Korean Journal of Cerebrovascular Surgery 2011;13(4):291-296.
Published online December 1, 2011.
Central Retinal Artery Occlusion After Carotid Artery Angioplasty and Stenting in an Elderly Patient: A Case Report.
Shin, Dong Seong , Kim, Bum Tae
Department of Neurosurgery Soonchunhyang University Bucheon Hospital, Bucheon, Korea. bumtkim@schmc.ac.kr
Carotid artery angioplasty and stenting (CAS) has become increasingly accepted as an alternative therapy to carotid endarterectomy for treatment of carotid artery stenosis. Central retinal artery occlusion (CRAO) is one of the diseases presented due to carotid artery stenosis. But CRAO without cerebral ischemia after CAS is uncommon. An 80-year-old man was admitted to the hospital with the right centrum ovale ischemic stroke and right proximal carotid artery stenosis. We performed CAS with a distal protection device after pre-ballooning 3 times, without post-ballooning. Then, 12 hours after the CAS, the patient complained of blindness in the right eye and was diagnosed with CRAO. However, Diffusion weighted magnetic resonance imaging (DW-MRI) showed no significant findings in the brain. CRAO after CAS without intracranial infarction is a rare complication.
Key Words: Stents, Central retinal artery occlusion, Carotid artery stenosis


Complications associated with carotid artery angioplasty and stenting (CAS) may occur during or after the procedure and generally present as neurological symptoms due to an embolism or thrombus.4) Physicians can prevent these complications by using protective filters.11) Cerebral infarction is a well-known CAS complication. However, without intracranial infarction, central retinal artery occlusion (CRAO) after CAS is not a common complication.

Case Report

An 80-year-old man, who complained of left side weakness and slurred speech, was admitted to the hospital. He had been diagnosed with and treated for hypertension for 10 years. Diffusion weighted magnetic resonance imaging (DW-MRI) showed a high signal lesion on his right centrum ovale, and a neck magnetic resonance angiogram (MRA) showed a right proximal carotid artery stenosis (Fig. 1). Single-photon emission computed tomography (SPECT) showed a decreasing perfusion in right fronto-parietal lobe under the non-acetazolamide challenge. Conventional angiography showed severe stenosis in the proximal part of right internal carotid artery (ICA). Normal ICA diameter was 4.52 mm. However, stenotic lesion was 1.78 mm. According to the North American Symptomatic Carotid Endarterectomy Trial (NASCET), 60% stenosis was shown (Fig. 2).

The patient underwent carotid angioplasty and CAS twenty days after ischemic attack, receiving an antiplatelet agent for one week. After inserting an 8Fr sheath via right femoral puncture, the physician used an exchange technique to place an 8Fr guiding catheter (Mach 1, Boston Scientific, Fremont, CA, USA) in the patient's right common carotid artery and placed an embolic protection device (FilterWire EZTM 190 cm, Boston Scientific) in the petrous portion of the internal carotid artery (ICA), followed by a balloon catheter (Ultrasoft SV 4.0/2.0 cm, Boston Scientific) on the stenosis lesion of the right proximal ICA. The patient underwent balloon angioplasty three times because the result of carotid angioplasty was not satisfactory in spite of two time trials (Fig. 3. A). After angioplasty, a carotid stent (Carotid Wallstent TM Monorail TM diameter 10.0 mm, length 30 mm, Boston Scientific) was applied, from the ICA to the common carotid artery, which effectively covered the ICA stenosis

lesion (Fig. 3. B). There was no further balloon angioplasty after applying the stent.

The angiography after the CAS revealed increasing intracranial cerebral flow and no significant abnormal findings (Fig. 4). However, the patient complained of blurred vision in his right eye three hours after the CAS and of blindness in the right eye 12 hours after CAS. DW MRI was shown no significant findings in the cerebrum (Fig.5). Right eye fundus photography revealed a cherry-red spot on the macula, the retina's white ground-glass appearance and attenuated arterioles (Fig. 6. A). A fluorescein angiogram (FAG) of the right eye showed delayed filling of the superior temporal and inferior nasal arteries, and a filling defect of the inferior temporal artery (Fig. 6. B). After five days, Patient’s visual acuity was improved to 0.02 on the standard Korean eye chart(logarithm of the minimum angle of resolution scale) and a follow-up FAG revealed recovery of the filling defect of the central retinal artery (Fig. 7). After one month, fundus photography showed resolution of the retina edema and generalized arterial attenuation (Fig. 8).


