A 69-yr-old man with a history of hypertension and diabetes mellitus was transferred to our hospital for sudden visual loss in his left eye which had occurred 9 hr ago. In medical history, he had no ophthalmic problem and had maintained good visual acuity. On examination, vision was light-perception in left and 20/20 in right eye. Fundus examination revealed white edematous retina and typical "cherry-red spot" as well as vessel fragmentations suggesting CRAO (Fig. 1A). Perfusion of retina was markedly diminished with arteriovenous (AV) transit time of 5 min while choroidal perfusion was normal on fundus fluorescein angiography of left eye (Fig. 1B). There was no strabismus and ocular movement was normal. Intraocular pressure was 9 mmHg and slit lamp examination of anterior segment, lid, and orbit showed normal findings. Because the neurological examination showed no abnormality and he had not recently experienced any neurological symptoms, we skipped the brain imaging studies which were usually performed in the stroke patients. Ten hours after symptom onset, we performed cerebral angiography with biplane angiographic unit (Integris Allura; Philips Medical Systems, Eindhoven, Netherlands). There was no atherosclerotic lesion in distal carotid and proximal cervical internal carotid artery on left carotid angiogram. Internal carotid angiogram showed no occlusion of left ophthalmic artery up to distal segment and normal choroidal blush (Fig. 2A). We changed diagnostic catheter for 6F guiding catheter (Envoy; Cordis, Warren, New Jersey). On selective angiogram at ophthalmic artery using a microcatheter (Excelsior SL-10; Boston Scientifics, Natick, Massachusetts), there was no definite occlusion in branches including ciliary arteries and muscular branches from ophthalmic artery (Fig. 2B). We could not confirm the central retinal artery on angiogram. After the microcatheter was placed in proximal segment of the ophthalmic artery, urokinase (Green Cross pharmacy, Yongin, Korea) and Abxicimab (Reopro; Lilly, Indianapolis, Indiana) which are usually used for IAT in intracerebral artery occlusion were hand-injected slowly up to 400,000 units and 4 mg, respectively. Urokinase was administrated firstly for finbrinolysis and Abxicimab was added for preventing from further platelet aggregation. Their doses were reduced due to small size and territory of central retinal artery and for safety. Compared with before preoperative angiograms, post-IAT angiography did not show the definite changes (Fig. 2B). There was no procedure-related complication or event.

During the procedure, we could not find any improvement of retinal perfusion on fundus examination and the patient had no subjective improvement of vision. After IAT, anticoagulation was not done, systemically. One hour after thrombolysis, the patient experienced marked restoration of vision and visual field. At one day after thrombolysis, his visual acuity was hand motion while he could see 20/100 using his temporal visual field. The fundus fluorescein angiography showed normalized retinal arterial filling with AV transit time of 18 sec (Fig. 3). The b wave amplitude of maximal combined response of electroretinogram was 331.7 uV in his right eye and 250.2 uV in his left eye. However, he had severe macular edema on optical coherence tomography and showed no further improvement of vision thereafter. Because there was no newly developed neurologic sign implying brain lesions, the brain imaging study was not performed, additionally.

A 47-yr-old man presented with sudden decrease of visual acuity in left eye for 10 hr. The best corrected visual acuity of his left eye was 20/70. On ophthalmic examination 1 month ago, he could have seen 20/20 with his left eye. Eight years ago, he had also experienced sudden visual loss in his right eye for CRAO. At that time, because he had visited at hospital 2 days after onset, he had not treated for visual loss and visual acuity was no light perception.

Fundus examination revealed edematous retina without fragmentation of vessels (Fig. 4A). On fundus fluorescein angiography, there was a delay in arterial filling and AV transit time was 70 sec (Fig. 4B). He was diagnosed as having CRAO and agreed to undergo IAT.

There was no steno-occlusive and remarkable lesion on carotid angiogram (Fig. 5A). The selective angiogram of ophthalmic artery showed a choroidal blush and no occlusion in its branches. A microcatheter was placed at the origin of ophthalmic artery and urokinase was hand-injected. During the injection, his visual acuity improved and retinal perfusion increased on fundus examination, so we stopped the IAT after the injection of 300,000 units of urokinase (Fig. 5B).

One day after IAT, his vision improved to 20/40 and fundus fluorescein angiography showed normal retinal perfusion with AV transit time of 12 seconds (Fig. 6A). Two weeks after IAT, his visual acuity improved to 20/25 and there was no more retinal edema (Fig. 6B).