Sequential bilateral retinal artery occlusion
An 86-year-old woman presented at the emergency room with sudden painless loss of visual field in her right eye (oculus dexter [OD]). Past medical history included primary systemic hypertension and hypercholesterolemia. She had undergone cataract surgery in both eyes (oculi uterque [OU]) 2 years previously. The patient had also experienced previous episodes of transient vision loss in her left eye (oculus sinister [OS]). Best-corrected visual acuity (BCVA) was 20/25 in OU. A confrontation test proved lower visual field defect in the OD. Intraocular pressure was normal, and anterior segment examination just revealed bilateral mild posterior capsular opacification. Fundoscopy disclosed superior BRAO in the OD, with a Hollenhorst plaque at the first bifurcation of the superior temporal arterial branch, attenuation, and “boxcarring” of the blood column in the involved region (). Small and medium-sized hard drusen were observed in OU. Oral antiplatelet therapy and rigorous follow-up of hypertension and hypercholesterolemia were recommended. Fourteen hours after discharge, the patient came back to the emergency room with sudden complete visual loss in the OS that had started 4 hours earlier. BCVA was 20/25 in the OD and hand motion in the OS, and there was a relative afferent pupillary defect in the OS. Fundus examination disclosed CRAO with cilioretinal artery sparing in the OS (). A cherry-red spot was observed in the macula. Fundoscopy of the OD showed previous BRAO with a small embolus after the second bifurcation of the superior temporal retinal vessel (). Spectral domain optical coherence tomography of the macula () showed a hyperreflective image in the OS, suggesting swelling of internal layers of the retina, and revealed 366±38 μm of foveal thickness (more prominent in the nasal quadrants). Fluorescein angiography showed impaired filling of the superior temporal arterial branch and branches of the central retinal artery (CRA) in the right and left eyes, respectively ().\nDespite some conservative maneuvers performed (paracentesis, ocular massage, intraocular hypotensive agents), there was no improvement of VA in the OS. Electrocardiogram results, erythrocyte-sedimentation rate, and serum C-reactive protein were completely normal in the acute phase. There was no evidence of systemic symptoms related to Horton’s disease. Systemic workup was completed by internal medicine and a cardiologist.\nSupra-aortic Doppler ultrasonography revealed mild right internal carotid artery stenosis (between 0% and 15%) ipsilateral to the eye with BRAO. There was moderate left internal carotid artery stenosis (between 15% and 50%), with a small, smooth, homogeneous plaque in the side of the CRAO. Transthoracic echocardiography revealed a severe calcification of the mitral valve with a mild–moderate rim of stenosis. The patient was informed about these findings and the high risk for cardiovascular disease, myocardial infarction and stroke.\nConsidering exploration and complementary studies, our patient experienced a sequential bilateral atherogenic embolic event (BRAO in the OD and nonarteritic CRAO with cilioretinal artery sparing in the OS). The patient was evaluated every month to monitor progression. Three months after BRAO, visual function remained stable, and both optic disks appeared pale ( and ).