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Show PHOTO ESSAY Bilateral Simultaneous Central Retinal Artery Occlusions in Atherosclerosis James D. her, MD FIG. 1. Central retinal artery occlusion with cilioretinal sparing in the OS ( A) and OD ( B). Photographs were taken 3 days after the nearly simultaneous onset of visual loss in both eyes. An 82- year- old woman with atherosclerosis developed central retinal artery occlusions ( CRAOs) in both eyes within an interval of 5 minutes. There was no evidence of a thromboembolic source, systemic hypotension, vasculitis, migraine, or hypercoagulable state. Virtually simultaneous binocular CRAOs have been rarely reported, and suggest the possibility of a systemic but still undefined " hypercoagulable trigger." ( JNeuro- Ophthalmol 2002; 22: 33- 34) An 82- year- old woman complained of acutely decreased vision in both eyes. Eight hours earlier, she had been watching television when the vision in her OS became " wavy and dim." Within 5 minutes, the vision in her OD dimmed. She experienced no other symptoms. She had a longstanding history of hypertension, hy-perlipidemiam, and polycythemia vera, which had not required treatment, of 15 years. She also reported a 60 pack-year history of tobacco use. Kellogg Eye Center, Department of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, Michigan, USA. Address correspondence to James D. Izer, MD, Kellogg Eye Center, 1000 Wall Street, Ann Arbor, MI 48015, USA; E- mail: jdtrobe@ umich. edu Blood pressure was 150/ 88; other vital signs and general physical examination were normal. Visual acuity was hand movements bilaterally. Pupils measured 5 mm in dim illumination and reacted sluggishly to direct light without an afferent defect. The ocular adnexal and motility examinations were normal. Moderate nuclear sclerosis was present bilaterally, and intraocular pressures were 15 mm Hg in both eyes. Fundus examination revealed ischemic whitening of the posterior retina and cherry red spots with cilioretinal artery sparing in both eyes ( Figs. 1 A, IB). A brain and orbit computed tomographic ( CT) scan was normal. White blood cell count was 10.1 K/ mm3, red cell count 4.59 M/ mm3, hemoglobin 15.1 g/ dL, hematocrit 44.5%, and platelets 200 K/ mm3. Eight hours after the onset of bilateral blindness, the patient underwent cerebral angiography, which revealed a normal aortic arch and patent carotid and ophthalmic arteries bilaterally. A total of 20 mg of tissue plasminogen activator ( tPA) was injected into each ophthalmic artery without complications. Intravenous heparin and methylprednisolone 125 mg qid were then administered for 4 days. Subsequent imaging studies included a normal chest x- ray, a carotid ultrasound that revealed no significant disease, and a transesophageal echocardiogram that showed J Neuro- Ophthalmol, Vol. 22, No. 1, 2002 33 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. JNeuro- Ophthalmol, Vol. 22, No. 1, 2002 PHOTO ESSAY mild mitral and tricuspid regurgitation but no masses. Clotting times, homocysteine levels and erythrocyte sedimentation rate were normal. Mutations for factor V Leiden, prothrombin 20210, methylenetetrahydrofolate reductase, and antiphospholipid antibodies were negative. Temporal artery biopsy was negative for mural inflammation but showed moderate atherosclerosis. Six days after the tPA installation, the patient was discharged with a visual acuity of 20/ 800 OD and 20/ 400 OS. Six months later, visual acuity was hand movements OD and 20/ 200 OS. She had developed pain in both eyes due to neovascular glaucoma OU. The patient underwent panretinal photocoagulation bilaterally, followed by laser cycloablation of the OD. One year after the retinal artery occlusions, she had visual acuities of light perception OD and finger counting OS. Central retinal artery occlusion ( CRAO) is binocular in only 1% of cases ( 1), occurring usually in the setting of temporal arteritis, homocystinuria, hypotension, polyarteritis nodosa, and migraine ( 2). However, in previous reports, the two eyes became involved consecutively, with an interval of days to months. We believe this is the first reported case of bilateral simultaneous CRAO, at least in the English literature. In a Japanese report, Nakamura et al. ( 3) described a 78- year- old woman with hypertension, atherosclerosis and history of deep vein thromboses who suffered consecutive binocular CRAOs with an interval of 21 hours. Evaluation was negative for clotting abnormalities or cardiac source, but the patient suffered an ischemic stroke within 1 day of suffering the retinal infarcts and was found to have carotid stenosis. In a Romanian report, Segal et al. ( 4) described two cases of bilateral simultaneous CRAOs without underlying systemic pathology. Our patient, who had ample atherosclerotic risk factors of hypertension, hyperlipidemia, and smoking, suffered bilateral CRAOs with an interval of five minutes. Extensive evaluation for underlying cardiac, clotting, or vasculitic disorders was negative. She gave no indication of having suffered a systemic hypotensive event, using a precipitating medication, or having been dehydrated. Although she had had a remote history of polycythemia vera, her blood counts had been normal without treatment. Atherosclerosis is now viewed as having inflammation as an important component ( 5). We wonder if some systemic factor, inflammatory or otherwise prothrombotic factor, could have contributed to the simultaneous clotting in two remote but symmetrical vessels. REFERENCES 1. Brown GC, Magargal LE. Central retinal artery occlusion and visual acuity. Ophthalmology 1982; 89: 14- 19. 2. Brown GC. Retinal arterial obstructive disease. In: Ryan SJ, ed. Retina. St Louis: Mosby, 1994: 1365- 8. 3. Nakamura H, Sakaue H, Yoshida H, et al. A case of bilateral continuous central retinal artery occulusion [ sic]. Nippon Ganka Gak-kai Zasshi- Acta Societatis Ophthalmologicae Japonicae 1999; 103: 327- 31. 4. Segal N, Spineau L. Ocluzie bilaterala simultana a arterei centrale a retinei. Oftalmologia. 1993; 37: 321- 5. 5. Ross R. Afherosclerosis- an inflammatory disease. N Eng J Med 1999; 340: 115- 26. 34 © 2002 Lippincott Williams & Wilkins Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. |