CAS can be a preferred treatment method for certain patients who are not good candidates for carotid endarterectomy, such as patients who experienced recurrent stenosis after a previous endarterectomy, who have medical problems, and suffer from an anatomically inaccessible lesion above the C2 level or radiation-induced stenosis.1-3)8) Complications associated with CAS are major or minor stroke, TIA, seizure, bradycardia, vasospasm, dissection and hypotension.10)11)14)

Embolic protection devices are useful for preventing CAS-induced thromboembolic infarctions, but several studies showed this is not a perfect solution. Kim et al.7) reported detecting a new, high signal intensity lesion on DW-MRI in about 39% of their CAS procedures with protection devices, with no apparent major arterial or territorial infarctions. du Mesnil et al.6) documented that 19 of 50 cases treated with CAS, including protection devices, showed punctuated new DW MRI lesions. These lesions have been detected in vascular territories independent of the stented carotid artery.

In particular, filter-type protection devices cannot prevent the transportation of embolic particles smaller than the filter pores, and the filter retrieval process itself might cause distal embolization.7) Another possible reason of thromboembolic infarction caused by CAS is post-procedural transport of in situ embolus on the carotid stent lesion. Embolic protection device can protect acute ischemia during CAS, but stent can’t cover in situ embolus after CAS. According to the above studies, such embolic events are probably correlated with certain catheterization procedures and the placement of large-caliber guiding catheters. Regarding the etiology of CRAO, procedure like carotid angiography or intravitreal steroid injection can result

in retinal artery occlusions.12)13) Sudden and profound visual loss is a disease presentation. After a retinal infarction, the patient's prognosis is poor. Even though DW-MRI after CAS did not show a newly developed ischemic lesion on the cerebrum, CRAO may have been an embolic complication in our case. The patient had some risk factors for CRAO or ischemic stroke. He had suffered from hypertension for 10 years, had carotid artery atherosclerotic disease, and was elderly.

Therefore, we hypothesized that an embolus had obstructed the retinal artery, as the symptoms occurred just 12 hours after his CAS. Atherosclerosis of the ophthalmic artery is another possible cause of CRAO. Even though we did not find a severe ophthalmic artery stenosis on our patient's angiography, he might have suffered an atherosclerotic change in the ophthalmic artery due to hypertension, old age, or systemic atherosclerosis. In addition, a dynamic change in ICA blood flow might have influenced the atherosclerotic ophthalmic artery after the CAS. We have usually been carrying out balloon angioplasty procedure once for extra-cranial carotid stenosis. However, we performed a balloon angioplasty 3 times before applying the stent. Repeated procedure might have worsened the unstable atherosclerosis of an ICA stenotic lesion. If we had performed angioplasty just once before applying the stent, we could have reduced this complication risk. Another possible cause of CRAO is external carotid artery (ECA) to ophthalmic artery anastomosis. A number of extra-orbital branches arise from the ophthalmic artery. Such extra-orbital ophthalmic branches have extensive anastomosis with the ECA.9) This anastomosis

might have offered an embolic route from the ECA to the ophthalmic artery, and we did not use an ECA protection device in this case. In our case, it was thought that the origin of CRAO was unstable in situ embolus in the carotid stenosis caused by multiple angioplasties. If CRAO had come from ophthalmic artery, angiography would have shown atherosclerosis of ophthalmic artery. Moreover, embolus might have passed ECA route. Because if embolus had passed ICA, DW-MRI would have shown new develop lesion. Patients can undergo treatment modalities that lower intraocular pressure and enhance retinal oxygenation, such as anterior chamber paracentesis, ocular massage, systemic acetazolamide, topical timolol maleate, and 5% carbon dioxide/95% oxygen inhalation. Despite these treatments, the prognosis of retinal infraction due to CRAO is poor and retinal cloudiness can become a continuing process. Currently, physicians sometimes try intravenous or intraarterial thrombolysis treatment for CRAO. The results of thrombolysis for CRAO appear to be better than either the natural history of CRAO or conservative treatment,5) but thrombolysis as a treatment for CRAO requires further studies. Embolism due to carotid atherosclerotic disease has been described as the most common cause of CRAO. Endovascular surgeons should keep in mind the risk of permanent vision loss because of carotid CAS.


CRAO after CAS without intracranial infarction is a rare complication. We here report a case in an elderly patient.


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