Open AccessFulminant toxoplasmic retinochoroiditis following intravitreal triamcinolone administration
Author(s) -
Ryan B Rush,
Saumil Sheth
Publication year - 2012
Publication title -
indian journal of ophthalmology/indian journal of ophthalmology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.542
H-Index - 51
eISSN - 1998-3689
pISSN - 0301-4738
DOI - 10.4103/0301-4738.94059
Subject(s) - medicine , triamcinolone acetonide , ophthalmology , vitrectomy , fulminant , endophthalmitis , macular edema , visual acuity , surgery
We report two cases of fulminant toxoplasmic retinochoroiditis following intravitreal triamcinolone acetonide (IVTA) administration. Case 1: A 42-year-old female received IVTA for presumed non-infectious panuveitis. Within 2 months, she developed diffuse macular retinochoroiditis with optic disc edema. Upon starting anti-toxoplasmic therapy (ATT), her intraocular inflammation resolved with catastrophic damage to the disc and macula. Case 2: A 30-year-old male received IVTA for presumed reactivation of previously scarred toxoplasmic retinochoroiditis. Despite simultaneous ATT, within 6 weeks, he developed extensive, multifocal macular retinochoroiditis. He continued to require ATT for 18 months and later underwent vitrectomy with silicone oil placement for severe epiretinal proliferation. Aqueous tap polymerase chain reactions were found positive for Toxoplasma gondii in both cases. In conclusion, IVTA administration can lead to fulminant toxoplasmic retinochoroiditis even when used with appropriate ATT. Extreme caution should be exercised while administering depot corticosteroids in eyes with panuveitis of unknown origin.