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Intravitreal injections of triamcinolone acetonide have increasingly been performed as treatment for intraocular diseases with intraretinal oedema and with subfoveal fluid accumulation, such as diffuse diabetic macular oedema, persistent pseudophakic cystoid macular oedema, central retinal vein occlusion, and exudative age related macular degeneration.1–4 In view of the widening spectrum of indications for intravitreal triamcinolone acetonide injections, it was the purpose of this study to evaluate whether intravitreal triamcinolone acetonide injections may be useful as treatment of longstanding central serous chorioretinopathy.
A 50 year old patient presented with a decrease in visual acuity to 1/20 in his right eye because of longstanding central serous chorioretinopathy. Six years earlier, visual acuity had started to deteriorate, and had remained at 1/20 for the past 2 years. Fluorescein angiograms showed a mottled appearance of the retinal pigment epithelium close to the foveola, and a leakage of dye in the late phase of the angiogram. There was no clear smoke stalk phenomenon (fig 1). In optical coherence tomography, the central retina was detached. Despite intensive topical treatment with prednisolone acetate eye drops and oral intake of carboanhydrase inhibitors, the morphological appearance of the fovea and visual acuity remained unchanged. Under topical anaesthesia, the patient received an intravitreal application of 20–25 mg of triamcinolone acetonide, which was transconjunctivally injected through the pars plana into the centre of the vitreous cavity. The technique has already been described in detail.2 The patient was fully informed about the experimental character of the treatment and had signed an informed consent. After the injection, all topical and systemic medication for his macular disorder was stopped.
Within the first 5 months after the injection, fluorescein angiograms and optical coherent tomograms did not show any marked changes in the macula (fig 2). Correspondingly, visual acuity remained at 1/20. Intraocular pressure increased up to levels of 30 mm Hg and was reduced to the normal values by topical application of a carbonic anhydrase inhibitor. Thirteen months after the injection, the fovea was still slightly detached. Visual acuity remained at 1/20.
The clinical course suggests that in this eye with longstanding central serous chorioretinopathy an intravitreal injection of a high dosage of triamcinolone acetonide was not accompanied by a fast resolution of the subfoveal fluid and an increase in visual acuity. For more than 5 months after the injection, the fovea remained clearly detached. The partial resorption of the subfoveal fluid 13 months after the injection may not have necessarily been caused by intravitreal triamcinolone but may be explained by the natural course of the disease. The report agrees with other investigations in which patients with central serous chorioretinopathy did not markedly benefit from systemic steroid treatment.5 This single case report, therefore, does not favour the use of intravitreal triamcinolone acetonide for this treatment.
Proprietary interest: None.