19.1 Features
Retinal vein occlusions (RVO) vary considerably based on distribution of the venous occlusive event, perfusion status of the affected retina, duration of untreated disease, and presence or absence of cystoid macular edema or retinal neovascularization and its sequelae. Because these factors result in myriad disease manifestations, clinicians must identify the correspondingly variable symptoms and examination findings.
A “typical” RVO presents at an older age (typically older than 50 years, with over 50% of affected patients being older than 60 years) and with known systemic vasculopathic risk factors (e.g., history of cigarette smoking, hypertension, hyperlipidemia, diabetes mellitus, peripheral vascular disease, renal disease, cerebrovascular accident, transient ischemic attacks, myocardial infarction, or thromboembolism). An “atypical” RVO may present at a younger age (i.e., younger than 50 years) without known systemic vasculopathic risk factors.
19.1.1 Common Symptoms
Vary from asymptomatic to acute, unilateral, painless vision loss. More widespread vision loss is typically present with central retinal vein occlusion (CRVO), compared to segmental visual field loss in patients with branch or hemiretinal vein occlusions (BRVO or HRVO).
19.1.2 Exam Findings
RVO is characterized by intraretinal hemorrhages confined primarily to the inner retina with accompanying engorged and tortuous retinal veins. The retinal distribution of findings depends on the type of RVO. Cystoid macular edema is common. There may be cotton wool spots and yellowish intraretinal exudates in the affected regions. Optic disc edema may be present. In later stages with more severe underlying ischemia, neovascularization of the retina or optic nerve head may occur resulting in vitreous hemorrhage, fibrovascular proliferation and traction, and/or neovascularization of the angle and iris with resulting neovascular glaucoma (▶ Fig. 19.1, ▶ Fig. 19.2, ▶ Fig. 19.3). Other findings in chronic RVO may include macular retinal pigment epithelium alterations due to long-standing edema, epiretinal membrane, and optociliary shunt vessels. In chronic RVO, many of the findings mentioned may be absent and diagnosis may require ancillary diagnostic testing (e.g., fluorescein angiography [FA], optical coherence tomography [OCT], OCT angiography [OCTA]). The subtypes of RVO are as follows:
Fig. 19.1 An 18-year-old female without known risk factors presented with (a) fundus and (b) fluorescein angiogram findings consistent with a central retinal vein occlusion. A hypercoagulable work-up suggested the possibility of a protein S deficiency. (a) The classic fundus findings of optic disc edema and hyperemia, blurring of the disc margins, engorged and tortuous retinal veins, intraretinal hemorrhage, and macular lipid exudates are seen. (b) Fluorescein angiography revealed dilated and tortuous retinal veins and blockage from intraretinal hemorrhage.
Fig. 19.2 (a) Ultra-widefield fundus imaging of a hemiretinal vein occlusion. There are intraretinal hemorrhages in the superotemporal and superonasal quadrants (superior hemisphere) respecting the horizontal raphe along with an engorged and tortuous superior retinal vein. (b) Ultra-widefield fluorescein angiography in the laminar venous filling phase shows delayed venous filling of the superior retinal vein in addition to blockage from superior intraretinal hemorrhage.
Fig. 19.3 (a) Fundus photograph and (b) fluorescein angiography showing superotemporal intraretinal hemorrhage respecting the horizontal raphe consistent with a branch retinal vein occlusion.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
