Central Retinal and Posterior Ciliary Artery Occlusion after Particle Embolization of the External Carotid Artery System ROBERT N. MAMES, MD,t LORY SNADY-McCOY, MD/ JOHN GUY, MD 1•3
Abstract: A 15-year-old boy underwent neuroradiologic embolization of the left internal maxillary artery with polyvinyl alcohol to stop traumatic epistaxis after failure of surgical clipping and nasal packing. Selective catheterization of the external carotid artery before embolization showed a faint choroidal blush. Although the procedure provided hemostasis, embolization to the central retinal artery and ciliary arteries resulted in loss of vision. The route of the eml:loli to the eye was via the anastomotic network of the lacrimal artery supplied by the external carotid artery system. Neuroradiologic embolization of the external carotid artery is an effective mode of therapy for dural-cavernous fistulas when fed by the external carotid artery system. Because the blood flow to the brain and eye is predominantly supplied by the internal carotid artery, embolization of the external carotid artery is considered relatively safe. The authors document the importance of recognition of the choroidal blush during selective external carotid artery angiography as a sign of collateral blood flow to the eye. Physicians and patients need to be aware of the risk of blindness as a complication of external carotid artery embolization when this sign is present. Ophthalmology 1991; 98:527-531
Occlusion of the central retinal artery and posterior ciliary arteries after selective embolization of the external carotid artery system is uncommon, since ocular blood flow is predominantly supplied by the internal carotid
artery system. Consequently, permanent loss of vision due to infarction of the neurosensory retina after particle embolization of the external carotid artery system is rare. The importance of a choroidal blush as the harbinger of collateral blood supply to the eye by the external carotid artery system is emphasized.
Originally received: August 13, 1990. Revision accepted: December 3, 1990. 1 2
3
Department of Ophthalmology, University of Florida, Gainesville. Department of Ophthalmology, Tufts New England Medical Center, Boston, and Brown University, Providence. Department of Neurology, University of Florida, Gainesville.
Supported in part by an unrestricted grant to the Department of Ophthalmology from Research to Prevent Blindness, Inc, New York, New York. Reprint requests to Robert N. Mames, MD, Retinal Vitreous Service, Department of Ophthalmology, Box J-284, JHMHC, University of Florida, Gainesville, FL 32610-0284.
CASE REPORT A 15-year-old boy was struck with a baseball over the nasal bridge. After 2 days of epistaxis from his left nares, he was admitted to a local hospital. Tomograms showed a comminuted nasal fracture. The nose was packed and intravenous antibiotics were administered. Twelve hours after admission, nasal arterial bleeding increased. Nasal packings were replaced but did not control the epistaxis. The hematocrit level fell from 37% on
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Fig 1. Cerebral angiography after injection of the left internal carotid artery reveals a choroidal blush (arrows) in the arterial (left) and arteriovenous (right) phases.
