BRIEF COMMUNICATION |
|
Year : 2012 | Volume
: 60
| Issue : 2 | Page : 141-143 |
|
Fulminant toxoplasmic retinochoroiditis following intravitreal triamcinolone administration
Ryan Rush1, Saumil Sheth2
1 Bascom Palmer Eye Institute, Miami, Florida, United States of America 2 Department of Retina, Sydney Eye Hospital, Sydney, Australia
Correspondence Address:
Saumil Sheth Department of Retina, Sydney Eye Hospital, 8, Macquarie Street, Sydney CBD, NSW 2000 Australia
Source of Support: None, Conflict of Interest: None | Check |
DOI: 10.4103/0301-4738.94059
|
|
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. |
|
|
|
[FULL TEXT] [PDF]* |
|
|
|