Open-Angle Glaucoma

Primary open-angle glaucoma in patients with scleritis may appear because of a preexisting abnormal outßow system that is further impaired by inßammation of the angle structures. Characteristics of these patients are normal angles, cupped disks, and glaucomatous Þeld defects; the increased intraocular pressure returns to normal with antiglaucomatous agents but does not respond to anti-inßammatory therapy for the scleritis [3].

Occlusion of the trabecular meshwork by inßammatory cells in anterior uveitis and scleral inßammation may cause a secondary open-angle glaucoma. Gonioscopically, inßammatory debris may be seen at the angle. Treatment with beta blockers, carbonate dehydratase inhibitors, and anti-inßammatory agents may control the intraocular pressure and the sclerouveal inßammation. If these fail to control the intraocular pressure, laser trabeculoplasty or Þltering surgery should be performed.

Steroid-induced open-angle glaucoma may appear in patients with scleritis receiving topical steroids or, more rarely, systemic steroids. The increased intraocular pressure may develop within 2 weeks of initiating steroid use or after many months or even years of use. The more potent drugs, such as dexamethasone and prednisolone are more likely to induce increased intraocular pressure sooner and to a higher level than weaker agents, such as hydrocortisone or ßuorometholone. This predisposition is genetically determined. Patients in whom glaucoma has been successfully controlled may develop unacceptable levels of intraocular pressure if steroid therapy is added. Nonsteroidal anti-inßammatory drugs and/or immunosuppressive agents may allow a reduction in the steroids. If spontaneous resolution does not occur within 2Ð6 weeks, if steroids cannot be stopped, or if the pressure is high, therapy for primary open-angle glaucoma may be initiated to prevent progression of optic nerve damage.

Neovascular Glaucoma

Angle neovascularization has been reported in enucleated eyes with scleral inßammation [9]. Long-standing hypoxic retinopathy, such as

central retinal artery or vein occlusion, may lead to the formation of a Þbrovascular membrane that may cover the trabecular meshwork, resulting in total angle closure. A combination of anti-inßam- matory therapy and panretinal photocoagulation, perhaps supplemented with direct goniophotocoagulation, medical antiglaucomatous treatment, or Þltering surgery, sometimes succeeds.

The presence of increased intraocular pres- sure-accompanying scleritis indicates an extension of the inßammatory process to the intraocular structures, with the development of complications leading to progressive visual loss. Intraocular pressure should always be measured in patients with scleral inßammation. The detection of glau- coma-accompanying scleritis requires early and aggressive therapy to control both the intraocular pressure and the scleral inßammation.

4.2.6.4 Cataract

The presence of long-standing anterior uveitis in patients with severe scleral inßammation, particularly of the necrotizing type, may lead to the formation of a cataract. Another cause of cataract is the use of long-term systemic or local steroid treatment. A comparison between a group of patients without scleritis and a group of patients with scleritis, both receiving long-term systemic or local steroid treatment, showed an increased risk of development of posterior subcapsular cataract in the group of patients with scleritis (36%) as opposed to the group of patients without scleritis (11%) [18].

Although cataract extraction usually is not complicated in patients with scleritis without uveitis, surgery should be attempted only in the absence of scleral inßammation. Cataract removal through a corneal incision is advisable.

Uneventful cataract extraction or any other surgical procedure can, although rarely, precipitate a necrotizing scleritis in patients with autoimmune or infectious diseases (surgically induced necrotizing scleritis, SINS) [161Ð166]. In seven of our patients, necrotizing scleritis developed after ocular surgery, including three patients after uneventful cataract extraction, three patients after retinal detachment repair, and one patient after pterygium excision and local mitomycin. The interval