admission to 29% 4 days later. Surgical ligation of the left anterior and posterior ethmoidal arteries and a submucous resection of the nasal septum were performed. However, epistaxis continued. The patient was transfused with two units of packed red blood cells. Ophthalmologic examination showed a visual acuity of 20/ 20 in each eye. The pupils reacted briskly to light without an afferent defect. Intraocular pressures were normal. Extraocular movements were full. A mild amount of periorbital edema surrounded the left eye. Vitreoretinal examination through dilated pupils was normal. Computed tomography (CT) showed several fractures involving the posterior wall of the frontal sinus and cribiform plate. Cerebral angiography with selective catheterization of the left internal carotid artery demonstrated a choroidal blush (Fig 1). After injection of contrast into the external carotid artery, a faint choroidal blush was not clearly seen until subtractions were made (Fig 2). Eight days after the injury, the patient experienced recurrent, uncontrolled epistaxis. Despite repacking of his nares in the operating room, a continuous flow of blood was noted. Consequently, embolization of the internal maxillary artery with polyvinyl alcohol was attempted. Under general anesthesia, using a right inguinal puncture, a catheter was advanced from the fern-
528
oral artery to the internal maxillary artery and a biplane angiographic run was made. A left internal maxillary artery injection with some reflux into the superficial temporal artery demonstrated a very faint choroidal blush, which was more evident after subtractions were made. Due to the risk of injected emboli occluding the choroidal vessels through potential middle meningeal artery to ciliary artery anastomoses, the catheter was advanced beyond the region of the middle meningeal artery. Two vials of 100 to 200 !Lm polyvinyl alcohol were then injected. The procedure appeared to be uncomplicated and successful, although postembolization films demonstrated partial obliteration of the middle meningeal artery beyond the foramen spinosum as well as obliteration of the second and third portions of the internal maxillary artery (Fig 3). The patient complained of loss of vision in the left eye upon awakening, 6 hours later. Visual acuity dropped to light perception. Retinal examination of the left eye showed attenuated vasculature and a pale edematous macula. Spherical emboli were visualized in the smaller retinal arterioles and choroidal vessels. To increase ocular perfusion, intraocular pressure was lowered by intravenous administration of 500 mg of acetazolamide, topical timolol maleate 0.5%, and paracentesis of the anterior segment with removal of 0.1 ml of aqueous fluid. Vasodilation was attempted by inhalation of a mixture of 95% oxygen and 5%
MAMES et al
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carbon dioxide gases. Eight hours later, visual acuity in the left eye improved to counting fingers at 6 inches. The fifth day after embolization, visual acuity was 20/400. The macula was still edematous (Fig 4). Fluorescein angiography showed markedly diminished to absent fluorescence of the temporal choroidal vasculature throughout most of the study (Fig 5). Not until 80 seconds was dye visible in the peripheral temporal choroidal circulation. Arteriovenous transit time was prolonged and lasted 14 seconds. Twenty days after the embolization procedure, there was a circinate pattern of exudation in the fovea. Pigment clumping was seen at the level of the retinal pigment epithelium and choroid in the temporal peripheral retina. One year later, visual acuity remained 20/400 in the left eye. There was optic atrophy, attenuated vessels, and pigment clumping in the temporal periphery and just temporal to the foveola (Fig 6). Fluorescein angiography demonstrated a region of temporal hypofluorescence and hyperfluorescence.
DISCUSSION Simultaneous infarction of the retina and choroid as seen in our patient is uncommon. When this occurs, it is usually attributed to ophthalmic artery occlusion. 1- 3 Ophthalmic artery occlusion is predominantly due to atherosclerosis involving the internal carotid artery system, although cardiac embolic disease and mucormycosis may result in a similar picture. 2•4- 7 Since blood flow to the macula is disrupted, the ophthalmoscopic picture of acute ophthalmic artery occlusion often does not include a cherry red spot, which represents preservation of the choroidal blood supply to the outer retina in the region of the macula. Our patient had disruption of the choroidal perfusion to the macula, and consequently he did not have a cherry red spot in this region. The retinal edema and ischemia in our patient were due to disruption of the circulation to the inner retina. Preservation of the nasal foveolar choroidal and retinal circulation blood supply by the patent cilioretinal artery may have contributed to the recovery of vision from light perception to 20/400 after treatment. The substantial retinal pigmentary alterations that later developed in our patient were due to the disruption of the blood supply to the outer retinal layers. The ophthalmic artery supplies blood to the inner retina via the central retinal artery and the outer retina and choroid via the posterior ciliary arteries. We suspect our patient had infarction of the outer retina from occlusion of the posterior ciliary arteries and of the inner retina by occlusion of the central retinal artery due to the small size (100-200 ttm) of the injected particles of polyvinyl alcohol. However, thrombosis of the ophthalmic artery was not excluded by selective angiography of the internal carotid artery after the embolization procedure and could have resulted in a clinical appearance similar to our patient who presumably suffered multiple emboli, occluding the central retinal artery and posterior ciliary arteries. Congenital variations of the anastomotic vascular supply to the brain and eye exist, although these organs are predominantly perfused by the internal carotid artery. Typically, the ophthalmic artery is the first branch of the
Fig 2. Selective injection of the left external carotid artery also shows a choroidal blush (arrows).
