TNOA Journal of Ophthalmic Science and Research

: 2022  |  Volume : 60  |  Issue : 1  |  Page : 52--54

Idiopathic posterior scleritis: A masquerade of acute angle-closure attack

Priyanka Sudhakar1, Meena Gopinath Menon1, Nidhi Dubey2,  
1 Department of Glaucoma, Sankara Eye Hospital, Bengaluru, Karnataka, India
2 Department of Uvea, Sankara Eye Hospital, Bengaluru, Karnataka, India

Correspondence Address:
Dr. Meena Gopinath Menon
Sankara Eye Hospital, Varthur Main Road, Near Kundalahalli Gate, Marathalli, Bengaluru - 560 037, Karnataka


We report a case of a 51-year-old gentleman who presented with diffuse conjunctival congestion, chemosis, and shallow anterior chamber only in his left eye (LE), with an intraocular pressure of 26 mmHg, and closed angles on gonioscopy. B-scan ultrasonography of the LE showed increased choroidal thickness with minimum suprachoroidal fluid effusion. A diagnosis of anterior and posterior scleritis with secondary angle closure was made. The patient showed a favorable response to oral and topical steroids with cycloplegics. Idiopathic scleritis can mimic an acute attack of angle closure. Prompt recognition of the same is vital to providing good clinical outcomes.

How to cite this article:
Sudhakar P, Menon MG, Dubey N. Idiopathic posterior scleritis: A masquerade of acute angle-closure attack.TNOA J Ophthalmic Sci Res 2022;60:52-54

How to cite this URL:
Sudhakar P, Menon MG, Dubey N. Idiopathic posterior scleritis: A masquerade of acute angle-closure attack. TNOA J Ophthalmic Sci Res [serial online] 2022 [cited 2022 Dec 1 ];60:52-54
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Full Text


Acute angle-closure attack, an ophthalmic emergency, warrants immediate intervention to alleviate the patient's symptoms and consequent disc damage. However, unilateral angle closure is a rare clinical entity and is usually secondary to an underlying pathology. Identification of the same is vital to providing the right treatment. We present one such unique case of a unilateral idiopathic scleritis, masquerading as an acute angle-closure attack.

 Case Report

A 51-year-old gentleman presented with a 2-day history of severe pain, exacerbating with eye movements and redness in his left eye (LE), with no prior significant antecedent history. Uncorrected visual acuity (UCVA) in LE was 6/12, with diffuse episcleral and conjunctival congestion [Figure 1], chemosis, a shallow anterior chamber (AC) [Figure 2], and 1+ cells in the AC, with few chorioretinal folds in the posterior pole on undilated fundus examination. Right eye (RE) was essentially normal, including normal AC depth [Figure 3]. Intraocular pressure (IOP) by applanation in RE and LE was 14 and 26 mmHg, respectively. Gonioscopy revealed closed angles in LE and open in RE. B-scan ultrasonography of the LE showed increased choroidal thickness with minimum suprachoroidal fluid effusion. A diagnosis of anterior and posterior scleritis with secondary angle closure was made. He was started on topical (prednisolone acetate 1% 4 times/day) and oral steroids (prednisolone 50 mg tapering dose) and oral antiglaucoma medication (tablet acetazolamide 250 mg, half dose twice daily). A panel of serological investigations to rule out associated systemic disorders was advised, which included, anti-neutrophilic cytoplasmic antibodies (c and p), antinuclear antibody, treponema pallidum hemagglutination, human immunodeficiency virus, and serum angiotensin-converting enzyme, all of which tested negative. Erythrocyte sedimentation rate was moderately raised, which in view of no other identifiable systemic comorbidity was regarded nonspecific. Chest X-ray and Mantoux were unremarkable. Over the next 2 weeks, LE improved symptomatically [Figure 4], with UCVA of 6/6, deepening of AC [Figure 5], and IOP of 16 mmHg. Tablet acetazolamide was stopped subsequently, and he was maintained on a tapering dose of steroids. IOP as on final visit at 3 weeks was 12 mmHg, with open angles on gonioscopy in LE [Figure 6].{Figure 1}{Figure 2}{Figure 3}{Figure 4}{Figure 5}{Figure 6}


