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Clinicopathologic Reports, Case Reports, and Small Case Series
November 2007

Spontaneous Filtration Bleb as a Consequence of Scleritis

Arch Ophthalmol. 2007;125(11):1578-1579. doi:10.1001/archopht.125.11.1578
Report of a Case

A 40-year-old woman with systemic lupus erythematosus was seen for evaluation of persistent redness and discomfort of variable intensity in the left eye during the previous 2 years. Her best-corrected visual acuity was 20/30 OD and 20/40 OS, with intraocular pressure of 10 mm Hg in the right eye and 11 mm Hg in the left eye. Slitlamp biomicroscopy showed mild dilatation of conjunctival and episcleral vessels of the right eye. The left eye demonstrated diffusely dilated episcleral vessels with a flat, superotemporal perilimbal avascular region with focal surrounding conjunctival edema. Magnetic resonance imaging performed to assess for orbital venous outflow disturbances was unrevealing. Topical corticosteroid therapy (1% prednisolone acetate) with subsequent tapering resulted in limited clinical improvement bilaterally.

At follow-up examination 2 years later, the patient reported substantial left eye pain. Visual acuity in both eyes was unchanged. Examination of the right eye demonstrated engorgement of both superficial vessels and the deeper scleral vascular plexus with a superotemporal perilimbal avascular patch (Figure 1). The left eye demonstrated apparent underlying scleral thinning and focal elevation of the bulbar conjunctiva with the appearance of a bleb along with dilatation of surrounding deep vessels (Figure 2). The anterior chamber remained deep, and examination of the posterior segment yielded normal findings. Intraocular pressure was 12 mm Hg in both eyes. Oral nonsteroidal anti-inflammatory drug therapy was instituted.

Figure 1.
Right eye. Note engorgement of both superficial vessels and the deeper scleral vascular plexus with a superotemporal perilimbal avascular patch.

Right eye. Note engorgement of both superficial vessels and the deeper scleral vascular plexus with a superotemporal perilimbal avascular patch.

Figure 2.
Left eye. Note underlying scleral thinning and focal elevation of the bulbar conjunctiva with the appearance of a bleb along with dilatation of surrounding deep vessels.

Left eye. Note underlying scleral thinning and focal elevation of the bulbar conjunctiva with the appearance of a bleb along with dilatation of surrounding deep vessels.

Clinical appearance was unchanged 8 months later, however, intraocular pressure was 11 mm Hg OD and 2 mm Hg OS. The bleb was Siedel testnegative. Gonioscopy of the right eye demonstrated normal-appearing lightly pigmented meshwork. Gonioscopy of the left eye demonstrated lightly pigmented trabecular meshwork, without evidence for a cyclodialysis cleft, cyclodestruction, or other basis for hypotony. Intraocular pressure during 15-month follow-up remained consistently asymmetric (range, 8-16 mm Hg OD and 2-9 mm Hg OS). During this period of observation, the morphologic bleb features remained stable without secondarycomplications from hypotony. Ophthalmic treatment during this interval included oral and topical nonsteroidal anti-inflammatory drugs and topical corticosteroid agents.

Comment

Scleral inflammatory disease is a deep and destructive inflammation presumed to be incited by autoimmune system dysregulation1 and is often classified on the basis of the site of pathologic findings and severity of inflammation.2 Scleritis is characterized by edema and inflammatory cell infiltration of the sclera and is commonly associated with identifiable systemic disease and often with ocular complications.3 The development of a spontaneous filtering bleb with consequential hypotony is an unusual complication of anterior scleritis, and, to our knowledge, our case is the first reported.

Thinning secondary to scleral inflammation, with a resultant focal aqueous shunt and collection external to the subconjunctival or sub-Tenon space, analogous to a deliberate guarded filtration procedure, is the presumed underlying mechanism. Ultrasound biomicroscopy to quantify scleral thinning was unavailable; however, its potential role in the assessment of scleritis subtypes, disclosing disease progression and judging treatment efficacy, has been demonstrated.4 This unusual complication emphasizes the destructive nature of scleral inflammatory processes and a management dilemma between the risks of infection and hypotony-related complications with observation compared with the potential to incite further, more substantial scleral inflammation with a surgical approach.

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Article Information

Correspondence: Dr Stock, Cornea Consultant, SC, 2500 N Mayfair Rd, Ste 340, Milwaukee, WI 53226 (corneaconsultant@gmail.com).

Financial Disclosure: None reported.

References
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Watson  PGHayreh  SS Scleritis and episcleritis. Br J Ophthalmol 1976;60 (3) 163- 191
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Heiligenhaus  ASchilling  MLung  ESteuhl  KP Ultrasound biomicroscopy in scleritis. Ophthalmology 1998;105 (3) 527- 534
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