Fig 3. After particle embolization, selective injection of contrast into the left internal maxillary artery shows obliteration of perfusion through the lacrimal artery and loss of the choroidal blush.
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Fig 4. Top left, five days after particle embolization, there is mild attenuation of the retinal vasculature and nerve fiber layer edema of the posterior pole in the left eye. Fig 5. Top right, early venous phase of the fluorescein angiogram of the left eye 5 days after embolization shows absence of choroidal fluorescence in the temporal fovea and peripheral retina. Notice the striking demarcation between the perfused and non perfused choroid. Fig 6. One year after particle embolization, there is optic atrophy, attenuation of the vessels, and pigmentary changes at the level of the retinal pigment epithelium in the temporal macula of the left eye (bottom left). The temporal retina has areas of retinal pigment epithelial atrophy and increased pigmentation consistent with a previous choroidal vascular insult (bottom right).
internal carotid artery. The central retinal artery and posterior ciliary arteries are supplied by the ophthalmic artery. Consequently a choroidal blush is commonly visualized by selective injection of contrast into the internal carotid artery. Some of the posterior ciliary arteries may also have branches from the lacrimal artery. The recurrent meningeal artery is a branch of the lacrimal artery and enters the cranial cavity to anastomose with a branch of the middle meningeal artery. Infrequently, the lacrimal artery, ophthalmic artery, and posterior ciliary arteries may branch directly from an anterior branch of the middle meningeal artery. The presence of a choroidal blush upon injection of the external carotid artery is evidence of anastomosis between the external carotid artery and internal carotid artery circulations. 6•8 The importance of this anatomic variation must be noted before injection of emboli.9 In our patient, a reflux of emboli may have entered the middle meningeal artery and passed into the ophthalmic circulation through the lacrimal artery via an anastomotic vessel (Fig 7). The literature cautions not to infuse particles 530
at a rate greater than that which the vessel can accept because of the increased risk of excessive run-off and unplanned embolization. 10•11 In general, embolization of the internal maxillary artery for uncontrolled posterior epistaxis has been reported to have potentially little risk. 12 Embolization of the external carotid artery system is also an accepted mode of therapy for dural-cavernous fistulas and may carry a similar risk to vision if the same anatomic variation seen in our patient is present. Anastomotic vasculature between the internal maxillary artery and the internal carotid artery also can provide a route of embolism to the brain. Kupersmith and associates 13 described transient contralateral hemiparesis after cyanoacrylate embolization of the external carotid artery for a carotid-cavernous fistula. Ophthalmologists should be aware of the potential for permanent blindness (Golnik KC, unpublished data; presented at the 1990 American Academy of Ophthalmology annual meeting) and neurologic deficits following embolization of this usually "safe" arterial system. A variety of nonadsorbable materials have been used
MAMES et al
•
CILIARY ARTERY OCCLUSION
tion. When this sign is present, patients must be advised of the risk of permanent visual loss as a result of selective external carotid artery embolization.
REFERENCES -MM
OA I
OPTIC N. -
',,
I
I
"§-
ICA
Fig 7. Illustration of a possible route of the polyvinyl alcohol (thin arrows) causing obstruction of the posterior ciliary arteries (PCA) and the central retinal artery (CRA). Notice the anastomotic vessel (ANA). The polyvinyl alcohol foam was injected within the IMA. (OA = ophthalmic artery; ICA = internal carotid artery; LA = lacrimal artery; MM = middle meningeal artery; IMA = internal maxillary artery; ECA = external carotid artery.)
