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Show Ocular Ischemic Syndrome After Occlusion of Both External Carotid Arteries Adeela M. Alizai, MD, Jonathan D. Trobe, MD, B. Gregory Thompson, MD, James D. Izer, MD, Wayne T. Cornblath, MD, and John P. Deveikis, MD Abstract: The ocular ischemic syndrome ( OIS) has been occlusion of the ECAs may cause the OIS if the eye is reported in association with high- grade stenosis or oc- predominantly supplied by the ECA and the endarterec-clusion of the common carotid artery ( CCA) or internal tomy surgeon does not meticulously remove the entire carotid artery ( ICA) but never with high- grade stenosis or plaque stump from that vessel. occlusion of the external carotid artery ( ECA) alone. We describe two patients who developed OIS with bilateral occlusion of the ECAs yet patent CCAs and ICAs. In one case, unilateral OIS followed consecutive bilateral carotid endarterectomies. In the other case, OIS developed spon- CASK RFPORTS taneously OU but was exacerbated in one eye after ip- Case 1 silateral carotid endarterectomy ( CE) in the setting of pre- A 70- year- old hypertensive woman underwent con-existing contralateral ECA occlusion. In some individuals, secutive carotid endarterectomies for asymptomatic carotid the ECA is the primary source of arterial blood flow to the stenosis. Sixteen months after the second endarterectomy eye. Because of this fact, the endarterectomy surgeon must and o n e m o n m after undergoing abdominal aortic aneu-avoid causing ECA occlusion by meticulously removing rysmal repair, she developed periocular pain, jaw claudi-not only the ICA plaque, but also the entire ECA plaque. cati0n, facial weakness, and blurred vision on the left side. (/ Neuro- Ophthalmol 2005; 25: 268- 272) Best- corrected visual acuities were 20/ 40 OD and 20/ 100 OS. The pupil OD measured 2.5 mm in dim illumination and reacted normally to light, whereas the pupil OS measured 3.5 mm and reacted minimally with an afferent T h e ocular ischemic syndrome ( OIS) has been reported pupillary defect OS. Intraocular pressures were 24 mm Hg in association with high- grade stenosis or occlusion of OD and 10 mm Hg OS. Ocular ductions and alignment were the common carotid artery ( CCA) or internal carotid artery normal. A left lower motor neuron seventh cranial nerve ( ICA) ( 1- 8). Yet the external carotid artery ( ECA) may palsy was present. Ms neovascularization was present in the occasionally be the principal source of blood flow to the OS. Ophthalmoscopy disclosed surface wrinkling macul-orbit and eye especially if there is hemodynamically sig- opathy OD and perivenous hemorrhages OS. nificant CCA or ICA stenosis ( 9). The OIS has not been Catheter cerebral angiography showed bilateral prox-reported in association with occlusion of the ECA when the jural ECA occlusions. Both ICAs filled normally. The right CCA and ICA are patent. ophthalmic artery ( OA) filled from the right OA, but the left We describe two patients who developed OIS in OA did not fill ( Fig. 1, A and B). After left ECA patch association with proximal bilateral ECA occlusion dem- grafting and stenting, angiography demonstrated ample onstrated on cerebral angiography. In both cases, cerebral flow in the ECA; the left OA filled via branches of the ECA angiography did not show high- grade stenosis or occlu- ( Fig. 1Q. The patient's periocular pain and jaw claudica-sion of the CCAs or ICAs. We hypothesize that bilateral tion resolved completely within days. The seventh nerve palsy resolved within months. However, she developed markedly increased intraocular pressure OS, presumably as Departments of Ophthalmology ( AMA, JDT, JDI, WTC), Neurology the result of restored blood flow to the ciliary body, which ( AMA, JDT, WTC), Neurosurgery ( JDT, BGT), Radiology ( BGT, JPD), c o u l d n Q W p r o d u c e a m o r e n o r m a l v o l u m e o f a q u e 0 U S ; i ts and Otolaryngology ( BGT), Kellogg Eye Center, University of Michigan, . _ , , 1 1 1 , 11 <• 1 Ann Arbor Michigan e om e eye blocked by angle closure from neovascular Address correspondence to Jonathan D Trobe, MD, Kellogg Eye Cen- glaucoma. Cyclocryotherapy returned the intraocular pres-ter, 1000 Wall street, Ann Arbor, MI 48104; E- mail: jdtrobe@ umich. edu sure to the normal range, and iris neovascularization and venous stasis retinopathy regressed several months after panretinal photocoagulation. Case 2 A 70- year- old man developed blurred vision in the OD and within a week, in the OS as well. He had diabetes melhtus, hypertension, hyperlipidemia, and arteriosclerotic peripheral vascular occlusive disease. Examination elsewhere disclosed hand movements vision OD and light perception OS. In the OD, ophthalmoscopy showed ischemic retinal whitening; in the OS, it showed pallid optic disc swelling. Brain MRI showed many small T2 white matter high-signal abnormalities consistent with small vessel occlusive disease. Magnetic resonance angiography ( MRA) showed occlusive disease of the left ECA but no significant stenosis of other