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Slowly Progressive Vision Loss in Giant Cell Arteritis
Arch Ophthalmol. 2006;124:416-418.
Vision loss in patients with giant cell arteritis (GCA) typically occurs over the course of seconds to days and often involves the other eye soon after. We describe a patient with arteritic anterior ischemic optic neuropathy and unusually slow progression of reversible vision loss for 1 month in the fellow eye.
Report of a Case
A 93-year-old man taking warfarin sodium (Coumadin) because of atrial fibrillation awoke with sudden painless vision loss in the right eye. Visual acuity was counting fingers OD and 20/30 OS. He identified 10 of 10 Ishihara color plates with the left eye. Funduscopy of the right eye revealed hyperemic optic nerve edema with hemorrhages and a small cup-disc ratio in the left eye. Strong bilateral, nontender temporal artery pulses were present. The patient denied systemic symptoms of GCA. The erythrocyte sedimentation rate (Westergren method) was 35 mm/h.
Seventeen days later, the patient described improvement of vision in the right eye and a gradual daily decline of vision in the left eye since his last visit. Visual acuity was counting fingers OD and 20/60 OS. Examination yielded otherwise stable findings. Magnetic resonance images of the orbit showed no abnormalities. One week later the patient noted continuation of the slowly progressive decline of vision in the left eye. Visual acuity was hand movements OD and counting fingers OS. The fluorescein angiogram showed marked delay in choroidal filling in the left eye (Figure 1A). The erythrocyte sedimentation rate was 25 mm/h, and the C-reactive protein level was 0.8 mg/L (normal, <2.0 mg/L). The temporal arteries were now pulseless and enlarged.
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Figure 1. Fluorescein angiogram of the left eye. A, At admission, the choroid began filling at 25.9 seconds and showed persistent, marked choroidal filling delay at 50.5 seconds. B, After treatment with corticosteroids, the choroidal filling time normalized, beginning at 26.6 seconds and complete by 32.2 seconds.
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The patient was given high-dose, intravenous solumedrol (250 mg every 6 hours). The next day, visual acuity was counting fingers OD and 20/50 OS. Temporal artery biopsy findings were positive for multiple giant cells (Figure 2). The subsequent fluorescein angiogram showed normalization of choroidal filling (Figure 1B). Nine months later, visual acuity in both eyes remained stable.
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Figure 2. Biopsy specimen of the left temporal artery. Note multiple giant cells (arrow; hematoxylin-eosin, original magnification x150).
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Comment
Our patient had atypical features of GCA. He denied systemic symptoms, the erythrocyte sedimentation rate and C-reactive protein level were normal, and the temporal arteries were grossly unremarkable at admission. In one study, 21.2% of patients had occult GCA (no systemic symptoms except vision loss), but nearly all had an elevated erythrocyte sedimentation rate or C-reactive protein level.1 The vision loss in the left eye was slowly progressive for 1 month, and improved dramatically within 24 hours of administration of high-dose corticosteroid therapy and remained stable.
We question whether our patient's baseline anticoagulant therapy contributed to the unusually slow progression of vision loss. A few reports propose beneficial effects of anticoagulation and antiplatelet therapy in GCA-related vision loss. Buono et al2 reported improvement in acuity and posterior ciliary artery blood flow with the addition of heparin sodium therapy in a patient with progressive visual loss despite corticosteroid therapy for 5 days. A retrospective study of 175 patients with GCA reported that patients taking aspirin had fewer cranial ischemic complications at admission and that fewer such complications developed, compared with patients not taking aspirin.3 The protective effect of aspirin therapy3 and improvement of vision and blood flow with heparin therapy2 imply that thrombosis may contribute to vision loss in patients with GCA. However, more studies are needed to validate the beneficial effects of anticoagulant therapy.
Visual loss secondary to choroidal ischemia has been previously described in GCA. One report described visual loss secondary to isolated choroidal nonperfusion over 1 to 2 days. The patient's vision improved with high-dose corticosteroid therapy.4 Another article described 3 patients with vision loss from choroidal ischemia that progressed over the course of seconds, several hours, and 3 days, respectively.5
The visual decline in patients with GCA typically occurs quickly, over the course of seconds to days. In our patient, vision loss from choroidal ischemia secondary to GCA progressed over 24 days. Giant cell arteritis must be considered in older patients with slowly progressive vision loss.
AUTHOR INFORMATION
Correspondence: Dr Lee, Department of Ophthalmology, University of Minnesota, 420 Delaware St SE, MMC 493, Minneapolis, MN 55455 (mikelee{at}umn.edu).
Financial Disclosure: None.
Anat Galor, MD;
Michael S. Lee, MD
REFERENCES
1. Hayreh SS, Podhajsky P, Zimmerman B. Occult giant cell arteritis: ocular manifestations. Am J Ophthalmol. 1998;125:521-526.
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2. Buono LM, Foroozan R, de Virgiliis M, Savino PJ. Heparin therapy in giant cell arteritis. Br J Ophthalmol. 2004;88:298-301.
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3. Nesher G, Berkun Y, Mates M, Baras M, Rubinow A, Sonnenblick M. Low-dose aspirin and prevention of cranial ischemic complications in giant cell arteritis. Arthritis Rheum. 2004;50:1332-1337.
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4. Quillen DA, Cantore WA, Schwartz SR, Brod RD, Sassani JW. Choroidal nonperfusion in giant cell arteritis. Am J Ophthalmol. 1993;116:171-175.
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5. Slavin ML, Barondes MJ. Visual loss caused by choroidal ischemia preceding anterior ischemic optic neuropathy in giant cell arteritis. Am J Ophthalmol. 1994;117:81-86.
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