for arterial embolization. These include beads composed of silicone, stainless steel, and lead, as well as isobutyl-2cyanoacrylate, and polyvinyl alcohol foam. 14- 18 In our patient, particulate polyvinyl alcohol sponges were used. Polyvinyl alcohol is converted into a sponge-like material by foaming agents and hardened with formaldehyde. It is inert, although it expands in liquid media. These materials all carry a risk of arterial occlusion. Our case emphasizes that a choroidal blush, during selective cerebral angiography of the external carotid artery, is an important sign of anastomoses between the posterior ciliary arteries and external carotid artery. This finding must be recognized before embolization procedures in a "safe" arterial system such as the external carotid artery. In our case, embolization of the ocular circulation may have been averted if digital subtraction arteriography or conventional subtractions were obtained before embolization. Digital subtraction arteriography or conventional subtractions should be obtained before cerebral embolization procedures and carefully reviewed to detect a choroidal blush associated with external carotid artery injec-
1. Brown GC, Magargal LE, Sergott R. Acute obstruction of the retinal and choroidal circulations. Ophthalmology 1986; 93:1373-82. 2. Brown GC, Magargal LE. Sudden occlusion of the retinal and posterior choroidal circulations in a youth. Am J Ophthalmol 1979; 88:690-3. 3. Wilson RS, Havener WH, McGrew RN. Bilateral retinal artery and cho· riocapillaris occlusion following the injection of long-acting corticoste· roid suspensions in combination with other drugs: I. Clinical studies. Ophthalmology 1978; 85:967-7 4. 4. Appen RE, Wray SH, Cogan DG. Central retinal artery occlusion. Am J Ophthalmol1975; 79:374-81. 5. Cogan DC, Wray SH. Vascular occlusions in the eye from cardiac myxomas. Am J Ophthalmol 1975; 80:396-403. 6. Russell EJ. Functional angiography of the head and neck. AJNR 1986; 7:927-36. 7. Qingli L, Orcutt JC, Seitter LS. Orbital mucormycosis with retinal and ciliary artery occlusions. Br J Ophthalmol 1989; 73:680-3. 8. Dilenge D, Ascher! GF Jr. Variations of the ophthalmic and middle meningeal arteries: relation to the embryonic stapedial artery. AJNR 1980; 1:45-53. 9. Carlson MR, Pilger IS, Rosenbaum AL. Central retinal artery occlusion after carotid angiography. Am J Ophthalmol1976; 81:103-4. 10. Kerber CW. Catheter therapy: fluoroscopic monitoring of deliberate embolic occlusion. Radiology 1977; 125:538-40. 11. Kerber CW. Flow-controlled therapeutic embolization: a physiologic and safe technique. AJR Am J Roentgenol 1980; 134:557-61. 12. Roberson GH, Reardon EJ. Angiography and embolization of the internal maxillary artery for posterior epistaxis. Arch Otolaryngol1979; 105:333-7. 13. Kupersmith MJ, Berenstein A, Flamm E, Ransohoff J. Neuroophthalmologic abnormalities and intravascular therapy of traumatic carotid cavernous fistulas. Ophthalmology 1986; 93:906-12. 14. Luessenhop AJ, Spence WT. Artificial embolization of cerebral arteries. Report of use in a case of arteriovenous malformation. JAMA 1960; 172:1153-5. 15. Dotter CT, Goldman ML, Rosch J. Instant selective arterial occlusion with isobutyl 2-cyanoacrylate. Radiology 1975; 114:227-30. 16. Doppman JL, Di Chiro G, Ommaya A. Obliteration of spinal-cord arteriovenous malformation by percutaneous embolisation [Letter]. Lancet 1968; 1:4 77. 17. Newton TH, Adams JE. Angiographic demonstration and nonsurgical embolization of spinal cord angioma. Radiology 1968; 91 :873-6. 18. Tadavarthy SM, Moiler JH, Amplatz K. Polyvinyl alcohol (lvalon)-new embolic material. AJR Am J Roentgenol 1975; 125:609-16.
