Associated Ocular Manifestations

In the series by Watson and Hayreh, the rate of complications in patients with scleritis was 57%, excluding scleral thinning [45]. Decreased visual acuity, keratitis, cataract, uveitis, and glaucoma are ocular associations indicating the spread of scleral inflammation to adjacent tissues [34, 42, 45]. Complications are more frequent in severe necrotizing scleritis and posterior scleritis [34,42,45]. Due to potential ocular complications related to scleritis, early diagnosis and treatment of scleritis and its associated ocular manifestations are critical.

Visual acuity may be compromised in patients with scleritis and must be monitored carefully. Decreased vision occurs most frequently with posterior scleritis (45-84%), necrotizing scleritis (74-82 %), nodular scleritis (26%), and least often with diffuse anterior scleritis (9%) [34, 42]. Vision may be limited due to keratitis, anterior uveitis, or cataract in anterior scleritis. In posterior scleritis, vision loss greater than 2 Snellen lines has been reported in 31-45% of patients [22, 34]. Vision loss in posterior scleritis from an axial hyperopic shift in refractive status can occur secondary to scleral edema with anterior displacement of the retina [22,34,40]. Decreased vision in posterior scleritis is most commonly related to macular changes followed by optic disc abnormalities, including macular edema, optic disc edema or atrophy, retinal detachment, epiretinal membrane formation, macular cyst or hole, and cataract [22,34,40,42,45]. In some patients the visual impairment can be severe and permanent, emphasizing the importance of early diagnosis and treatment [22].

A mild to moderate anterior uveitis has been observed in 30-42 % of patients with scleritis, most frequently (69 %) with necrotizing scleritis [36,45]. Almost half of the patients with posterior scleritis have an anterior uveitis [34] and 2-100% have a posterior vitritis, depending on the case series [22,45]. The anterior uveitis often follows a long-standing and intractable course [36, 45], with one-third of cases being bilateral [36]. Approximately half of patients with scleri-tis-associated uveitis have an associated systemic illness [34, 36], most frequently (19%) rheumatoid arthritis [36]. Anterior uveitis may be an indicator of the activity and extent of scleral inflammation, as the uveitis subsides when the scleral inflammation is adequately treated. Additionally, vision loss (49%), peripheral ulcerative keratitis (22%), and glaucoma (19%) occurred more frequently in patients with uveitis compared with those without uveitis [36]. Due to extension of scleral inflammation to other ocular tissues, scleritis-associated uveitis portends a worse prognosis.

A keratopathy has been associated with 14-29% of patients with scleritis, including peripheral corneal thinning, stromal keratitis, and peripheral ulcerative keratitis [34, 37, 42, 45]. Corneal changes are most frequently seen in patients with necrotizing scleritis (relative risk of 5.3) and least often in patients with diffuse scleritis [37].An associated systemic illness was found in 87% of patients who had both peripheral keratopathy and scleritis [37]. Patients with scleritis-associated peripheral keratopathy are at increased risk for complications, such as decreased vision (81%), anterior uveitis (62%), and impending corneal perforation (62%) [37]. Peripheral corneal thinning is the most benign form with a well-demarcated peripheral zone of circumferential thinning that precedes corneal vascularization. Indicative of extension of scler-al inflammation, stromal keratitis with central or peripheral infiltrates can progress to diffuse corneal clouding or sclerocornea [45]. The most destructive keratopathy is peripheral ulcerative keratitis inferring a worse prognosis [37, 45], with a higher prevalence of necrotizing scleritis (67%), and a greater association with impending corneal perforation (100%) [45].

During any stage of scleral inflammation, the intraocular pressure may be elevated due to several different mechanisms, such as obstruction of the aqueous outflow channels, elevated epis-cleral pressure, angle closure, or secondary to a steroid response [45]. Although the elevation in intraocular pressure may be transient, glaucoma has been reported in 12-13 % of cases of scleritis [34, 45]. Patients with an associated anterior uveitis are at an increased risk for ocular hypertension due to possible obstruction of the tra-becular meshwork by inflammatory cells, corti-costeroid usage, or secondary angle closure from peripheral anterior synechiae [45]. Intraocular pressure was elevated in 12 % of patients with posterior scleritis [22]. In 4-16% of posterior scleritis cases with ocular hypertension, annular ciliochorodial effusions were present, causing secondary angle closure from anterior displacement of the iris-lens diaphragm [3,22].

Cataracts have been observed in 7-17% of cases of scleritis [34, 45]. Cataract formation may be accelerated by long-standing inflammation or secondary to steroid use. The prevalence of cataract was associated with the type of scle-ritis, seen most frequently with necrotizing scleritis (41%) and least frequently with diffuse scleritis (9%) [34]. Cataract extraction can precipitate scleral inflammation, usually in the form of a necrotizing scleritis [19,37,32,38].

Scleral thinning (22 %) most commonly occurs in necrotizing scleritis and may progress to ectasia [45]. Staphyloma formation occurs only in the presence of increased intraocular pressure, usually greater than 30mmHg. Scleral defects can develop due to necrosis and sequestration, but rarely result in perforation. If the inflammation is controlled medically,new collagen may form over small defects. Large defects are less likely to become adequately covered with new granulation tissue [45].

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