Retinal Review, Issue 66
Authored by Burton Wisotsky, MD
A 68 year old woman was referred for vision loss OS. She noted the sudden onset of diffuse visual blur three weeks ago. It did not improve. The patient was noted to have retinal hemorrhaging and was referred for evaluation. Past medical history is significant for hypertension and hyperlipidemia. Past ocular history is not contributory. On examination, VA was OD: 20/25 and OS: CF. IOP’s were OD: 23 and OS: 18. The SLE was normal OU. Visual field with a 24-2 program was full OD and showed central depression and scotoma OS. DFE is noted below:
Examination of the right eye revealed hypertensive retinopathy (arteriolar narrowing). The cup was moderate but the rim appeared intact. The macula was unremarkable. In the left eye there was a hemorrhagic CRVO with extensive hemorrhaging and diffuse macular edema. OCT confirmed the flat macula in the right eye and the extensive macular edema in the left. Fluorescein angiography was difficult to assess due the extensive intraretinal hemorrhaging and resulting blocked fluorescence.
Before discussing the left eye, it is important to mention that patients with vascular occlusion in one eye have an increased likelihood of COAG in the fellow eye. The reasons are unknown. One should always fully evaluate the fellow eye in a patient with vascular occlusion for evidence of glaucoma. Our patient’s fellow eye has a moderate cup with high IOP – she is a glaucoma suspect and should be monitored carefully.
There are three issues regarding the CRVO. First is the potential medical implication. Many patients with CRVO have an underlying medical issue associated with vascular occlusion. These can include atherosclerosis, hypertension, hyperlipidemia, diabetes, systemic inflammation, and clotting disorder. The most common risk factor is hypertension, which our patient had. No further medical testing is indicated. Second issue is ischemia. CRVO’s are broken into three groups – perfused, nonperfused, and indeterminate. Perfused, or nonishemic CRVO has an 8% risk of developing progressive ischemia, which can then lead to rubeotic glaucoma. Perfused CRVO patients should be observed for ischemia but not treated unless they progress. Nonperfused (ischemic) CRVO has a high risk of progression to rubeotic glaucoma. These patients typically have 10 or more disc areas of nonperfusion on fluorescein angiography. They should be observed carefully for rubeosis. If they develop rubeosis of the angle or iris, they should undergo immediate heavy panretinal photocoagulation to reduce the risk of rubeotic glaucoma. Indeterminate patients have extensive retinal hemorrhaging which blocks the ability to determine the fluorescein nonperfusion. Based on CRVO studies, 80% of these patients will go on to develop ischemia. They need to be observed carefully like the nonperfused patients for signs of increasing ischemia and rubeosis. Our patient was indeterminate, but had no signs of rubeosis.
The third issue is macular edema and vision. Our patient’s vision is reduced due to retinal hemorrhaging, presumed retinal ischemia, and macular edema. Initial treatment for CRVO is antiVEGF therapy. This should be instituted as soon as possible after the diagnosis is made, assuming the vision is significantly reduced. The effect of antiVEGF is unknown on ischemia, but is well known to reduce macular edema and improve vision. An occasional patient can be observed for a short time before instituting antiVEGF therapy if the CRVO looks mild, or if they are young (can spontaneously resolve). There are several strategies for antiVEGF including monthly injections, treat and extend regimens, and PRN dosing. Most of the studies suggest that numerous injections the first year and less numerous injections the second year yield the best visual results. Most specialists now treat in this manner rather than the “few injections then wait and see approach”.
We scheduled the patient for 3 monthly injections of Avastin. The results were dramatic. The hemorrhaging and macular edema almost fully resolved (see photos, angiograms, and OCT below). Vision returned to 20/30. We will now inject the patient every few months for the next year or so and hope to stop at that point. If the patient had not responded well to antiVEGF or had continued to recur, Ozurdex intravitreal steroid implant could have been used. If ischemia had worsened laser could have been applied. Fortunately for our patient, she had an excellent response to Avastin and will likely not need any other type of treatment.