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Abstract: A 15-year-old boy underwent neuroradiologic embolization of the left internal maxillary artery with polyvinyl alcohol to stop traumatic epistaxis after failure of surgical clipping and nasal packing. Selective catheterization of the external carotid artery before embolization showed a faint choroidal blush. Although the procedure provided hemostasis, embolization to the central retinal artery and ciliary arteries resulted in loss of vision. The route of the eml:loli to the eye was via the anastomotic network of the lacrimal artery supplied by the external carotid artery system. Neuroradiologic embolization of the external carotid artery is an effective mode of therapy for dural-cavernous fistulas when fed by the external carotid artery system. Because the blood flow to the brain and eye is predominantly supplied by the internal carotid artery, embolization of the external carotid artery is considered relatively safe. The authors document the importance of recognition of the choroidal blush during selective external carotid artery angiography as a sign of collateral blood flow to the eye. Physicians and patients need to be aware of the risk of blindness as a complication of external carotid artery embolization when this sign is present. Ophthalmology 1991; 98:527-531
Occlusion of the central retinal artery and posterior ciliary arteries after selective embolization of the external carotid artery system is uncommon, since ocular blood flow is predominantly supplied by the internal carotid
artery system. Consequently, permanent loss of vision due to infarction of the neurosensory retina after particle embolization of the external carotid artery system is rare. The importance of a choroidal blush as the harbinger of collateral blood supply to the eye by the external carotid artery system is emphasized.
Originally received: August 13, 1990. Revision accepted: December 3, 1990. 1 2
3
Department of Ophthalmology, University of Florida, Gainesville. Department of Ophthalmology, Tufts New England Medical Center, Boston, and Brown University, Providence. Department of Neurology, University of Florida, Gainesville.
Supported in part by an unrestricted grant to the Department of Ophthalmology from Research to Prevent Blindness, Inc, New York, New York. Reprint requests to Robert N. Mames, MD, Retinal Vitreous Service, Department of Ophthalmology, Box J-284, JHMHC, University of Florida, Gainesville, FL 32610-0284.
CASE REPORT A 15-year-old boy was struck with a baseball over the nasal bridge. After 2 days of epistaxis from his left nares, he was admitted to a local hospital. Tomograms showed a comminuted nasal fracture. The nose was packed and intravenous antibiotics were administered. Twelve hours after admission, nasal arterial bleeding increased. Nasal packings were replaced but did not control the epistaxis. The hematocrit level fell from 37% on
527
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VOLUME 98
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Fig 1. Cerebral angiography after injection of the left internal carotid artery reveals a choroidal blush (arrows) in the arterial (left) and arteriovenous (right) phases.
admission to 29% 4 days later. Surgical ligation of the left anterior and posterior ethmoidal arteries and a submucous resection of the nasal septum were performed. However, epistaxis continued. The patient was transfused with two units of packed red blood cells. Ophthalmologic examination showed a visual acuity of 20/ 20 in each eye. The pupils reacted briskly to light without an afferent defect. Intraocular pressures were normal. Extraocular movements were full. A mild amount of periorbital edema surrounded the left eye. Vitreoretinal examination through dilated pupils was normal. Computed tomography (CT) showed several fractures involving the posterior wall of the frontal sinus and cribiform plate. Cerebral angiography with selective catheterization of the left internal carotid artery demonstrated a choroidal blush (Fig 1). After injection of contrast into the external carotid artery, a faint choroidal blush was not clearly seen until subtractions were made (Fig 2). Eight days after the injury, the patient experienced recurrent, uncontrolled epistaxis. Despite repacking of his nares in the operating room, a continuous flow of blood was noted. Consequently, embolization of the internal maxillary artery with polyvinyl alcohol was attempted. Under general anesthesia, using a right inguinal puncture, a catheter was advanced from the fern-
528
