Chronic secondary glaucoma is a common and serious complication of uveitis, even if intraocular pressure (IOP) is low during episodes of ocular inflammation. Management of the glaucoma is difficult because of the often chronic course of the underlying disease, and blindness is a common consequence. Several pathophysiologic mechanisms may be involved in the development of uveitic glaucoma. The glaucoma can be acute or chronic, and associated with open or closed anterior chamber angle. Elevated IOP can be the result of active inflammation, corticosteroid therapy, insufficient glaucoma therapy, or permanent changes in ocular structures that alter aqueous humor dynamics. Because the etiologic factors and pathologic mechanisms involved in uveitic glaucoma are so complex, diagnostic and therapeutic decisions are guided by carefully delineating the pathophysiology of each individual case. The goal of treatment is to minimize permanent structural alterations of aqueous outflow and to prevent damage to the optic nerve. New aspects of uveitic glaucoma physiopathology are presented.