extremely ominous. The uveitis associated with scleritis is more frequently anterior, mild to moderate in intensity, and appears during the late course of the scleral inßammation [6].

In our series, 132 of the 500 patients (26%) with scleritis had had at least one episode of anterior uveitis (Table 4.4). There was no difference in the sex and age distribution between the patients with scleritis with and without uveitis. The presence of anterior uveitis was highly associated with the presence of necrotizing anterior scleritis (45%), diffuse anterior scleritis (28%), and posterior scleritis (26%); Þve of the eight patients with posterior scleritis and anterior uveitis also had some degree of anterior scleritis.

Posterior uveitis was present in all cases of posterior scleritis. Because the presence of posterior uveitis in association with anterior scleritis is rare, the detection of posterior uveitis in a patient with anterior scleral inßammation obligates one to search for posterior scleritis [3].

Decrease in vision in patients with scleritis may be caused by complications, such as keratitis, uveitis, cataract, glaucoma, or macular edema. Long-standing uveitis may cause cataract, glaucoma, or macular edema. The presence of anterior uveitis with scleritis was highly associated with the presence of ocular complications (including decrease in vision, peripheral keratitis, or ocular hypertension) indicating that uveitis occurs with scleritis cases undergoing complications that may lead to visual loss.

The presence of uveitis-accompanying scleritis should be considered as a grave sign because it indicates not only an extension of the inßammatory process to the intraocular structures, but also the presence of complications that may cause progressive visual loss. The detection of uveitisaccompanying scleritis requires early and aggressive therapy to control both the uveal and scleral inßammation.

4.2.6.3 Glaucoma

Increased intraocular pressure is caused by the accompanying scleral edema and uveal inßammation. Fraunfelder and Watson [1] found that 46% of 30 enucleated eyes with a primary histological

diagnosis of scleritis showed signs of having had glaucoma; scleritis with glaucoma and uveitis was the most common cause of enucleation. Whilhelmus et al. [9], in another series of 92 enucleated eyes with a primary histological diagnosis of scleritis, found that 49% of them had had glaucoma [9]. These data suggest that the presence of scleritis with glaucoma, particularly when associated with uveitis, should be considered as an ominous sign [1]. The reported incidence of increased intraocular pressure in patients with scleritis varies between 12% and 22% [2, 9, 18]. In our series of 500 patients with scleritis, 71 (14%) had increased intraocular pressure (Table 4.4). Angleclosure glaucoma, open-angle glaucoma, and neovascular glaucoma are some of the possible mechanisms.

Angle-Closure Glaucoma

A primary angle-closure attack can appear in scleral inßammation, particularly if the patient has narrow angles. Swelling of the angle structures combined with a mildly dilated pupil may account for the closure of the angle. The therapy includes the standard antiglaucomatous treatment, primarily with hyperosmotic agents, miotics, beta blockers, and laser iridectomy, combined with anti-inßammatory treatment for controlling the scleral inßammation.

Secondary angle closure in patients with scleritis may be caused by anterior synechiae, iridolenticular adhesions, or ciliary body edema secondary to long-standing anterior uveitis [9]. In this case, relief of anterior adhesions (laser iridogonioplasty or Þltering procedures) and/or pupillary block (laser iridectomy) and control of the sclerouveal inßammation may restore the intraocular pressure to normal.

Secondary angle closure may occur in patients with posterior scleritis when a ciliochoroidal effusion displaces the iris-lens diaphragm forward, shallowing the anterior chamber and closing the Þltration angle [100]. In this case, treatment with miotics may cause further shallowing of the anterior chamber, whereas treatment of the scleral inßammation with anti-inßammatory drugs resolves the inßammatory effusion and allows the angle to reopen.