Visual Morbidity in Giant Cell Arteritis
Authors: Grant T. Liu, Joel S. Glaser, Norman J. Schatz, J. Lawton Smith
Journal: Ophthalmology (1994)

Purpose: To characterize visual morbidity in giant cell arteritis and to assess prognosis with respect to treatment. Methods: Record review of 185 patients with coded diagnosis of giant cell (cranial) arteritis examined at the Bascom Palmer Eye Institute from January 1, 1980, to January 31, 1993. Results: Forty-five patients with biopsy-proven giant cell arteritis had visual symptoms, and 41 individuals (63 eyes) lost vision. The visual loss was unilateral in 19 patients (46%), sequential in 15 (37%), and simultaneous in 7 (17%). Anterior ischemic optic neuropathy developed in 88% of eyes, visual acuity was 20/200 or worse in 70%, 21% had no light perception, and the majority of field defects in testable eyes, aside from central scotomas associated with loss, showed altitudinal or arcuate patterns. Six patients lost vision during corticosteroid therapy for systemic symptoms of giant cell arteritis, whereas in 39 patients visual symptoms prompted steroid treatment. For visual symptoms, 25 patients received intravenous methylprednisolone, whereas 20 received oral prednisone alone. In the 41 patients with visual loss, vision was unchanged in 20 (49%), it worsened in 7 (17%), and it improved in 14 (34%). Subsequent fellow eye involvement was observed only with oral therapy, and a greater percentage of patients (9/23 [39%] versus 5/18 [28%]) improved after intravenous treatment. Conclusions: In the authors' series, patients with visual loss due to giant cell arteritis had a 34% chance for some improvement in visual function after corticosteroid treatment. Intravenous therapy may diminish the likelihood of fellow eye involvement and was associated with a slightly better prognosis for visual improvement. Purpose: To characterize visual morbidity in giant cell arteritis and to assess prognosis with respect to treatment. Methods: Record review of 185 patients with coded diagnosis of giant cell (cranial) arteritis examined at the Bascom Palmer Eye Institute from January 1, 1980, to January 31, 1993. Results: Forty-five patients with biopsy-proven giant cell arteritis had visual symptoms, and 41 individuals (63 eyes) lost vision. The visual loss was unilateral in 19 patients (46%), sequential in 15 (37%), and simultaneous in 7 (17%). Anterior ischemic optic neuropathy developed in 88% of eyes, visual acuity was 20/200 or worse in 70%, 21% had no light perception, and the majority of field defects in testable eyes, aside from central scotomas associated with loss, showed altitudinal or arcuate patterns. Six patients lost vision during corticosteroid therapy for systemic symptoms of giant cell arteritis, whereas in 39 patients visual symptoms prompted steroid treatment. For visual symptoms, 25 patients received intravenous methylprednisolone, whereas 20 received oral prednisone alone. In the 41 patients with visual loss, vision was unchanged in 20 (49%), it worsened in 7 (17%), and it improved in 14 (34%). Subsequent fellow eye involvement was observed only with oral therapy, and a greater percentage of patients (9/23 [39%] versus 5/18 [28%]) improved after intravenous treatment. Conclusions: In the authors' series, patients with visual loss due to giant cell arteritis had a 34% chance for some improvement in visual function after corticosteroid treatment. Intravenous therapy may diminish the likelihood of fellow eye involvement and was associated with a slightly better prognosis for visual improvement.