NEWS & EVENTS
Retinal Review, Issue 37
CASE NUMBER 37
A 72 year old man noted the sudden onset of a scotoma in his right eye over the past week. The scotoma was painless and nonprogressive. Past ocular history is significant for moderate myopia and early cataracts. Past medical history is significant for atherosclerotic heart disease for which he is on numerous medications including plavix. On examination, VA measured OD: 20/60 and OS: 20/20. IOP’s were normal. The anterior segments were intact. There were early nuclear sclerotic cataracts in both eyes. Dilated examination, red free photograph, and fluorescein angiograms were as follows:
In the left eye there was peripapillary atrophy with mild macular RPE disease. No exudation was noted. In the right eye there was similar peripapillary atrophy. There was a large subretinal hemorrhage extending from the optic nerve to the macula. The fovea was involved. Fluorescein angiography demonstrated blocked fluorescence from the blood, but there was no obvious leakage site. There are two considerations in further evaluating this patient and in determining a treatment course: 1) What is the etiology of the subretinal hemorrhage and 2) Does the medical history play a role? The differential diagnosis for subretinal hemorrhage in this patient includes exudative AMD, retinal arteriolar macroaneurysm, trauma, valsalva retinopathy, and anomalous blood vessel. Although the view of the retina and subretinal space are compromised by the hemorrhage, there is no obvious anomalous blood vessel or macroaneurysm. The patient denies a history of trauma or straining. This leaves exudative AMD as the leading diagnosis. Regarding the medical history, blood thinners such as plavix typically do not cause spontaneous subretinal hemorrhages, but can certainly change a small hemorrhage into a larger one. There are several treatment options. Subretinal hemorrhage is thought to be toxic to the retina. If the subretinal hemorrhage is large enough, it is often recommended to displace the hemorrhage from the macula via intravitreal gas injection alone or in combination with TPA (tissue plasminogen activator), a thrombolysis agent. This can allow rapid displacement of subretinal hemorrhage and an improvement in final vision. Another option is beginning a course of antiVEGF therapy. Presumably there is a CNVM under the hemorrhage and with treatment the CNVM and hemorrhage with gradually resolve. A third option is observation. The hemorrhage is below the fovea but fairly thin. These hemorrhages often clear on their own and after resolution the CNVM can be treated if necessary. We elected observation. The patient’s medical doctor was contacted and he temporarily discontinued his plavix. Over the course of several weeks, the peripapillary hemorrhage gradually resolved:
Visual acuity with improvement of the hemorrhage (please note some residual yellow subretinal hemorrhage) increased to 20/25. A small grayish CNVM was noted temporal to the optic nerve. Laser was applied to the lesion. Thermal laser was chosen rather than antiVEGF therapy because the lesion was far enough from the fovea that a scotoma would likely not be noticed. Laser can often ablate a CNVM in one session rather than multiple sessions of antiVEGF therapy.
The CNVM was successfully ablated by laser, the rest of the subretinal hemorrhage fully resolved and the vision returned to 20/20. The patient resumed his plavix and as of yet has not had any further issues. In this case patience and observation were the keys to a successful result.