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Chronic intraocular inflammation such as chronic uveitis can lead to cystoid macular oedema, papilloedema, and vitreous opacities temporarily or permanently reducing visual acuity. Chronic uveitis has usually been treated by topical or systemic application of steroids. Topical treatment, however, often has not been sufficiently effective to suppress intraocular inflammation and to reduce cystoid macular oedema. Systemic treatment with steroids inevitably leads to secondary side effects such as systemic suppression of the whole immune system and Cushing’s syndrome. Taking into account that the eye comprises only 0.01% of the whole body volume, and considering that for achieving high concentrations of a drug at its site of action it is best to apply it directly into the region of required action, we describe the clinical outcome in a patient receiving an intravitreal injection of a crystalline cortisone.
A 17 year old woman suffering from chronic idiopathic uveitis in both eyes for 5 years had been treated topically, peribulbarly, and systemically with corticosteroids. As a steroid responder, she had developed secondary ocular hypertension. Steroid induced cataract in her right eye was operated on by phacoaspiration, transpupillary anterior vitrectomy, and posterior chamber lens implantation. To reduce the systemic side effects of steroid treatment, systemic cyclosporin A had been added to the treatment scheme since January 1998. In February 2000, she presented again with a severe uveitis with papilloedema and cystoid macular oedema. Despite intensive topical treatment with steroids given hourly, and systemic acetazolamide, visual acuity remained in the range 0.10–0.16. To avoid the side effects of systemic steroid treatment and to achieve high and longstanding concentrations of steroids in the eye, we injected 20 mg crystalline triamcinolone acetonide into the vitreous cavity of the right eye in July 2000 with topical anaesthesia.
Within the next 5 weeks, visual acuity increased to 0.5. Intraocular pressure increased to a maximum of 38 mm Hg, and was reduced to the normal range with topical antiglaucomatous medication. Four months after the injection, the steroid crystals were resorbed, visual acuity returned to the preoperative level of 0.1, and with topical steroids given, intraocular pressure decreased to values of less than 23 mm Hg without further antiglaucomatous medication.
In ophthalmology, corticosteroids applied topically or systemically are well known and have widely been used to suppress intraocular inflammation. Based on experimental studies performed by Machemer, Peyman and others, as well as on clinical observations, intravitreal injections of triamcinolone acetonide have increasingly been reported as treatment for intraocular neovascular, oedematous, or inflammatory diseases. These include diffuse diabetic macular oedema, proliferate diabetic retinopathy, neovascular glaucoma, exudative age related macular degeneration, and uveitis.1–5 In agreement with these previous studies, the results of the present report suggest that the intravitreal injection of triamcinolone acetonide may be an additional option in the treatment of chronic uveitis. Future studies may address which types of uveitis intravitreal steroid injection are best for, and whether the use of intravitreally implanted slow release devices6 can decrease the recurrence rate of uveitis for a longer period than a single intravitreal injection dose.
Proprietary interest: none.
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