This Article  • Extract  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on ISI (1)  • Contact me when this article is cited  Related Content  • Similar articles in this journal

Arch Ophthalmol. 2002;120:857-860.

Therapeutic embolization is an accepted component in the management of vascular tumors, arteriovenous malformations, and active bleeding sites.¹ Complications are rare, but include infarction by unintended occlusion of vessels.¹ This occurs either when particles are injected from a proximally placed catheter or when they reflux from distal vessels during flushing.

Inadvertent occlusion of the ophthalmic or central retinal artery during external carotid artery embolization has been reported in 4 cases,^2-4 with immediate loss of vision. We report a case in which stepwise decline of vision related to progressive swelling of polyvinyl alcohol (PVA) particles lodged in retinal arterioles occurred throughout a period of 8 days.

Report of a Case
A 39-year-old woman underwent preresection embolization of a left-posterior frontal convexity meningioma. A preembolization arteriogram visualized the middle meningeal branches to the tumor, as well as an anastomosis to the ophthalmic artery via the sphenoidal artery (Figure 1 and Figure 2A).

View larger version (32K): [in this window] [in a new window] Figure 1. Preembolization left external carotid arteriogram showing middle meningeal artery (asterisk), parietal branch (solid arrow) to tumor (blush of small vessels), sphenoidal artery (open arrow), and ophthalmic artery (arrowhead).

View larger version (84K): [in this window] [in a new window] Figure 2. Schematic view of tumor and retinal embolization. A, Left middle meningeal branches, including supply to convexity meningioma, and anastomosis to ophthalmic artery. B, Catheter injecting polyvinyl alcohol (PVA) particles to occlude vessels in the tumor bed. It is positioned in a meningeal branch distal to the branch that leads to the sphenoidal artery. C, Catheter has been pulled back to proximal meningeal artery in preparation for postembolization arteriogram. The pull-back is done to avoid reflux of loose PVA particles lying in tumor vessels. Those PVA particles residing in the microcatheter are inadvertently flushed into meningeal branches that anastomose to sphenoidal, ophthalmic, and retinal arteries. These particles occlude retinal arterioles and, as they swell, sequentially infarct the retina.

A 5F catheter was positioned in the left external carotid artery, and through this catheter, a 2F microcatheter was advanced into the middle meningeal artery supplying the lesion. The patient was systemically heparinized during the procedure. The catheter was positioned distal to the take-off of the sphenoidal artery (Figure 2B). To confirm that the catheter was beyond all dangerous anastomoses, provocative testing was performed by injecting amobarbital and lidocaine through the microcatheter.⁵ When this testing produced novisual or other neurological deficits, 45- to 150-µm PVA particles suspended in radiographic contrast were slowly injected under fluoroscopic guidance into the tumor (Figure 2B). After slowed flow to the tumor was seen, the microcatheter was flushed with heparinized saline to evacuate any remaining particles in the catheter. To prevent reflux of emboli that had been deposited in the distal vessels supplying the tumor, the catheter was then pulled back proximal to the sphenoidal artery take-off (Figure 2C), and contrast was injected to confirm devascularization of the meningioma. As the contrast was injected, the patient reported a sudden flash of light in the left eye, and she soon developed an inferior scotoma on that side. Polyvinyl alcohol particles retained within the catheter had evidently been flushed into the ophthalmic artery anastomosis and reached the retinal arterioles (Figure 2C).

Ophthalmic examination performed 3 hours after the procedure disclosed visual acuities of 20/25 OD and 20/25 OS, and a left afferent pupil defect. Ophthalmoscopy revealed ischemic clouding of the retina superotemporally. Small, yellow-white particles were visible in retinal arterioles of the superior and inferior arcades, including the vessel that was occluded in the superior arcade (Figure 3A). A formal visual field test (Humphrey Field Analyzer Program 24-2; Humphrey Instruments, San Leandro, Calif) disclosed a corresponding inferonasal scotoma (Figure 3B). Seven days later, the patient reported a further decline in vision in her left eye. Ophthalmoscopy revealed enlargement of the superior retinal infarct (Figure 4A) and of the corresponding scotoma (Figure 4B). The particle in the proximal inferior temporal arteriole had enlarged. Despite 4 mg of oral dexamethasone taken 3 times daily, she developed loss of the superior field one day later. Visual acuity had fallen to 20/400; ophthalmoscopy showed that the particle in the inferior temporal artery had further enlarged, that the inferior retina was now infarcted (Figure 5A), and that the scotoma involved most of the visual field (Figure 5B). Follow-up examination 2 months later showed a pale left optic disc and no change in visual function.

View larger version (32K): [in this window] [in a new window] Figure 3. Fundus photographs and visual fields of the left eye on the day of procedure. A, Superior branch retinal artery occlusion as ischemic whitening. Several yellow-white polyvinyl alcohol particles are impacted within proximal retinal arterioles. B, Corresponding inferior nerve fiber bundle defect.

View larger version (29K): [in this window] [in a new window] Figure 4. Fundus photographs and visual fields of the left eye 7 days after the procedure. A, Retinal infarction has extended nasally. B, Enlargement of visual field defect, corresponding to enlarged area of infarction.

View larger version (28K): [in this window] [in a new window] Figure 5. Fundus photographs and visual fields of the left eye 8 days after the procedure. A, Retinal infarction now also involves the inferior branch artery. The particle lodged in the proximal inferior temporal retinal arteriole has enlarged. B, Visual field defect now involves the upper field, corresponding to new infarction of the inferior retina.