oral artery to the internal maxillary artery and a biplane angiographic run was made. A left internal maxillary artery injection with some reflux into the superficial temporal artery demonstrated a very faint choroidal blush, which was more evident after subtractions were made. Due to the risk of injected emboli occluding the choroidal vessels through potential middle meningeal artery to ciliary artery anastomoses, the catheter was advanced beyond the region of the middle meningeal artery. Two vials of 100 to 200 !Lm polyvinyl alcohol were then injected. The procedure appeared to be uncomplicated and successful, although postembolization films demonstrated partial obliteration of the middle meningeal artery beyond the foramen spinosum as well as obliteration of the second and third portions of the internal maxillary artery (Fig 3). The patient complained of loss of vision in the left eye upon awakening, 6 hours later. Visual acuity dropped to light perception. Retinal examination of the left eye showed attenuated vasculature and a pale edematous macula. Spherical emboli were visualized in the smaller retinal arterioles and choroidal vessels. To increase ocular perfusion, intraocular pressure was lowered by intravenous administration of 500 mg of acetazolamide, topical timolol maleate 0.5%, and paracentesis of the anterior segment with removal of 0.1 ml of aqueous fluid. Vasodilation was attempted by inhalation of a mixture of 95% oxygen and 5%
MAMES et al
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CILIARY ARTERY OCCLUSION
carbon dioxide gases. Eight hours later, visual acuity in the left eye improved to counting fingers at 6 inches. The fifth day after embolization, visual acuity was 20/400. The macula was still edematous (Fig 4). Fluorescein angiography showed markedly diminished to absent fluorescence of the temporal choroidal vasculature throughout most of the study (Fig 5). Not until 80 seconds was dye visible in the peripheral temporal choroidal circulation. Arteriovenous transit time was prolonged and lasted 14 seconds. Twenty days after the embolization procedure, there was a circinate pattern of exudation in the fovea. Pigment clumping was seen at the level of the retinal pigment epithelium and choroid in the temporal peripheral retina. One year later, visual acuity remained 20/400 in the left eye. There was optic atrophy, attenuated vessels, and pigment clumping in the temporal periphery and just temporal to the foveola (Fig 6). Fluorescein angiography demonstrated a region of temporal hypofluorescence and hyperfluorescence.
DISCUSSION Simultaneous infarction of the retina and choroid as seen in our patient is uncommon. When this occurs, it is usually attributed to ophthalmic artery occlusion. 1- 3 Ophthalmic artery occlusion is predominantly due to atherosclerosis involving the internal carotid artery system, although cardiac embolic disease and mucormycosis may result in a similar picture. 2•4- 7 Since blood flow to the macula is disrupted, the ophthalmoscopic picture of acute ophthalmic artery occlusion often does not include a cherry red spot, which represents preservation of the choroidal blood supply to the outer retina in the region of the macula. Our patient had disruption of the choroidal perfusion to the macula, and consequently he did not have a cherry red spot in this region. The retinal edema and ischemia in our patient were due to disruption of the circulation to the inner retina. Preservation of the nasal foveolar choroidal and retinal circulation blood supply by the patent cilioretinal artery may have contributed to the recovery of vision from light perception to 20/400 after treatment. The substantial retinal pigmentary alterations that later developed in our patient were due to the disruption of the blood supply to the outer retinal layers. The ophthalmic artery supplies blood to the inner retina via the central retinal artery and the outer retina and choroid via the posterior ciliary arteries. We suspect our patient had infarction of the outer retina from occlusion of the posterior ciliary arteries and of the inner retina by occlusion of the central retinal artery due to the small size (100-200 ttm) of the injected particles of polyvinyl alcohol. However, thrombosis of the ophthalmic artery was not excluded by selective angiography of the internal carotid artery after the embolization procedure and could have resulted in a clinical appearance similar to our patient who presumably suffered multiple emboli, occluding the central retinal artery and posterior ciliary arteries. Congenital variations of the anastomotic vascular supply to the brain and eye exist, although these organs are predominantly perfused by the internal carotid artery. Typically, the ophthalmic artery is the first branch of the
Fig 2. Selective injection of the left external carotid artery also shows a choroidal blush (arrows).
