This 64YO male presented with one year of decreased vision in his left eye. Vision was 20/20 in his normal OD and 20/200 OS.
Optos color RGB imaging shows sheathing and ischemia throughout the posterior pole, sparing the superotemporal quadrant. Collateral vessels are noted on the nerve. Triton swept-source OCT shows diffuse inner retinal thinning with disorganization of inner retinal layers (DRIL) and a variably adherent epiretinal membrane. Fluorescein angiography shows profound retinal ischemia throughout the distribution of the hemiretinal vein occlusion (HRVO) with innumerable buds of retinal neovascularization. Collateral vessels cross the temporal horizontal meridian.
Learning Points:
Branch retinal vein occlusions are virtually always caused by a retinal artery compressing a retinal vein within its common adventitial sheath. Some people are born with an anomalous two-trunked central retinal vein that independently drains the superior and inferior retinal hemispheres. HRVO, similar to central retinal vein occlusion, is caused by compression of the retinal vein posterior to the lamina cribrosa (see Hayreh, Arch Ophthalmol 1980;98:1600-1609).
HRVO-related macular edema and retinal neovascularization are treated similarly to branch retinal vein occlusion. In 1986, the Branch Vein Occlusion Study Group reported that scatter laser decreased the risk of vitreous hemorrhage from retinal neovascularization in BRVO and suggested applying laser once neovascularization develops (Arch Ophthalmol 1986;104:34-41). We scheduled this treatment for our patient.
