Intravitreal injections of triamcinolone acetonide have increasingly been used for treatment of various intraocular neovascular, proliferative, or edematous diseases, such as diffuse diabetic macular edema, proliferative diabetic retinopathy, proliferative vitreoretinopathy, chronic uveitis, and persistent pseudophakic cystoid macular edema.1- 6 In view of the widening spectrum of therapeutic indications of intravitreal triamcinolone acetonide, we report the clinical course of a patient who repeatedly received intravitreal injections of triamcinolone acetonide 14 months apart, who showed intravitreal triamcinolone acetonide crystals still present 9 months after the second injection, and who developed secondary open-angle glaucoma uncontrollable by topical antiglaucomatous medication.
A 79-year-old woman sought treatment for progressive exudative age-related macular degeneration with subfoveal occult neovascularization in her left eye. Snellen chart visual acuity decreased from 0.80 to 0.50 OS with the accompanying complaint of marked metamorphopsia. Intraocular pressure measured 16 mmHg, and the appearance of the optic nerve head was normal. The right eye demonstrated a large subfoveal disciform scar due to exudative macular degeneration covering the whole macular region between the temporal vascular arcades. Visual acuity was reduced to hand movements OD. The intraocular pressure measurement was within the reference range. In an attempt to reduce subfoveal exudation and to suppress subretinal angiogenesis, the patient received a transconjunctival intravitreal injection of 25 mg of crystalline triamcinolone acetonide in 0.2 mL of Ringer solution in her left eye. The procedure was carried out under topical anesthesia after paracentesis was performed to decrease the volume of the globe. The patient was fully informed about the experimental nature of the therapy. She signed an informed consent form. The ethics committee of the university approved the study, which followed the tenets of the Declaration of Helsinki.
After the injection, the patient's vision remained stable for 4 months. On indirect ophthalmoscopy as well as Goldmann contact lens ophthalmoscopy, the triamcinolone acetonide crystals were localized in the preretinal vitreous cortex at the 6-o'clock position in the periphery of the fundus. Two months after the injection, intraocular pressure increased to as much as 32 mmHg, necessitating antiglaucomatous topical treatment with latanoprost, timolol maleate, and dorzolamide hydrochloride, under which intraocular pressure normalized. Five months after the injection, visual acuity started to decrease. Simultaneously, the triamcinolone acetonide crystals were no longer detectable on indirect ophthalmoscopy and Goldmann contact lens ophthalmoscopy. Eight months after the injection, uncomplicated phacoemulsification was performed with implantation of a foldable posterior chamber lens. Fourteen months after the injection, visual acuity was 0.30 OS with enlargement of the subfoveal neovascular membrane and an increase of the subretinal exudation. In view of the stabilization of visual acuity after the first injection, a second intravitreal injection of 25 mg of triamcinolone acetonide was performed. For 6 months after the second injection, visual acuity remained at 0.30 OS (Snellen charts). Despite maximally tolerable antiglaucomatous topical treatment, intraocular pressure ranged between 20 mmHg and 30 mmHg with the eventual development of glaucomatous changes in the appearance of the optic nerve head. Because intraocular pressure remained uncontrolled and triamcinolone acetonide crystals were still detectable in the vitreous cavity on indirect ophthalmoscopy, although 9 months had passed since the last triamcinolone acetonide injection, a standard trabeculectomy was carried out using mitomycin C intraoperatively in a concentration of 0.25 mg/mL. Postoperatively, the anterior chamber was well formed, there was no leakage at the limbal wound edge, and intraocular pressure ranged between 5 mmHg and 10 mmHg in the first postoperative weeks. Concentration of triamcinolone in the aqueous humor sample obtained at the start of the trabeculectomy by anterior chamber fluid aspiration was 11.2 µg/L.
The clinical course of this patient demonstrates that, in contrast to previous reports on an intraocular presence of triamcinolone for as long as 6 months after the injection, 3 triamcinolone acetonide crystals can be present in the vitreous and soluble triamcinolone can be detected in the aqueous humor for 9 months or longer after intravitreal injection of 25 mg of triamcinolone acetonide. This long intraocular presence of triamcinolone acetonide, especially in patients receiving repeated intravitreal injections of triamcinolone, may not only lead tosecondary ocular hypertension but also to steroid-induced secondary open-angle glaucoma necessitating trabeculectomy. This case may also demonstrate that intraocular concentrations of triamcinolone can be achieved for 9 months or longer by a single injection of 25 mg of triamcinolone acetonide. This finding may be interesting for the discussion of when to repeat intravitreal injections and when to use an intraocular slow-release device for corticosteroids.
The authors have no relevant financial interest in this article.
Corresponding author: Jost B.Jonas, MD, Universitäts-Augenklinik, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany (e-mail: firstname.lastname@example.org).
Jonas JB, Kreissig I, Degenring R. Secondary Chronic Open-Angle Glaucoma After Intravitreal Triamcinolone Acetonide. Arch Ophthalmol. 2003;121(5):729-730. doi:10.1001/archopht.121.5.729