Raised intraocular pressure is a common and frequently serious complic
ation of anterior uveitis. The milieu of inflammatory cells, the media
tors they release, and the corticosteroid therapy used to treat the uv
eitis can participate in the pathogenesis of uveitic glaucoma. These f
actors 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 an
gle closure with pupillary block glaucoma, or chronic, such as combine
d steroid-induced and secondary open angle glaucoma. Management of uve
itic glaucoma may be difficult because of the numerous mechanisms invo
lved in its pathogenesis. Diagnostic and therapeutic decisions are gui
ded by careful delineation of the pathophysiology of each individual c
ase. The goal of treatment is to minimize permanent structural alterat
ion of aqueous outflow and to prevent damage to the optic nerve head.
This article reviews the pathogenesis of uveitic glaucoma, with specif
ic attention to etiology. Medical and surgical therapies are also disc
ussed, with emphasis on the more recent developments in each category.
(C) 1997 by Elsevier Science Inc.