cells and atypical endothelial cell morphology in the involved eye.

Therapy is directed toward the corneal edema and secondary glaucoma. Hypertonic saline solutions and medications to reduce the IOP, when elevated, can be effective in controlling the corneal edema. The ACG can be treated medically with aqueous suppressants and prostaglandin analogues. Miotics are often ineffective. When medical therapy fails, filtering surgery (trabeculectomy or a glaucoma drainage device) can be effective. Late failures have been reported with trabeculectomy secondary to endothelialization of the fistula. The fistula can be reopened in some cases with the Nd:YAG laser. Laser trabeculoplasty has no useful role in treating glaucoma related to ICE syndrome.

Tumors

Tumors in the posterior segment of the eye or anterior uveal cysts may cause a unilateral secondary ACG. Primary choroidal melanomas, ocular metastases, and retinoblastoma are the most common tumors to cause secondary angle closure. The mechanism of the ACG is determined by the size, location, and pathology of the tumor. Choroidal and retinal tumors tend to shift the lens–iris interface forward as the tumors enlarge, causing secondary angle closure. Breakdown of the blood–aqueous barrier and inflammation from tissue necrosis can result in posterior and PAS formation, further exacerbating other underlying mechanisms of angle closure. Iris neovascularization can occur frequently with retinoblastomas, medulloepitheliomas, and choroidal melanomas, resulting in secondary angle closure and neovascular glaucoma.

Inflammation

Secondary ACG can result from ocular inflammation. Fibrin and increased aqueous proteins from the breakdown of the blood–aqueous barrier may predispose to the formation of posterior synechiae (Fig 5-18) and PAS. If left untreated, these posterior synechiae can result in a secluded pupil, iris bombé, and secondary angle closure (Fig 5-19).

Figure 5-18 Inflammatory glaucoma. A fibrinous anterior chamber reaction and posterior synechiae formation are shown in a patient with ankylosing spondylitis.

Figure 5-19 Inflammatory glaucoma. A secluded pupil is shown in a patient with long-standing uveitis with classic iris bombé

and secondary angle closure. (Courtesy of Steven T. Simmons, MD.)

Inflammation may prompt PAS to form through peripheral iris edema, organization of inflammatory debris in the angle, and the bridging of the angle by large keratic precipitates (sarcoidosis). Unlike with PAC, in which the PAS occur preferentially in the superior angle, with inflammatory etiologies they occur most frequently in the inferior angle (Fig 5-20). These PAS tend to be nonuniform in shape and height, which further differentiates inflammatory disease from PAC (Fig 5-21). In rare instances, ischemia secondary to inflammation may cause rubeosis iridis and neovascular glaucoma.

Figure 5-20 Inflammatory glaucoma. Keratic precipitates can be seen bridging the inferior anterior chamber angle in this patient with long-standing uveitis, resulting in the formation of PAS.