Fig 3. After particle embolization, selective injection of contrast into the left internal maxillary artery shows obliteration of perfusion through the lacrimal artery and loss of the choroidal blush.
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Fig 4. Top left, five days after particle embolization, there is mild attenuation of the retinal vasculature and nerve fiber layer edema of the posterior pole in the left eye. Fig 5. Top right, early venous phase of the fluorescein angiogram of the left eye 5 days after embolization shows absence of choroidal fluorescence in the temporal fovea and peripheral retina. Notice the striking demarcation between the perfused and non perfused choroid. Fig 6. One year after particle embolization, there is optic atrophy, attenuation of the vessels, and pigmentary changes at the level of the retinal pigment epithelium in the temporal macula of the left eye (bottom left). The temporal retina has areas of retinal pigment epithelial atrophy and increased pigmentation consistent with a previous choroidal vascular insult (bottom right).
internal carotid artery. The central retinal artery and posterior ciliary arteries are supplied by the ophthalmic artery. Consequently a choroidal blush is commonly visualized by selective injection of contrast into the internal carotid artery. Some of the posterior ciliary arteries may also have branches from the lacrimal artery. The recurrent meningeal artery is a branch of the lacrimal artery and enters the cranial cavity to anastomose with a branch of the middle meningeal artery. Infrequently, the lacrimal artery, ophthalmic artery, and posterior ciliary arteries may branch directly from an anterior branch of the middle meningeal artery. The presence of a choroidal blush upon injection of the external carotid artery is evidence of anastomosis between the external carotid artery and internal carotid artery circulations. 6•8 The importance of this anatomic variation must be noted before injection of emboli.9 In our patient, a reflux of emboli may have entered the middle meningeal artery and passed into the ophthalmic circulation through the lacrimal artery via an anastomotic vessel (Fig 7). The literature cautions not to infuse particles 530
at a rate greater than that which the vessel can accept because of the increased risk of excessive run-off and unplanned embolization. 10•11 In general, embolization of the internal maxillary artery for uncontrolled posterior epistaxis has been reported to have potentially little risk. 12 Embolization of the external carotid artery system is also an accepted mode of therapy for dural-cavernous fistulas and may carry a similar risk to vision if the same anatomic variation seen in our patient is present. Anastomotic vasculature between the internal maxillary artery and the internal carotid artery also can provide a route of embolism to the brain. Kupersmith and associates 13 described transient contralateral hemiparesis after cyanoacrylate embolization of the external carotid artery for a carotid-cavernous fistula. Ophthalmologists should be aware of the potential for permanent blindness (Golnik KC, unpublished data; presented at the 1990 American Academy of Ophthalmology annual meeting) and neurologic deficits following embolization of this usually "safe" arterial system. A variety of nonadsorbable materials have been used
MAMES et al
•
CILIARY ARTERY OCCLUSION
tion. When this sign is present, patients must be advised of the risk of permanent visual loss as a result of selective external carotid artery embolization.
REFERENCES -MM
OA I
OPTIC N. -
',,
I
I
"§-
ICA
Fig 7. Illustration of a possible route of the polyvinyl alcohol (thin arrows) causing obstruction of the posterior ciliary arteries (PCA) and the central retinal artery (CRA). Notice the anastomotic vessel (ANA). The polyvinyl alcohol foam was injected within the IMA. (OA = ophthalmic artery; ICA = internal carotid artery; LA = lacrimal artery; MM = middle meningeal artery; IMA = internal maxillary artery; ECA = external carotid artery.)
