Abstract
Raised intraocular pressure is a frequently encountered complication of uveitis. Intraocular homeostasis, maintained by the impermeable blood-ocular barrier, is important to guarantee optimal visual function. During uveitis breakdown of the blood-ocular barrier occurs, allowing the influx of proteins as well as inflammatory and immunocompetent cells. The combination of action of inflammatory cells and the mediators they release; and the chronic corticosteroid therapy used to treat the uveitis can participate in the pathogenesis of uveitic glaucoma. These factors alter the normal anatomic structure of the anterior chamber and angle. Management of uveitic glaucoma may be difficult because of the numerous mechanisms involved in its pathogenesis and is guided by careful delineation of the pathophysiology involved in each individual case. This article reviews, in detail, the pathogenesis of uveitic glaucoma and its therapies, with emphasis on the recent developments in the subject.
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