Raised intraocular pressure is a common and frequently serious complication of anterior uveitis. The milieu of inflammatory cells, the mediators they release, and the 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, influencing aqueous production and outflow. These changes act to disrupt the homeostatic mechanisms of intraocular pressure control. Structural changes in the angle can be acute, such as in secondary angle closure with pupillary block glaucoma, or chronic, such as combined steroid-induced and secondary open angle glaucoma. Management of uveitic glaucoma may be difficult because of the numerous mechanisms involved in its pathogenesis. Diagnostic and therapeutic decisions are guided by careful delineation of the pathophysiology of each individual case. The goal of treatment is to minimize permanent structural alteration of aqueous outflow and to prevent damage to the optic nerve head. This article reviews the pathogenesis of uveitic glaucoma, with specific attention to etiology. Medical and surgical therapies are also discussed, with emphasis on the more recent developments in each category.