Uveitic glaucoma often results from a combination of mechanisms. Glaucoma associated with uveitis is best classified by morphologic changes in angle structure; thus, uveitic glaucoma may be divided into secondary angle-closure and secondary open-angle glaucoma. These entities may be further subdivided into acute and chronic types. In addition, corticosteroid-induced ocular hypertension and glaucoma are other components that must be addressed in cases of chronic uveitic glaucoma. See also BCSC Section 10, Glaucoma.
Secondary angle-closure glaucoma
Acute with central shallowing of the anterior chamber Acute secondary angle-closure glaucoma may occur when choroidal inflammation results in forward rotation of the ciliary body and lens–iris diaphragm. It can be the presenting sign of Vogt-Koyanagi-Harada (VKH) syndrome or sympathetic ophthalmia. Patients present with pain, elevated IOP, and no posterior synechiae. Ultrasound biomicroscopy (UBM) or ultrasound evaluation showing choroidal thickening and anterior rotation of the ciliary body is diagnostic. Treatment is with aggressive corticosteroid therapy, aqueous suppressants, and cycloplegia to induce a posterior rotation of the ciliary body. As the inflammation subsides, the chamber deepens and the IOP normalizes. Peripheral iridotomy or iridectomy is not useful in these acute cases because the underlying cause is not pupillary block.
Acute without central shallowing of the anterior chamber Chronic or acute recurrent anterior segment inflammation may result in the formation of circumferential posterior synechiae with pupillary block due to seclusion of the pupil and resultant iris bombé, producing secondary peripheral angle closure. Whereas synechiae formation usually occurs over time, the development of iris bombé may be an acute event. Peripheral laser iridotomy or surgical iridectomy results in resolution of the bombé and angle closure if performed before permanent peripheral anterior synechiae form. Iridotomies should be multiple, created as large as possible. Exacerbation of inflammation can be anticipated after laser iridotomy in these eyes, making the iridotomies prone to close and requiring re-treatment or surgical iridectomy. Intensive topical corticosteroid and cycloplegic therapy is given following the procedure. In patients with brown irides, pretreatment of the iris with an argon laser before using the Nd:YAG laser may lessen the chance of bleeding and facilitate a wider opening. If laser iridotomy is not successful, surgical iridectomy is required. The procedure may be supplemented with goniosynechialysis if peripheral anterior synechiae have started to develop, but this approach is controversial.
Chronic In addition to posterior synechiae, chronic intraocular inflammation may result in peripheral anterior synechiae and chronic secondary angle-closure glaucoma. Eyes with these complications often have chronic secondary open-angle glaucoma and corticosteroid-induced glaucoma superimposed. Topical aqueous suppressants may be inadequate to prevent progression of optic nerve head damage. These eyes may require goniosynechialysis and trabeculectomy with mitomycin C or placement of a glaucoma drainage device. See BCSC Section 10, Glaucoma, for a more detailed discussion on surgical treatment of glaucoma.
Secondary open-angle glaucoma
Acute Inflammatory open-angle glaucoma occurs when the trabecular meshwork is inflamed (trabeculitis), as commonly occurs with infectious causes of uveitis such as toxoplasmic retinochoroiditis, necrotizing herpetic retinitis, herpes simplex and varicella-zoster anterior uveitis, cytomegalovirus anterior uveitis (including the Posner-Schlossman type), and sarcoid uveitis or when inflammatory debris clogs the angle. This type of glaucoma usually responds to specific treatment of the infectious agent supplemented by topical cycloplegics and corticosteroids.
Chronic Chronic outflow obstruction is caused by direct damage to the trabecular meshwork. The management of chronic secondary open-angle glaucoma is similar to that of primary open-angle glaucoma (see BCSC Section 10, Glaucoma), with the added complexity of maintaining strict control of intraocular inflammation through the use of IMT.
Combined-mechanism uveitic glaucoma
Multiple mechanisms may be responsible for elevated pressure in uveitic eyes. Treatment should be aimed at controlling the inflammation and IOP through a multimodal approach, including both medical and surgical therapy aimed at the responsible mechanisms.
Excerpted from BCSC 2020-2021 series: Section 9 - Uveitis and Ocular Inflammation. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.