Poster 29 - Corneal Endothelial Precipitates in Human Immunodeficiency Virus-Positive Patients

POSTER 29 Corneal Endothelial Precipitates in Human lmmunodeficiencv virus-Positive Patients Andrew Horvath, 0 .D. VA llliana Health Care System, 1900 East Main Street, Danville, Illinois 61832 Background: Human immunodeficiency virus (HIV)compromises a person's immune system by depleting CD4positive T lymphocytes and, subsequently,the generation of CD8-positive T lymphocytes. The absence or reduction in number of these cells results in hiaher-than-nor" ma1 susceptibility to systemic andlor ocular infections. Method: In order to keep a person's immune system adept to fighting off these infections, a number of different drugs are prescribed. These medications often have considerable side effects, as well as ocular implications. Case Report: Our case report and illustrations describe an asymptomatic veteran with noteworthy corneal endothelial precipitates. JG, a 68-year-old veteran, came to the eye clinic for a yearly eye examination. Ocular and medical history was remarkable only for the diagnosis of HIV in 1985. Current medications consist of 600-mg Efavirenz, 150-mg Lamivudine, and 300-mg Tenofovir Disoproxil Fumarate. His latest HIV-1 viral load was < 400 and CD4 count at 357. Uncorrected distance visual acuity was 20130-2 O.D. and 20125 O.S., correctable to 20120 0.D.IO.S. Pupils were equal, round, and reactive to light, with no afferent pupillary defect; extraocular motilities exhibited full range of motion; and confrontation visual fields were full. Slit-lamp evaluation was remarkable for yellow-brown corneal endothelial deposits, 4 mm wide, peripheral > central, 360' circu&corneal OU. ~ o l d m a k napplanation tonometry found pressures to be 13 mmHg O.D. and 14 mmHg O.S. The dilated fundus examination revealed 0.3 CID, distinct margins, 0.6 vessels, clear macula, no retinal detachments, holes, or tears in the periphery, a clear vitreous, and no evidence of HIV retinopathy. Conclusion: Patient was diagnosed with corneal endothelial deposits secondary to HIV precipitate vs. medicinal precipitate. Patient has yearly followups. Past literature states that HIV or the medication probably causes corneal endothelial precipitates. HIV is relatively new and its medication is constantly evolving.

POSTER 30 Muttifocal and Punctate Inner Choroidopathies: Is There a Link? Erin Nosel, 0.D., Ralph Parkansky, M.S., M.B.A., 0.D., and H. Simon Ghazi-Birry, M.D., Ph.D., 0 .D. Southern College of Optometry, 1245 Madison Avenue, Memphis, Tennessee 38104 Background: The white-spot syndromes are a group of inflammatory diseases of the retina characterized by visual loss in association with areas of retinal whitening. The etiology is presumed to be an immunologic vasculitic obstruction of the choriocapillaris, with secondary infarction of the retinal pigment epithelium. These syndromes include multifocal choroiditis (MFC),punctate inner choroidopathy (PIC),multiple evanescent white-

dot syndrome, serpiginous choroiditis, and acute posterior multifocal placoid pigment epitheliopathy. Method: This voster will vresent a case of MFC and a case of PIC demonstrating the commonality of etiology, manifestations, diagnosis, testing, management, and prognosis between two cases, and explore the possible link between the pathologies. Case Reports: Case 1: A 50-year-old woman came to us with blurry vision and photopsia. Medical history: non-contributory. Exam findings: visual acuities of 20130 O.D.; 20125 O.S.. Funduscopy revealed a mild vitritis overlying multiple yellowlwhite discrete oval retinal spots. These retinal pigment epitheliumlchoriocapillaris lesions varied in size and were scattered mainly in the periphery. Fluorescein angiography showed mild blockage of the early florescence and hyperfluorescence around some lesions. Serology was negative. MPC was diagnosed and oral steroids improved the vitritis and visual acuity. A year later, visual acuity worsened, with minimal response to additional steroid treatment. Case 2: A 21-year-old woman came to us with rapid onset decrease in vision OU, with bright spots in her field of vision. PMH indicated recent pyrexia of unknown origin. Examination findings: visual acuities of 20125 O.D.; 201800 O.S. Funduscopy revealed multiple atrophic lesions around the macula OU, with cor;esponding visual-field defects. Fluorescein angiography confirmed PIC and the ~ a t i e nwas t started on a reaimen of oral Prednisone for days and given a home L s l e r grid. A month after the steroids were stopped, a further decrease in vision and metamorphopsia occurred. Despite additional steroid treatment, further deterioration occurred. Low vision devices helped the patient complete her graduate studies.

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POSTER 31 Successful Management of a Central Bacterial Corneal Ulcer with Topical Moxifloxacin and Importance of Concurrent Corticosteroid Use Diane Calderon, O.D., Alan Kabat, O.D., Zoeanne Schinas, 0.D., and Christine Corella, 0 .D. Nova Southeastern University, College of Optometry, 3200 South University Drive, Ft. Lauderdale, Florida 33328 Background: The management of central corneal ulcers of an infectious etiology necessitates an aggressive approach. What is often overlooked is the significance of adding a corticosteroid to the treatment plan. The antiinflammatory properties inherent in corticosteroids serve to promote healing and lead to faster resolution of the infection and reduction of likely scar formation. Case Report: A 16-year-oldgirl was brought to us with symptoms of redness, pain, and photophobia O.S. Ocular history was remarkable only for soft daily wear contact lens use. Best-corrected acuity was 20120 O.D., 20160 O.S. Biomicroscopy revealed a central corneal epithelial defect, 1.5 mm in diameter, with underlying stromal infiltration. Also noted were grade 3 + cells and trace flare in the anterior chamber. The patient was diagnosed with central corneal ulcer of a presumed pseudomonal etiology. She was cyclopleged and given a loading dose of 0.5% 77

VOLUME 76lNUMBER 6/JUNE 2005

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