for arterial embolization. These include beads composed of silicone, stainless steel, and lead, as well as isobutyl-2cyanoacrylate, and polyvinyl alcohol foam. 14- 18 In our patient, particulate polyvinyl alcohol sponges were used. Polyvinyl alcohol is converted into a sponge-like material by foaming agents and hardened with formaldehyde. It is inert, although it expands in liquid media. These materials all carry a risk of arterial occlusion. Our case emphasizes that a choroidal blush, during selective cerebral angiography of the external carotid artery, is an important sign of anastomoses between the posterior ciliary arteries and external carotid artery. This finding must be recognized before embolization procedures in a "safe" arterial system such as the external carotid artery. In our case, embolization of the ocular circulation may have been averted if digital subtraction arteriography or conventional subtractions were obtained before embolization. Digital subtraction arteriography or conventional subtractions should be obtained before cerebral embolization procedures and carefully reviewed to detect a choroidal blush associated with external carotid artery injec-
1. Brown GC, Magargal LE, Sergott R. Acute obstruction of the retinal and choroidal circulations. Ophthalmology 1986; 93:1373-82. 2. Brown GC, Magargal LE. Sudden occlusion of the retinal and posterior choroidal circulations in a youth. Am J Ophthalmol 1979; 88:690-3. 3. Wilson RS, Havener WH, McGrew RN. Bilateral retinal artery and cho· riocapillaris occlusion following the injection of long-acting corticoste· roid suspensions in combination with other drugs: I. Clinical studies. Ophthalmology 1978; 85:967-7 4. 4. Appen RE, Wray SH, Cogan DG. Central retinal artery occlusion. Am J Ophthalmol1975; 79:374-81. 5. Cogan DC, Wray SH. Vascular occlusions in the eye from cardiac myxomas. Am J Ophthalmol 1975; 80:396-403. 6. Russell EJ. Functional angiography of the head and neck. AJNR 1986; 7:927-36. 7. Qingli L, Orcutt JC, Seitter LS. Orbital mucormycosis with retinal and ciliary artery occlusions. Br J Ophthalmol 1989; 73:680-3. 8. Dilenge D, Ascher! GF Jr. Variations of the ophthalmic and middle meningeal arteries: relation to the embryonic stapedial artery. AJNR 1980; 1:45-53. 9. Carlson MR, Pilger IS, Rosenbaum AL. Central retinal artery occlusion after carotid angiography. Am J Ophthalmol1976; 81:103-4. 10. Kerber CW. Catheter therapy: fluoroscopic monitoring of deliberate embolic occlusion. Radiology 1977; 125:538-40. 11. Kerber CW. Flow-controlled therapeutic embolization: a physiologic and safe technique. AJR Am J Roentgenol 1980; 134:557-61. 12. Roberson GH, Reardon EJ. Angiography and embolization of the internal maxillary artery for posterior epistaxis. Arch Otolaryngol1979; 105:333-7. 13. Kupersmith MJ, Berenstein A, Flamm E, Ransohoff J. Neuroophthalmologic abnormalities and intravascular therapy of traumatic carotid cavernous fistulas. Ophthalmology 1986; 93:906-12. 14. Luessenhop AJ, Spence WT. Artificial embolization of cerebral arteries. Report of use in a case of arteriovenous malformation. JAMA 1960; 172:1153-5. 15. Dotter CT, Goldman ML, Rosch J. Instant selective arterial occlusion with isobutyl 2-cyanoacrylate. Radiology 1975; 114:227-30. 16. Doppman JL, Di Chiro G, Ommaya A. Obliteration of spinal-cord arteriovenous malformation by percutaneous embolisation [Letter]. Lancet 1968; 1:4 77. 17. Newton TH, Adams JE. Angiographic demonstration and nonsurgical embolization of spinal cord angioma. Radiology 1968; 91 :873-6. 18. Tadavarthy SM, Moiler JH, Amplatz K. Polyvinyl alcohol (lvalon)-new embolic material. AJR Am J Roentgenol 1975; 125:609-16.
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