Secondary angle closure can occur as a result of ocular inflammation. Fibrin and increased aqueous proteins released due to the breakdown of the blood–aqueous barrier may predispose to formation of posterior synechiae (Fig 20-10) and PAS. If left untreated, these posterior synechiae can lead to a secluded pupil, iris bombé, and secondary angle closure (Fig 21-10).
Figure 10-20 Inflammatory glaucoma in a patient with ankylosing spondylitis. A fibrinous anterior chamber reaction and posterior synechiae formation are evident.
(Courtesy of Steven T. Simmons, MD.)
Figure 10-21 Clinical photograph showing inflammatory glaucoma. A secluded pupil is seen in a patient with long-standing uveitis with classic iris bombé and secondary angle closure.
(Courtesy of Steven T. Simmons, MD.)
Figure 10-22 Inflammatory glaucoma. PAS in uveitis occur typically in the inferior anterior chamber angle and are nonuniform in height and shape, as shown in this photograph.
(Courtesy of Joseph Krug, MD.)
Peripheral iris edema, organization of inflammatory debris in the angle, and bridging of the angle by large keratic precipitates (seen in sarcoidosis) can accompany the ocular inflammation and lead to formation of PAS. These PAS most often form in the inferior anterior chamber angle, unlike the PAS in PAC, which typically occur in the superior angle. The PAS are usually not uniform in shape or height, further distinguishing inflammatory disease from PAC (Fig 22-10). In rare instances, ischemia secondary to inflammation may cause rubeosis iridis and neovascular glaucoma.
Ocular inflammation can lead to the shallowing and closure of the anterior chamber angle by other mechanisms as well, such as uveal effusion and subsequent anterior rotation of the ciliary body. Significant posterior uveitis can cause massive exudative retinal detachment or choroidal effusions that push the lens–iris interface forward, resulting in secondary angle closure. Treatment is primarily directed at the underlying cause of the uveitis. Aqueous suppressants and corticosteroids are the primary agents for reducing IOP and preventing synechial angle closure in this situation. Although prostaglandin analogues can cause increased inflammation in some eyes, they may be considered if needed to control IOP.
Interstitial keratitis may be associated with open-angle glaucoma or angle closure. The angle-closure component may be caused by chronic inflammation and PAS formation or by multiple cysts of the iris pigment epithelium.
Shallow or flat anterior chamber after surgery
A flat anterior chamber from any cause can result in the formation of PAS. Hypotony in an eye with a flat chamber after cataract surgery or filtering surgery indicates the presence of a wound leak unless proven otherwise. A Seidel test should be performed to locate the leak. Simple pressure patching or bandage contact lens application will often seal the leak and allow the chamber to re-form. If the chamber does not re-form, the leak should be repaired surgically to prevent synechial angle closure or other complications of hypotony.
Debate continues concerning how long a postoperative flat chamber should be managed conservatively before surgical intervention is undertaken. Some ophthalmologists repair the wound leak and re-form a flat chamber following cataract surgery within 24 hours. Others prefer observation in conjunction with corticosteroid therapy for several days to prevent formation of synechiae. Although iridocorneal contact is well tolerated, contact between the cornea and the hyaloid face or an IOL requires re-formation of the chamber without delay to minimize corneal endothelial damage. Early intervention should also be considered in the presence of corneal edema, excessive inflammation, or posterior synechiae formation.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.