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Case Reports and Small Case Series
June 2000

Retinal Artery Occlusion Following Coil Embolization of Carotid-Ophthalmic Aneurysms

Arch Ophthalmol. 2000;118(6):851-852. doi:

Paraclinoid aneurysms, such as carotid-ophthalmic aneurysms, represent 5% of all intracranial aneurysms. In the past, treatment involved surgical clipping of the aneurysm, which is associated with 4% morbidity and 1% mortality even in elective cases.1 A nonsurgical alternative treatment for intracranial aneurysms was developed in 1990 that utilizes detachable coils placed by an endovascular route to embolize the aneurysm and induce thrombus formation within the aneurysmal sac. The procedure has the advantage of avoiding the risks of neurosurgery and enabling treatment of aneurysms that are unclippable or otherwise associated with a high morbidity. However, cerebral embolization can complicate this procedure.2,3 We report 2 cases of retinal artery occlusion following coil embolization of nonruptured carotid-ophthalmic aneurysms.

Report of Cases
Case 1

A 54-year-old man had a subarachnoid hemorrhage on November 1996 secondary to rupture of a left carotid-ophthalmic aneurysm that was successfully embolized with coils. He also had a small right carotid-ophthalmic aneurysm measuring 4 mm in diameter that was intact and not treated. The patient had full recovery and demonstrated no neurological deficits. In January 1999, he underwent coil embolization of the right paraclinoid aneurysm. While heparinized, there was perforation of the dome of the aneurysm during the procedure. The aneurysm was completely packed with coils and the heparin was reversed. A few hours after the procedure, the patient complained of blurred vision in his right eye. Visual acuity was initially 20/20 OU, and the fundi showed no signs of ischemia. Confrontation testing showed constriction of the right visual field. Eight hours later, visual acuity deteriorated to hand motions OD and a relative afferent pupillary defect was noted. Fundus examination revealed a central retinal artery occlusion in the right eye (Figure 1). Cerebral angiography showed that the coils were in satisfactory position occluding the aneurysm and that the right ophthalmic artery was patent. Because of perforation of the aneurysm and the potential risk of disturbing the coils while trying to catheterize the ophthalmic artery, thrombolytic therapy was contraindicated and intravenous heparin was given instead. Topical timolol and intravenous acetozolamide were administered, an anterior chamber tap was performed, and the eye was massaged, but there was no visual recovery. His visual acuity remained hand motions OD in the remaining temporal field 4 months later.

Figure 1.
Fundus photograph of the right eye 2 weeks after central retinal artery occlusion and after coil embolization of the paraclinoid aneurysm. Note the diffuse macular edema and the irregular attenuated appearance of the arterioles due to hypoperfusion of the retina. The classic cherry-red spot seen in the acute phase of central retinal artery occlusion has evolved to formation of hard exudates and intraretinal and subretinal hemorrhage in the macula at this time.

Fundus photograph of the right eye 2 weeks after central retinal artery occlusion and after coil embolization of the paraclinoid aneurysm. Note the diffuse macular edema and the irregular attenuated appearance of the arterioles due to hypoperfusion of the retina. The classic cherry-red spot seen in the acute phase of central retinal artery occlusion has evolved to formation of hard exudates and intraretinal and subretinal hemorrhage in the macula at this time.

Case 2

A 13-year-old girl with tuberous sclerosis was found to have an intracranial aneurysm of the right carotid artery on magnetic resonance imaging. Angiography showed that the aneurysm was located in the ophthalmic branch and measured 8.6 mm in diameter with a wide neck (Figure 2). The patient had no focal neurological deficits at the time, and the aneurysm was embolized with Guglielmi detachable coils. The aneurysm was 95% occluded, but there was some coil protrusion into the parent artery. Anticoagulation with intravenous heparin was administered for 48 hours in hopes of preventing thrombus formation. Shortly after discontinuation of heparin therapy, the patient complained of 2 episodes of inferior visual field loss in the right eye. Visual acuity was 20/20 OU, but confrontation visual field testing demonstrated an inferonasal field defect in the right eye. No relative afferent pupillary defect was noted. Fundus examination showed whitening of the retina along the superotemporal arcade with sparing of the fovea consistent with a branch retinal artery occlusion (Figure 3). Angiography was performed to determine if thrombus was present in the carotid artery, but none was found. The position of the coils remained unchanged. The patient was again given anticoagulation therapy with intravenous heparin. Because of the presence of an incompletely occluded aneurysm, coil protrusion, and an embolic episode, she underwent surgical removal of the coil and clipping of the aneurysm 4 days after the initial procedure. Visual acuity remained 20/20 OD postoperatively, and the inferonasal field defect persisted.

