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Show J. Clill. Neuro-ophthalmol. 4: 141-142, 1984. Therapeutic Temporal Artery Biopsy To the Editor: I would like to briefly present for your consideration and review, a case history that is amazing and extraordinary. On September 13, 1983, I saw a 69-year-old white male who on September 12, 1983, noted a marked decrease in visual acuity in the left eye. This was sudden and nonprogressive. He had no complaints in the right eye. Past medical history revealed that the patient had a long history of adenocarcinoma of the colon that is presently in remission. He had a known history of systemic hypertension that was easily controlled with Dyazide. He had taken no other medication other than Dyazide. He had no known allergies to medicine and no prior history of eye disease, other than an aunt with adult onset diabetis mellitus. There is no other significant family history. Examination revealed a corrected visual acuity of 20/60 in the right eye, and 3/200 in the left eye. External examination revealed the globes and orbits to be quiet and white on each side. He had a marked decrease in color and brightness perception in the left eye. Pupillary examination revealed a +4 out of 4 positive swinging light test in the left eye. Motility examination was totally unremarkable. Visual fields were full in the right eye and full in the left eye peripherally, but a large central scotoma was noted centrally. Intraocular pressure was 20 mm Hg in each eye. Hertel exophthalmometry revealed no evidence of proptosis. There were no orbital or carotid bruits. Slit lamp examination was unremarkable except for modest lenticular opacities. There was a decrease in the amplitude of the pulsation of the left carotid artery, but no bruit was heard. Dilated examination of the fundi, including Goldmann three-mirror lens examination revealed an unremarkable retinal periphery in each eye. The posterior pole of the left eye revealed a translucent appearance of the retina with nerve fiber layer hemorrhage on the surface and at the edge of the superior left disc. There were few scattered macular hemorrhages in the superficial retina. There were no spontaneous venous pulsations on the left side, but spontaneous venous pulsations were present on the right side. The patient had a sedimentation rate of 81, by the Westergren method. A left superficial temporal artery biopsy was undertaken on September 15, 1983. At the time of ligation of the left superficial temporal artery June 1984 and before the skin sutures were applied, the patient exclaimed that his visual acuity in the affected eye had improved dramatically. At that time in the operating room, he was able to read fine print with the left eye. The biopsy of the left superficial temporal artery with multiple serial sections was negative for giant cell arteritis. The patient was seen again on September 16, 1983. At that time, his visual acuity in the left eye was 20/30 +2. There was a negative swinging light test on the left side. He had equal color and brightness perception. Digital subtraction angiography, undertaken on September 20, 1983, showed mild irregularities about the left carotid bifurcation. No evidence of high-grade stenosis was seen. The patient has maintained his visual acuity and has no complaints whatsoever. I consider this as an unusual and dramatic case report; to my knowledge, this is the first example of a therapeutic temporal artery biopsy. Robert A. Laibovitz, M.D. Austin, Texas Response: And now to the case of the millennium! The first assumption I am going to make about this man is that his problem has a vascular substrate. I also assume it is neither neoplastic nor traumatic. The vasculopathies obviously include aneurysms and arteriovenous malformations which seem to be ruled out easily, and the more pedestrian entities like central retinal artery or branch artery occlusion, venous obstructive processes, and ischemic optic neuropathies. The description of the fundus leaves me perplexed, but the lack of hemorrhages in the periphery and the absence of venous congestion would seem to make a central retinal vein occlusion ordinaire unlikely. In some ways, the description sounds like an arterial occlusive process, but perhaps with an excess of hemorrhages. I think that a fluorescein angiogram and fundus photographs would go a long way toward explaining the nature of the process responsible for the visual loss, and a late photograph and description of the fundus so we could know what the fundus looked like when "the smoke cleared" might be helpful. Unfortunately, we have none of these. Could some of the changes that were described have reflected subretinal accumulations of liquid perhaps related to a vascular choroidopathy? I will proceed on the assumption that this is not an 141 |
