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Show PHOTO ESSAY Optic Nerve Enhancement in Hypotensive Ischemic Optic Neuropathy Michael S. Vaphiades, DO FIG. 1. Axial ( A) and coronal ( B) T1 postcontrast fat- suppressed orbital MRIs performed eight weeks after coronary artery bypass surgery at the time blindness was first identified. The scans show enhancement of both optic nerves. Abstract: A 57- year- old woman who had hypotension and cardiac arrest during coronary artery bypass grafting developed hypotensive ischemic optic neuropathy with no light perception vision OU. Bilateral mid- orbital optic nerve enhancement was found on magnetic resonance imaging ( MRI) eight weeks after surgery. Re- examination 16 weeks after surgery showed no light perception vision, dilated un-reactive pupils, and pale optic discs. Bilateral optic nerve enhancement persisted on MRI. Optic nerve enhancement has been reported commonly in radiation- induced ischemic optic neuropathy, occasionally in arteritic ischemic optic neuropathy, and rarely in nonarteritic ischemic optic neuropathy. It has never been reported in hypotensive ischemic optic neuropathy. ( JNeuro- Ophthalmol 2004; 24: 235- 236) A57- year- old woman with a 34- year history of diabetes mellitus underwent coronary artery bypass grafting. During the procedure, hypotension developed, she had a cardiac arrest, and she was placed on a ventilator for several Department of Ophthalmology, University of Alabama, Birmingham, Alabama. This work was supported in part by an unrestricted grant from the Research to Prevent Blindness, Inc., New York, NY. Address correspondence to Michael S. Vaphiades, DO, University of Alabama, Department of Ophthalmology, Suite 601, 700 South 18th Street, Birmingham, AL 53233; E- mail: vaph@ uab. edu weeks. She was unconscious except for a brief period of time during the first week on the ventilator, when the patient reported that she could see normally. After eight weeks on the ventilator, when the patient regained consciousness, she reported being blind OU. She was examined by the staff ophthalmologist, who noted no light perception vision OU without response to the optokinetic drum or mirror test. The pupils were fixed and dilated at 6 mm OU. The intraocular pressures were normal and there was very mild optic nerve pallor without edema OU. The retina appeared normal. Magnetic resonance imaging ( MRI) showed mid-orbital optic nerve enhancement bilaterally ( Fig. 1). Complete blood count, metabolic panel, antinuclear antibody, and angiotensin- converting enzyme were normal. On re- examination 16 weeks after surgery, she was alert with a normal mood and affect. She affirmed that her vision had been normal before the surgery. Visual acuity remained no light perception OU and the pupils were fixed and dilated at 6 mm OU. Fundus examination disclosed markedly pale optic discs. Repeat MRI showed persistent optic nerve enhancement OU ( Fig. 2). Intravenous high-dose methylprednisolone, 1 g per day for three days, did not improve vision. Her examination was unchanged at 20 weeks after surgery. The visual loss in this patient resulted from posterior ischemic optic neuropathy ( 1- 4) presumably related to hypotension. The unusual feature is the presence of optic nerve enhancement on MRI and its persistence 16 weeks J Neuro- Ophthalmol, Vol. 24, No. 3, 2004 235 JNeuro- Ophthalmol, Vol. 24, No. 3, 2004 Vaphiades FIG. 2. Axial precontrast ( A) and postcontrast ( B1, B2) and coronal precontrast ( C) and postcontrast ( D) T1 fat- suppressed orbital MRIs performed 16 weeks after coronary bypass surgery. They show persistent enhancement of both optic nerves. ( B1 and B2, representing different axial levels, are both shown to best visualize each optic nerve.) after the inducing event. There have been no reported cases of optic nerve enhancement in patients with hypotensive ischemic optic neuropathy. It has been described frequently in posterior ischemic optic neuropathy ( PION) after intracranial radiation therapy ( 5). Lee et al ( 6) have reported it in three patients who had arteritic AION ( AAION). The scans for their cases were performed within three weeks of the visual loss. Rizzo et al ( 7) reported, but did not display, optic nerve MRI enhancement in two ( 6%) of 32 patients with non- arteritic anterior ischemic optic neuropathy ( NAION). The scans were performed within 20 days of visual loss. By contrast, 30 ( 97%) of 31 patients with optic neuritis in that study displayed enhancement of the optic nerve. The authors pointed out that optic nerve enhancement is a useful way to distinguish optic neuritis from NAION. Enhancement reflects marked compromise of the blood- brain barrier, a phenomenon that apparently occurs rarely in NAION, may occur in AAION, and often occurs in PION after intracranial irradiation. It is reported here for the first time in hypotensive ION. In this latter condition, the breach in the blood- brain barrier may evidently persist for at least four months, as this case exemplifies. REFERENCES 1. Williams EL, Hart WM Jr., Tempelhoff R. Postoperative ischemic optic neuropathy. Anesth Analg 1995; 80: 1018- 29. 2. Cheng MA, Sigurdson W, Tempelhoff R, Lauryssen C. Visual loss after spine surgery: a survey. Neurosurgery 2000; 46: 625- 31. 3. Sadda SR, Nee M, Miller NR Biousse V, Newman NJ, Kouzis A. Clinical spectrum of posterior ischemic optic neuropathy. Am J Ophthalmol 2001; 132: 743- 50. 4. Johnson MW, Kincaid MC, Trobe JD. Bilateral retrobulbar optic nerve infarctions after blood loss and hypotension. A clinicopatho-logic case study. Ophthalmology 1987; 94: 1577- 84. 5. McClellan RL, El Gammal T, Kline LB. Early bilateral radiation-induced optic neuropathy with follow- up MRI. Neuroradiology 1995; 37: 131- 3. 6. Lee AG, Eggenberger ER, Kaufman DI, Manrique C. Optic nerve enhancement on magnetic resonance imaging in arteritic ischemic optic neuropathy. JNeuroophthalmol 1999; 19: 235- 7. 7. Rizzo JF 3rd, Andreoli CM, Rabinov JD. Use of magnetic resonance imaging to differentiate optic neuritis and nonarteritic anterior ischemic optic neuropathy. Ophthalmology 2002; 109: 1679- 84. 236 © 2004 Lippincott Williams & Wilkins |
