A 48-year-old African American woman with a history of hypertension and a 15 pack-year smoking history experienced an acute onset of visual loss in the right eye and retrobulbar pain 20 minutes after striking her right temple against a bed post. Review of systems was otherwise negative. She drove herself to an emergency room where computed tomography (CT) of the brain was normal and magnetic resonance imaging demonstrated mild induration of the intraconal fat and subtle enhancement of the optic nerve. She was instructed to see a neurologist as an outpatient, and 2 days later, her vision spontaneously returned to baseline.
Two weeks later, the patient again acutely lost vision in her right eye and was admitted to a hospital where a temporal artery biopsy was negative. She was transferred to our facility and neurological examination was normal except for loss of vision in the right eye. Visual acuity was light perception, right eye, and 20/30, left eye. Pupillary examination revealed a right relative afferent pupillary defect. Intraocular pressure was normal in both eyes as was the left visual field. The right fundus revealed splinter hemorrhages, segmental arteriolar narrowing, optic disc pallor, and macular ischemia with a prominent cherry red spot in the macula (Fig. 1). The left fundus was unremarkable. Fluorescein angiography demonstrated delayed choroidal and optic disc perfusion in the right eye (Fig. 2). The constellation of clinical findings were consistent with a right ophthalmic artery occlusion. Within a few days, vision in the right eye was no light perception.
Laboratory workup yielded normal results for erythrocyte sedimentation rate, anti-nuclear antibody, perinuclear anti-neutrophil cytoplasmic antibody, and cytoplasmic antinuclear cytoplasmic antibody, vitamin B12 and folate, rapid plasma reagin, thyroid function, lipid profile, liver function studies, and hypercoaguable panel. Transthoracic echocardiogram, electrocardiogram, and carotid Doppler failed to reveal a source of thromboemboli. Magnetic resonance angiogram (MRA) and magnetic resonance venogram were normal as was cerebrospinal fluid analysis. Cerebral angiography demonstrated nonvisualization of the origin of the right ophthalmic artery from the right internal carotid artery (ICA) with distal refilling of the ophthalmic artery via flow from the meningolacrimal branch of the right middle meningeal artery. In addition, there was a 1.73 × 1.75 mm irregular dilation of the ophthalmic segment of the right ICA associated with distal narrowing of the right supraclinoid ICA, consistent with dissecting pseudoaneurysm (Fig. 3).
A Pipeline embolization device (PED; Covidien Vascular Therapies, Mansfield, MA) was positioned within the supraclinoid ICA from the level of the anterior choroidal artery extending into the anterior genu of the cavernous ICA. Angiography performed following embolization demonstrated complete obliteration of the pseudoaneurysm (Fig. 4). The patient's vision in the right eye remained unchanged 12 months later.
Ophthalmic artery occlusion is uncommon and compromises blood flow to the retinal and choroidal circulations. It is usually due to embolic phenomena related to atherosclerotic disease, myxoma, mural thrombus, or vasculitis (1).
Our patient's vision returned to baseline 2 days after the initial presentation and was subsequently lost a second time. This may be explained by the hypothesis of Duker and Brown (2) that ophthalmic artery occlusion often causes hypoperfusion of choroidal and retinal vessels, thus compromising retinal cell function without necessarily causing cell death. It is likely that retinal perfusion recovered because of resolution of the initial thromboembolic occlusion but a second thromboembolic event resulted in permanent loss of vision. A less likely explanation is that visual loss may have resolved and recurred because of ophthalmic artery vasospasm, which is known to occur in the setting of trauma.
Traumatic intracranial aneurysms are rare (3–5) and result from shearing of intracranial vessels due to rapid deceleration forces (5). Arteries arising nearby may become occluded because of local thromboembolism, hemodynamic compromise, and changes in vessel morphology brought about by aneurysmal expansion and dissection (6). Mortality secondary to rupture of traumatic intracranial aneurysms approaches 50% in the first 3 weeks (7–9), necessitating prompt treatment. These aneurysms are less amenable to surgical intervention or endovascular coil embolization because of their thin walls, wide necks, and propensity for intraoperative rupture (10,11).
The PED is an implantable, platinum-based mesh conduit designed to divert arterial flow away from the aneurysm, resulting in intra-aneurysmal hemostasis and thrombosis. Parent vessel reconstruction with the PED was decided upon in our patient for its ability to treat the pseudoaneurysm without the need for aneurysmal catheterization and without risk of coil migration.
Computed tomography angiography (CTA) and MRA are favored over conventional angiography as an initial screening method for intracranial vascular pathology because of their increased availability and lower frequency of complications. However, traumatic intracranial aneurysms often are small in size (3,8,12,13), and CTA and MRA have a sensitivity of 30%–60% for aneurysms <5 mm in size (14). Therefore, patients suspected of posttraumatic pseudoaneurysm may require cerebral catheter angiography for both diagnosis and treatment.
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