A 65-year-old male presented with acute, painless vision loss in the lower portion of his left eye (OS) for one day. Past medical history was significant for hypertension, hyperlipidemia, and coronary artery disease with previous coronary artery stenting. Significant medications included aspirin and clopidogrel (Plavix). He smoked one pack of cigarettes per day for many years. He denied jaw claudication, scalp pain, headache, fever, chills, or malaise and had no history of obstructive sleep apnea. He was not using any phosphodiesterase inhibitors (erectile dysfunction medications). External examination was negative for temporal nodularity or scalp tenderness. Visual acuity was 20/20 in the right eye (OD) and 20/400 OS. The pupils measured 4 mm in the dark and 2 mm in the light in both eyes (OU), but there was a relative afferent pupillary defect (RAPD) OS. The remainder of the anterior segment examination was within normal limits. Automated visual field testing (Humphrey 24-2) was normal OD but showed a dense inferior arcuate field defect OS (Fig. 6.1). Dilated fundus examination OD was normal and showed a cup-to-disc ratio of 0.1 (Fig. 6.2). There was superior (sectoral) disc edema OS (Fig. 6.3) that resolved over time to residual sectoral optic atrophy OS. Optical coherence tomography (OCT) of the optic nerve OS showed a thinned superior nerve fiber layer (Fig. 6.4) six months later. Laboratory workup at the time of presentation revealed a normal erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level. General physical examination was normal and carotid Doppler testing performed by internal medicine showed less than 40% stenosis bilaterally.
|Original language||English (US)|
|Title of host publication||Questions and Answers in Neuro-Ophthalmology: A Case-Based Approach|
|Publisher||World Scientific Publishing Co.|
|Number of pages||13|
|State||Published - Jan 1 2014|
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