Current management approaches for uveitic glaucoma.

Abstract

Uveitic glaucoma is a term that encompasses a myriad of disease entities with different etiologies, mechanisms, and prognoses. The prevalence of glaucoma in inflammatory diseases of the eye ranges from 10% to 20% in non‐population-based studies. 1‐3 The mechanisms by which intraocular inflammation causes an elevation of intraocular pressure (IOP) and subsequent secondary glaucoma vary according to the specific uveitic etiology, ocular anatomic features, ocular physiology, and treatment modalities employed which can affect eye pressure. Aqueous outflow obstruction in uveitis may be either macroscopic (ie, with synechial seclusion of the pupil, secondary pupillary block and chronic synechial, and/or neovascular angle closure) or ultrastructural (ie, with open-angle glaucoma due to microanatomic changes to aqueous outflow pathways). In acute uveitis, decreased IOP may be observed due to reduced aqueous secretion by the inflamed ciliary body (cyclitis), 4 and theoretically, facilitation of aqueous uveoscleral outflow secondary to increased aqueous concentration of prostaglandins. 5,6 Eventually, IOP may paradoxically rise secondary to increased inflammatory mediators, cells and proteins, trabecular meshwork (TM) cell dysfunction and trabeculitis, with an associated increase in resistance to trabecular aqueous outflow. 7 In addition, the prolonged use of topical corticosteroids, a mainstay of uveitis treatment, and to a lesser extent, periocular or systemic corticosteroids, may result in trabecular damage and glycosaminoglycan deposition resulting in steroid-induced glaucoma. 8‐10 The use of corticosteroid intravitreal implants in the treatment of uveitic glaucoma has also been associated with a significant elevation of IOP. 11 The corticosteroid-induced IOP rise appears to be especially pronounced in eyes where damage to the