f6-opth-5-075: Fundus autofluorescence of right a) and left b) eyes 28 months postingestion demonstrating diffuse hyperfluorescence without evidence of RPE atrophic lesions OU.Abbreviations: RPE, retinal pigment epithelium, OU, both eyes.

Mentions: The patient was last seen at the Ophthalmology clinic at 28 months postingestion. At this time, her uncorrected VA was 20/20 OD and 20/20 OS. Farnworth D-15 color vision testing demonstrated mild blue-yellow color deficiencies. There were no changes worth noting between the patient’s Humphrey visual fields or FA between this visit and her visit at 15 months postingestion. Cirrus spectral-domain OCT revealed central subfield thicknesses that were 283 microns OD and 279 microns OS and average retinal thicknesses that were 213 microns OD and 211 microns OS (normal average retinal thickness is 264 ± 21.9 microns).7 Although the central retinal thicknesses on the Cirrus OCT were within the normal range, the average macular thicknesses were decreased, a finding consistent with retinal atrophy and to the peripheral constriction seen on the visual fields. FAF photography (TRC-50DX; Topcon, Oakland, NJ) revealed a generalized hyperfluorescent pattern without evidence of atrophic retinal pigment epithelial changes (Figures 5, 6).

Christoforidis J, Ricketts R, Loizos T, Chang S - Clin Ophthalmol (2011)

Bottom Line: Fundus autofluorescence did not reveal any retinal pigmentary abnormalities.Quinine toxicity as seen by OCT reveals increased thickness with inner retinal hyperreflectivity acutely with development of significant retinal atrophy in the long-term.Fundus autofluorescence reveals an intact retinal pigment epithelial layer at 28 months.These findings suggest that quinine poisoning may produce a direct toxic effect on the inner retina in the acute phase resulting in long-term retinal atrophy.

Affiliation: The Ohio State University College of Medicine, Columbus, OH, USA.

Abstract: To report a case of acute quinine poisoning, document acute and chronic macular changes with optical coherence tomography imaging and fluorescein angiography (FA), and to review the literature on ocular toxicity of quinine.A 32-year-old white female presented to our Emergency Department after ingesting over 7.5 g of quinine. She underwent a complete ophthalmologic examination, fluorescein angiography, Stratus time-domain optical coherence tomography (OCT), and electroretinography at 72 hours and 15 months postingestion. Stratus time-domain and Cirrus spectral-domain OCT, fundus autofluorescence, and FA were obtained at 28 months postingestion.Fluorescein angiography at 72 hours postingestion revealed normal filling times and vasculature. OCT showed marked thickening of the inner retina bilaterally. At 15 and 28 months follow-up, fundus photography and fluorescein angiography demonstrated optic nerve pallor, severely attenuated retinal vessels while OCT showed inner retinal atrophy. Fundus autofluorescence did not reveal any retinal pigmentary abnormalities.Quinine toxicity as seen by OCT reveals increased thickness with inner retinal hyperreflectivity acutely with development of significant retinal atrophy in the long-term. Fundus autofluorescence reveals an intact retinal pigment epithelial layer at 28 months. These findings suggest that quinine poisoning may produce a direct toxic effect on the inner retina in the acute phase resulting in long-term retinal atrophy.