neck vessels. A right temporal artery biopsy showed arteriosclerosis but no arteritis. As a desperate measure, a right carotid endarterec-tomy ( CE) was performed despite the lack of convincing MRA evidence of hemodynamically significant cervical carotid stenosis. Several days later, the patient developed a large area of brawny skin necrosis in the right frontal scalp region ( Fig. 2), decreased sensation in the first division of the right fifth cranial nerve, no light perception binocularly complete ptosis of the right upper lid ( Fig. 3), and complete ophthalmoplegia of the OD ( Fig. 4). Both pupils measured 6 mm and were unreactive to light. The right cornea was opacified with Descemet folds ( Fig. 5). Intraocular pressures measured 6 mm Hg OD and 7 mm Hg OS. In the OS, ophthalmoscopy revealed pallid disc swelling. Catheter cerebral angiography showed non- filling of both ECAs, non- stenosing atherosclerosis of both ICAs, non- filling of the right ophthalmic artery, and filling of the left ophthalmic artery ( Fig. 6). A second temporal artery biopsy, performed on the left side, failed to show arteritis. DISCUSSION Our two patients manifested the OIS in the setting of bilateral ECA occlusions and adequate caliber CCAs and ICAs. In Case 1, bilateral ECA occlusion followed consecutive carotid endarterectomies. The left OA did not fill, presumably because it had depended on the left ECA. The patient developed left OIS. The right OA filled from the right ICA, preserving adequate blood flow to the eye and preventing OIS. In Case 2, after the patient had developed OIS bilaterally, left ECA stenosis was found by MRA. After a right CE, OIS worsened in the OD. Catheter angiography revealed bilateral ECA occlusions with patent ICAs. The left OA filled from the left ICA; the right OA did not fill. We do not know if CE produced a right ECA occlusion that was not evident preoperatively on MRA. We presume that OIS developed because the eyes of our two patients depended on arterial blood predominantly from the ECA, not the ICA, which remained patent throughout. OIS has been documented in CCA ( 1- 4) and ICA ( 5- 8) occlusive disease, but not in ECA occlusive disease alone. The ICA is usually the main feeder of the ophthalmic artery, but some autopsy dissections have disclosed that the ECA is the principal supply line ( Fig. 7) via angular, middle meningeal, lacrimal, or anterior ethmoidal branches ( 9). Notably, in lower animals like deer and antelope, the eye and orbit are supplied entirely by a branch of the ECA ( 10) ( Fig. 8). Because of extensive cross flow between the two ECAs, occlusion of one ECA would be unlikely to cause the OIS. In our two patients, occlusion of both ECAs was present. As in our Case 1, this phenomenon may occur iatrogenically when the ECA plaque is incompletely removed during carotid endarterectomy ( CE). A common surgical approach in CE is to concentrate on meticulous plaque removal in the CCA and ICA with the assumption that residual plaque and stenosis of the ECA is inconsequential ( 11,12). This assumption may prove problematic in patients who develop stump emboli that flow into the ICA from an occluded ECA and in patients whose eyes depend on flow from the ECAs. Iatrogenic ECA occlusion after endarterectomy could arise in one of two ways ( Fig. 9). The more common way is through unintentional fracturing of the ECA plaque. The less common way is through incomplete remove of the distal portion of the ECA plaque. In either case, ECA stenosis may be aggravated producing turbulent flow that may lead to ECA thrombosis or thromboembolism from the closure, the removal of plaque should be sufficiently distal occluded stump back into the ICA. so that palpation will reveal an increased pulse in To avoid ECA occlusion, the endarterectomized a compressible ECA without any residual palpably non-vessel must be carefully inspected to assure adequate compressible plaque. After closure of the arteriotomy, an plaque removal before and after arteriotomy closure. Before intraoperative micro- Doppler probe is also useful to assess arteriotomy closure, use of the operating microscope or adequacy of flow in the ECA. After the use of the standard loupe illumination and magnification will facilitate a thor- longitudinal endarterectomy incision, if the plaque frac-ough removal of plaque. ECA " eversion endarterectomy" tares too proximally and the ECA cannot be adequately ( wherein the CCA just below the bifurcation, or the ECA everted over it to allow for ECA plaque removal, then just above the bifurcation, is transected and " everted" or a separate linear incision in the ECA, or a " Y" incision unrolled in a caudal- cephalad fashion) may also be helpful from the CCA into the ECA, is required to complete the in removing the most distal ECA plaque. After arteriotomy endarterectomy. REFERENCES 1. Borruat FX, Bogousslavsky J, Uffer S, et al. Orbital infarction 7. Fisher M. Transient monocular blindness associated with hemiplegia, syndrome. 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