More on Retinal Vein Occlusions
A 58-year-old man sought medical attention because of the recent sudden onset of blurred vision in his left eye. His vision had not improved over several days. The patient had hypertension and had recently sustained a myocardial infarction. He was taking metoprolol, 25 mg/d, and aspirin, 81 mg/d.
His best-corrected visual acuity was 20/30 in the right eye and 20/80 in the left eye. No afferent pupillary defect was noted. Biomicroscopy revealed early nuclear sclerotic cataracts.
Results of the funduscopic examination of the right eye were unremarkable. The fundus of the left eye showed dot, blot, and flame-shaped hemorrhages throughout, including the macula. The macular reflex was blunted, and the macula appeared edematous. The retinal veins were engorged and tortuous. No evidence of ischemia (cotton-wool spots) was seen. Because the central retinal vein occlusion (CRVO) had occurred recently, the optic nerve head also appeared edematous. The patient’s blood pressure was normal. Bilateral carotid artery bruits were audible with auscultation. The patient was referred to his internist for further workup.
CRVO is caused by localized thrombosis at the level of the lamina cribrosa of the optic nerve. Intra-retinal hemorrhages are visible throughout the fundus grounds in patients with CRVO. Cotton-wool spots and an afferent pupillary defect are signs of ischemia. Poor initial visual acuity also correlates with the degree of ischemia. If ischemia is present initially or occurs over time, neovascularization of the retina and iris (rubeosis) may develop. This can lead to neovascular glaucoma, severe eye pain, and further loss of vision.
The management of CRVO includes strict control of arterial blood pressure, hypercholesterolemia, and cardiovascular risk factors. Patients need to be monitored monthly by an ophthalmologist for the possible development of neovascularization.