The authors report a case of a 48-year-old woman with a branch retinal artery occlusion after the neurosurgical coiling of a paraclinoid aneurysm. Clinical examination revealed a Hollenhorst plaque at the bifurcation of the inferior arcade and at a branch of the superior arcade with associated retinal whitening in the right eye. Follow-up examination at 8 months demonstrated improved visual acuity with near complete resolution of the retinal infarction but a persistent inferior Hollenhorst plaque. This case illustrates a retinal artery occlusion as a possible complication of paraclinoid aneurysmal coiling procedure.
[Ophthalmic Surg Lasers Imaging Retina. 2014;45:e26–e28.]
From the Retina Service, Scheie Eye Institute, University of Pennsylvania, Philadelphia, Pennsylvania.
The authors have no proprietary or financial interest in the materials presented herein.
Address correspondence to Alexander J. Brucker, MD, Retina Service, Scheie Eye Institute, 51 N. 39th Street, Philadelphia, PA 19104; email:
Received: July 13, 2013
Accepted: November 14, 2013
Posted Online: April 04, 2014
Retinal artery occlusions may result from a variety of etiologies. These occlusions may involve the central retinal artery or its branches. The embolic source may originate from calcific plaques in valvular heart disease, cholesterol emboli from carotid arterial disease, or embolization of local thrombi.1 We report a case of branch retinal artery occlusion secondary to embolization following neurosurgical coiling of a paraclinoid aneurysm.
A 48-year-old African-American woman with a medical history significant for a right paraclinoid aneurysm underwent endovascular stent placement in July 2007 (Figure 1A). During this procedure, coil embolization was also attempted but failed because the coil continued to prolapse out of the parent vessel. Several hours after the procedure, the patient noted a “darkening” of her vision in the right eye. Best corrected visual acuity (BCVA) was hand motion in the right eye and 20/20 in the left eye with no relative afferent papillary defect. Her right fundus revealed a Hollenhorst plaque at the bifurcation of the branch retinal artery of the inferior arcade and superior arcade with associated retinal whitening. A second Hollenhorst plaque was also present downstream in the same vessel within the inferior arcade with multiple peripapillary cotton-wool spots (Figure 1B). One month later, BCVA was 20/400 in the right eye and 20/20 in the left eye, with resolving retinal whitening in the region supplied by the occluded vessels. Goldmann visual field testing confirmed the presence of three adjacent central scotomas in her right eye. Optical coherence tomography revealed retinal thinning greatest superiorly and temporally, where the ischemic insult occurred (Figure 1C). Eight months after the initial embolic branch retinal artery occlusion, BCVA was 20/20 in the right eye and 20/20 in the left eye. The occluded vessels were now perfused despite a persistent Hollenhorst plaque at the inferior arcade (Figure 1D).
(A) MRI/MRA of the brain demonstrating right-sided paraclinoid aneurysm (white arrow). (B) Right fundus photograph with multiple branch retinal arteriolar occlusions with visible Hollenhorst plaques and peripapillary cotton-wool spots. (C) Time-domain OCT of the right macula with inner retinal thinning. (D) Right fundus photograph 8 months after presentation with fine residual lipid exudates nasal to macula and resolved retinal whitening. Note persistent Hollenhorst plaque at inferior arcade.
Paraclinoid or ophthalmic segment aneurysms arise from the internal carotid artery between the roof of the cavernous sinus and the origin of the posterior communicating artery. These aneurysms represent 5% of all intracranial aneurysms.1 Cerebrovascular ischemia from embolism is a known and reported complication of endovascular coiling for intracranial aneurysms. In one of the largest studies of coil embolization of intracranial aneurysms, Vinuela et al reported a 2.5% incidence of cerebrovascular ischemia from embolism.2 There are many sources of embolism during endovascular coiling, including friable plaques, air bubbles, iatrogenic dissection within parent vessels, and thrombus or fresh clots within aneurysms and the catheters themselves.3 At present the rate of retinal artery occlusion following endovascular coiling of intracranial aneurysms has yet to be reported.
In the case described here, it is believed that the microemboli that caused the branch retinal artery occlusion arose from a thrombus that may have formed within the walls of the aneurysm or at the site of the stent itself. Furthermore, the resultant central scotomas and retinal thinning are consistent with retinal artery occlusion. Vision loss following intracranial coiling procedures has been described, secondary to mircroemboli and ischemia from vasospasm.4
Retinal artery occlusions can be visually devastating; however, as perfusion returns, as in this case, partial or complete visual acuity improvement is possible. Retinal artery occlusions therefore are an important complication of intracranial aneurysm coiling procedures; ophthalmologists and interventional radiologists should be aware of and be certain to educate patients about this complication.
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- Vinuela F, Duckwiler G, Mawad M. Guglielmi detachable coil embolization of acute intracranial aneursym: perioperative anatomical and clinical outcome in 403 patients. J Neurosurg. 1997;86(3):457–482. doi:10.3171/jns.1997.86.3.0475 [CrossRef]
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