Figure 2.
Left, Angiogram of the right internal carotid artery showing an 8.6-mm carotid-ophthalmic aneurysm (arrowheads) with a wide neck. Right, After coil embolization, the aneurysm is 95% occluded, but some coil protrusion into the parent artery is noted. The ophthalmic artery is seen immediately proximal to the aneurysm (arrows) and remains patent on the postembolization angiogram.

Left, Angiogram of the right internal carotid artery showing an 8.6-mm carotid-ophthalmic aneurysm (arrowheads) with a wide neck. Right, After coil embolization, the aneurysm is 95% occluded, but some coil protrusion into the parent artery is noted. The ophthalmic artery is seen immediately proximal to the aneurysm (arrows) and remains patent on the postembolization angiogram.

Figure 3.
Fundus photograph of the right eye showing occlusion of the superotemporal retinal artery branch after coil embolization of the paraclinoid aneurysm shown in Figure 2. The fovea is spared from ischemia, and the patient maintains 20/20 visual acuity.

Fundus photograph of the right eye showing occlusion of the superotemporal retinal artery branch after coil embolization of the paraclinoid aneurysm shown in Figure 2. The fovea is spared from ischemia, and the patient maintains 20/20 visual acuity.

Comment

Cerebrovascular ischemia from embolism is a known complication of coil embolization of cerebral aneurysms. In one large case series involving 403 patients, Vinuela et al3 reported an incidence of 2.5%. The complication of retinal artery occlusion following this procedure, however, has not yet been reported in the literature to our knowledge. These 2 cases represent the only ophthalmic embolic complications of 71 paraclinoid carotid aneurysms that have been treated with detachable coils at our institution. In both cases, the ophthalmic arteries were patent at angiography and the retinal artery was too small to be visualized. The microemboli that caused the retinal artery occlusion presumably arose from the thrombus that formed around the coils in the aneurysm. Visual loss following surgical clipping of paraclinoid aneurysms has been reported, but the cause has been considered to be improper placement of clips on the ophthalmic artery, direct trauma to the nerve, or ischemia from vasospasm.4 Retinal artery occlusion, either branch or central, can be a devastating complication. Ophthalmologists and interventional neuroradiologists should be aware of this complication so that prompt treatment may be given. However, in the context of a recently coiled paraclinoid aneurysm associated with subarachnoid hemorrhage, we consider fibrinolysis too risky and we only administer anticoagulation therapy to the patient. In elective cases, it is prudent to perform an ophthalmic examination with perimetery prior to treatment.

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Article Information

Supported in part by an unrestricted grant from Research to Prevent Blindness Inc, New York, NY, and a core grant from the National Eye Institute, Bethesda, Md.

Corresponding author: Jose S. Pulido, MD, Department of Ophthalmology, University of Illinois at Chicago Eye Center, 1855 W Taylor St, Chicago, IL 60612.

References
1.
King  JBerlin  JFlamm  E Morbidity and mortality from elective surgery for asymptomatic, unruptured, intracranial aneurysms: a meta-analysis. J Neurosurg. 1994;81837- 842Article
2.
Klotzsch  CNahser  HHenkes  HKuhne  DBerlit  P Detection of microemboli distal to cerebral aneurysms before and after therapeutic embolization. Am J Neuroradiol. 1998;191315- 1318
3.
Vinuela  FDuckwiler  GMawad  M Guglielmi detachable coil embolization of acute intracranial aneurysm: perioperative anatomical and clinical outcome in 403 patients. J Neurosurg. 1997;86475- 482Article
4.
Rizzo  J Visual loss after neurosurgical repair of paraclinoid aneurysms. Ophthalmology. 1995;102905- 910Article
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