Moorthy R S, Mermoud A, Baerveldt G, Minckler D S, Lee P P, Rao N A
Doheny Eye Institute, University of Southern California School of Medicine, Los Angeles, USA.
Surv Ophthalmol. 1997 Mar-Apr;41(5):361-94. doi: 10.1016/s0039-6257(97)00006-4.
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.
眼压升高是前葡萄膜炎常见且往往较为严重的并发症。炎症细胞的环境、它们释放的介质以及用于治疗葡萄膜炎的皮质类固醇疗法都可能参与葡萄膜炎性青光眼的发病机制。这些因素改变了前房和房角的正常解剖结构，影响房水的生成和流出。这些变化会破坏眼压控制的稳态机制。房角的结构变化可以是急性的，如瞳孔阻滞性青光眼继发的房角关闭，也可以是慢性的，如类固醇诱导性和继发性开角型青光眼合并存在。由于葡萄膜炎性青光眼发病机制涉及多种因素，其治疗可能较为困难。诊断和治疗决策需依据对每个病例病理生理学的仔细剖析来指导。治疗的目标是尽量减少房水流出的永久性结构改变，并防止对视神经乳头造成损害。本文回顾了葡萄膜炎性青光眼的发病机制，特别关注病因。还讨论了药物和手术治疗方法，重点介绍了每一类别的最新进展。
