DECADRON
      DEXASONE
      HEXADROL
      Click for Drug Monograph
      implant or triamcinoloneSome Trade Names
      ARISTOCORT
      KENACORT
      KENALOG
      NASACORT
      Click for Drug Monograph
      .
    • Focal laser photocoagulation is useful in some cases of macular edema secondary to a branch retinal vein occlusion, and panretinal laser photocoagulation should be done for retinal or anterior segment neovascularization.

    Last full review/revision December 2012 by Sunir J. Garg, MD, FACS

    Content last modified January 2013

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