Comment
Our patient had a rare complication of therapeutic PVA embolization, namely, inadvertent occlusion of branches of the central retinal artery. This complication is based on known anastomoses between the external carotid circulation and the ophthalmic artery.^6-8 External carotid branches may replace the internal carotid artery as the predominant supply of the ophthalmic artery in 5% of patients with otherwise normal cephalic vessels⁷ and in a much higher proportion in those with arteriosclerosis, which preferentially affects the internal carotid system.

Aware that this anastomosis might cause a serious problem, our interventional neuroradiologist (J.P.D.) positioned the catheter far distal to it, performed preembolization pharmacologic provocative testing, embolized gently without repositioning the catheter, and flushed the catheter after embolization. However, these techniques failed to prevent errant emboli from reaching the retinal vessels. Some particles were undoubtedly present in the catheter even after careful flushing with saline, suggesting that it may not be possible to completely remove all particles from the microcatheter.

Four additional measures might have prevented this complication. First, embolization could have been performed with particulate agents too large to enter the anastomotic pathway, but there are 2 drawbacks to this maneuver. The first is that the size of anastomoses and particles vary, making it impossible to be sure that some particles will not enter the anastomosis. The second drawback is that large particles are less effective in devascularizing the tumor bed.⁹ The second measure would have been to selectively occlude the anastomosis with a microcoil prior to embolization of the tumor bed. This would have prevented small particles from entering the anastomosis, but this is not feasible if the anastomosis is too small or tortuous to be selectively catheterized. A third preventive measure would have been to remove the microcatheter used for injecting emboli, and to then introduce a new microcatheter to perform the postembolization arteriographic studies. The drawback to this measure is that if further embolization of the tumor through a distal site is found to be necessary, additional time and risk would be added to the procedure. Fourth, we could have injected contrast dye during the follow-up arteriogram through the guiding catheter positioned in the external carotid artery, rather than through the microcatheter. This would have avoided the need to manipulate the microcatheter and would have virtually eliminated the risk of injecting retained PVA emboli. The main disadvantage of this otherwise practical solution is that a guiding catheter must have a large enough inner lumen to allow passage of the inner microcatheter and leave enough room around it to inject viscous contrast material. Perhaps a larger 6F guiding catheter would have been preferable in this case.

An unusual aspect of our case is the sequential nature of the branch retinal artery occlusions occurring throughout a period of 8 days. We attribute this phenomenon, (not previously reported) to progressive swelling and/or thrombus formation in these vessels. Swelling is a feature that makes PVA a useful agent for therapeutic embolization, but that increases the possibility that errant PVA particles will cause neurological deficits. Unfortunately, there is no antidote to reverse the swelling of the particles.

Although our case has unusual features, we doubt that inadvertent occlusion of the retinal artery during preoperative embolization via the external carotid system is as rare as the published literature would suggest. An authoritative textbook¹⁰ describes 2 unpublished cases. In presenting this case to gatherings of ophthalmologists and neuroradiologists, many members of our audiences have told us of similar experiences.

AUTHOR INFORMATION

Tina Turner, MD; Jonathan D. Trobe, MD; John P. Deveikis, MD
Ann Arbor, Mich

Corresponding author: Jonathan D. Trobe, MD, Kellogg Eye Center, 1000 Wall St, Ann Arbor, MI 48105 (e-mail: jdtrobe{at}umich.edu).

REFERENCES
1. Taylor W, Rodesch G. Recent advances: interventional neuroradiology. BMJ. 1995;311:789-792. FREE FULL TEXT 2. Soong HK, Newman SA, Kumar AAJ. Branch artery occlusion: an unusual complication of external carotid embolization. Arch Ophthalmol. 1982;100:1909-1911. PUBMED 3. Mames RN, Snady-McCoy L, Guy J. Central retinal and posterior ciliary artery occlusion after particle embolization of the external carotid artery system. Ophthalmology. 1991;98:527-531. ISI | PUBMED 4. Shimizu Y, Kiyosawa M, Miura T, Takahashi A, Tamai M. Acute obstruction of the retinal and choroidal circulation as a complication of interventional angiography. Graefes Arch Clin Exp Ophthalmol. 1993;231:43-47. PUBMED 5. Deveikis JP. Sequential injections of amobarbital sodium and lidocaine for provocative testing in the external carotid circulation. AJNR Am J Neuroradiol. 1996;17:1143-1147. ABSTRACT 6. Gillilan LA. The collateral circulation of the human orbit. Arch Ophthalmol. 1961;65:684-694. FREE FULL TEXT 7. Hayreh SS. Arteries of the orbit in the human being. Br J Surg. 1963;50:938-953 PUBMED 8. Ahn HS, Kerber CW, Deeb ZL. Extra- to internal arterial anastomoses in therapeutic embolization: recognition and role. AJNR Am J Neuroradiol. 1980;1:71-75. ABSTRACT 9. Wakhloo AK, Juengling FD, Velthoven W, Schumacher M, Hennig J, Schwechheimer K. Extended preoperative polyvinyl alcohol microembolization of intracranial meningiomas: assessment of two embolization techniques. AJNR Am J Neuroradiol. 1993;14:571-582. ABSTRACT 10. Kupersmith MJ, Berenstein A. Embolic and noninflammatory occlusive vascular disease of the visual and ocular motor system. In: Kupersmith MJ, Berenstein A. Neurovascular Neuro-ophthalmology. Berlin, Germany: Springer-Verlag; 1993:126, 358.

SECTION EDITOR: W. RICHARD GREEN, MD