Eyeworld

159 EW RESIDENTS March 2015 Introduction Acute visual loss in otherwise healthy elderly individuals gener- ally warrants an extensive investi- gation into a panoply of potential etiologies. Because the differential includes vision-threatening ailments such as giant cell arteritis, optic neuropathy/neuritis, retinal detach- ment, vitreous hemorrhage, macular edema/maculopathy, neovascu- larization, and stroke, appropriate evaluation leading to a prompt and accurate diagnosis is critical. The ensuing lab studies and imaging, however, may distract a clinician from considering less emergent etiologies. Case presentation A phakic 64-year-old woman with a past medical history of hyperlip- idemia and no prior ophthalmic history presented to her general ophthalmologist one July morning complaining of profoundly de- creased visual acuity in her previous- ly 20/20 right eye. She complained of no other ophthalmic symptoms aside from a chalazion of her right upper eyelid and specifically denied flashes, floaters, curtains, scotomas, diplopia, photophobia, amauro- sis, or similar prior episodes. She reported no recent illnesses, fevers, night sweats, headaches, weight loss, or jaw claudication. Refraction did not improve her acuity better than 20/150 OD and was best corrected 20/20 OS. A slit lamp examination was unremarkable for any pathol- ogy in the anterior segment, and intraocular pressures by applanation were in the normal range OU. A dilated fundus examination revealed mild nuclear sclerotic cataracts and clear vitreous in both eyes. The optic nerves were both sharp, pink, and flat with normal symmetric cup-to-disc ratios, and the maculae, blood vessels, and peripheral retinae were unremarkable. An OCT of the maculae in both eyes demonstrated no obvious maculopathy. In the ab- sence of an obviously intraocular eti- ology, the general ophthalmologist referred the patient to a neuro-oph- thalmologist. The neuro-ophthalmologist was also unable to explain the patient's vision loss. There was no obvious abnormality of the optic nerves, and the patient demonstrated normal color vision, no afferent pupillary defect, and healthy appearance on exam. A complete neuro-ophthal- mologic evaluation including labs evaluating for infectious and auto- immune/inflammatory etiologies was negative. MRI of the brain and orbits were also unremarkable. At a loss, the neuro-ophthal- mologist decided that he could not rule out a subtle corneal topographic abnormality and referred the patient to a cornea specialist for further evaluation. Upon examination by the cornea specialist, the patient's vision remained unchanged. Anterior segment evaluation was significant only for the finding of a Krukenberg spindle that had not previously been noted. Computerized corneal topog- raphies revealed profound flattening of the central cornea of the right eye (Figures 1A and B). The topography was unremarkable in the left eye. Hard contact lens over-refraction corrected the visual acuity in the right eye to 20/30. Because the patient had no history of refractive surgery and the substantial topographic abnormality seemed to account for the vision loss, her cornea specialist sought an etiology to explain the rapid onset of central corneal flattening in an otherwise normal cornea. A more detailed interview of the patient revealed that the develop- ment of the chalazion of her right upper eyelid had immediately pre- ceded the onset of her vision loss. Further examination demonstrated the right upper lid internal chal- azion lay directly over the area of topographic flattening. The cornea specialist recommended a regimen of warm compresses to the right eye 3 to 4 times per day and follow-up within a week. It was planned that she would be referred to oculoplas- tics for excision of the lesion if it persisted. She returned 4 weeks later with complete resolution of her chalazi- on with conservative management. Her visual acuity was improved to 20/70+2 in the right eye, refract- ing to 20/30+1 with +1.00 sphere, An unexpected etiology of acute vision loss in an elderly patient by Sarwar Zahid, MD Figure 1A: A wire frame 3D representation of the refractive indices reflecting superior flattening and inferior steepening of the right cornea noted at the first clinic visit. The superior flattening corresponded to the location of her right upper lid chalazion. Figure 1B: Corneal topography of the right cornea revealing superonasal flattening and corresponding inferotemporal steepening in the right cornea at the first clinic visit. Figure 2: Corneal topography of the right cornea 4 months after initial presentation demonstrating improvement. Source (all): Madison Ophthalmology PLLC continued on page 160

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