Retinal Vein Occlusion (RVO) Clinical Presentation

Updated: Sep 20, 2019
  • Author: Jesse Borke, MD, FACEP, FAAEM; Chief Editor: Gregory Sugalski, MD  more...
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The history should focus on timing, severity, and character of vision loss, the presence or absence of trauma, unilateral versus bilateral, and associated symptoms. It is also important to ask about risk factors.

Branch retinal vein occlusion (BRVO) may be asymptomatic and noted incidentally on funduscopic examination, or patients may complain of relative scotoma or areas of blurred vision, classically worsening over hours to days.

Patients with central retinal vein occlusion (CRVO) are symptomatic as a rule, classically presenting with sudden painless monocular vision loss or dense central scotoma. In some cases, this loss of vision is subtle in character, with intermittent episodes of blurred vision. In other cases, it may be sudden and dramatic. The nonischemic type is often the more subtle of the two, while the ischemic type is prone to the more acute clinical presentations.



Visual acuity is the vital sign of the eye and should be documented by triage or the physician. As with any vital sign, if the documented value does not make sense, it should be rechecked by the physician personally.

Extraocular motility should be checked in every case of suspected RVO. It should be normal.

Pupillary function should be checked in every case of suspected RVO. It often appears normal during examination by a nonophthalmologist but commonly demonstrates ipsilateral relative afferent pupillary defect (RAPD) in cases of ischemic CRVO. A 2007 article in the American Journal of Ophthalmology noted that the finding of an afferent pupillary defect in ischemic CRVO is of diagnostic value. [11]

Intraocular pressure should be checked in every case of suspected RVO. IOP is generally normal in an initial acute presentation or prior to neovascularization.

Anterior slit lamp examination should be performed in every case of suspected RVO and typically yields normal findings.

Funduscopic examination is diagnostic in RVO, as it shows retinal hemorrhage, edema, and dilated veins (see image below). In patients with CRVO or hemiretinal vein occlusion (HRVO), the retinal hemorrhage is scattered and diffuse, giving the classic "blood and thunder" fundus (or hemi-fundus).

A: Central retinal vein occlusion (CRVO). B: Hemir A: Central retinal vein occlusion (CRVO). B: Hemiretinal retinal vein occlusion (HRVO). C: Branch retinal vein occlusion (CRVO).


The risk factors for both BRVO and CRVO largely mirror those for vascular disease in general, including increasing age, hypertension, diabetes, smoking, obesity, and hypercoagulable disorders (such as protein C resistance-factor V Leiden, protein C and S deficiency, and antiphospholipid syndrome). Glaucoma, which causes stasis and decreased outflow, is also a significant risk factor. Increased levels of physical activity, advantageous cholesterol profiles, and alcohol consumption may be protective.

Trauma, local ocular disease, and orbital structural lesions have also been implicated in the development of RVO. Clotting can be caused by many systemic diseases, including hypercholesterolemia, hyperhomocysteinemia, systemic lupus erythematosus (SLE), sarcoidosis, tuberculosis, syphilis, multiple myeloma, cryoglobulinemia, leukemia, lymphoma, Waldenstrom macroglobulinemia, polycythemia vera, and sickle cell disease. In CRVO, a positive association has been found in ACE inhibitor use with atrial fibrillation. A negative association has been reported with the use of estrogen in postmenopausal women.



The primary concern is vision loss. Neovascularization can result in neovascular glaucoma, vitreous hemorrhage, and, in late or severe cases, retinal detachment. Visual morbidity and blindness in RVO are due to macular edema, retinal hemorrhage, macular ischemia, and neovascular glaucoma (see Mortality/Morbidity).