In primary acute angle-closure glaucoma (ACG), examination of the fellow eye usually reveals a shallow AC. However, in case of a normal fellow eye, one should rule out the following etiological possibilities of unilateral angle closure: (A) lens related: lens dislocation and intumescent cataract; (B) tumors: retrobulbar and intraocular (choroidal melanoma); (C) retinal: central retinal vein occlusion, choroidal hemorrhage, panretinal photocoagulation, neovascular glaucoma, massive vitreous hemorrhage, scleral buckling surgery, and persistent primary hyperplastic vitreous; and (D) and other causes like –Weber syndrome, chronic uveitis, iridocorneal endothelial syndromes, episcleritis and posterior scleritis, uveal effusion syndrome.

Posterior scleritis accounts for 2%–12% of all scleritis cases, with 29% having an underlying systemic association.[1] It is more common in middle-aged women (40–60 years), bilateral in 40%–80% of cases, the risk being higher in patients with rheumatoid arthritis or other collagen-vascular diseases.[1] Although many patients present unilaterally, other eye can become symptomatic months or years later. The most common presenting symptoms of posterior scleritis are pain often proportional to the severity of anterior involvement, decreased vision, and redness of the eye. Literature states that some anterior scleral involvement is commonly found in patients with posterior scleritis. Characteristic fundus findings include any of these: circumscribed fundal mass, choroidal folds, retinal striae, disc edema sometimes with annular choroidal detachment, exudative macular detachment, cystoid macular edema, or peripheral retinal detachment. Ultrasonography and computed tomography show sub-Tenon effusion and any thickening of the posterior sclera, described as the T-sign, which though diagnostic, may not be seen in peripheral posterior scleritis, not involving the posterior pole.

Scleritis may be complicated by glaucoma in 11.6% to 49% of cases,[2],[3] the postulated pathophysiology of which include:[1]

Ciliochoroidal effusion causing an anterior rotation of iris–lens diaphragm (ILD) forwardInflammatory cells clogging trabecular meshworkPlasma cells and lymphocytic infiltration of ciliary body (CB) and trabecular meshworkRaised episcleral venous pressure by lymphocytic cuffing of episcleral vesselsLymphocytic cuffing around Schlemm's canalSteroid-induced glaucoma due to chronic steroid usage.

Although secondary ACG in scleritis is uncommon, it is not completely unknown. Inflamed and thickened sclera attributes to impaired permeability of the transscleral outflow, resulting in fluid accumulation in the choroidal space, which on extending to CB can cause CB edema and anterior rotation with an anterior shift of ILD. When these changes become more severe, ACG develops by direct angle closure. As early as 1978, Quinlan et al. reported three cases of posterior scleritis presenting with ACG and peripheral choroidal detachment.[4] Jain et al. reported a case of young male presenting with angle-closure attack and exudative RD, secondary to presumed tubercular posterior scleritis, resolving completely with oral corticosteroids.[5] Bashir et al. reported a case of 50-year-old woman with panscleritis presenting as unilateral case of acute ACG.[6]

The importance of identifying the underlying pathophysiology in a case of unilateral acute angle-closure attack lies in the difference in management strategy. Posterior scleritis masquerading as acute angle-closure attack is secondary to anterior rotation of CB. Thus, the conventional approach of laser iridotomy as in an acute ACG would not be effective in these cases, as would use of topical pilocarpine which could be detrimental. In addition to a course of topical and oral steroids, they would benefit well with cycloplegics, which would help to relieve angle compression by posterior displacement of ILD.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


1Benson WE. Posterior scleritis. In: Survey of Ophthalmology. Vol. 32.: Elsevier,USA; 1988. p. 297-316.
2Watson, P G, and S S Hayreh. “Scleritis and episcleritis.” The British journal of ophthalmology vol. 60,3 (1976):163-91.
3Wilhelmus KR, Grierson I, Watson PG. Histopathologic and clinical associations of scleritis and glaucoma. Am J Ophthalmol 1981;91:697-705.
4Quinlan MP, Hitchings RA. Angle-closure glaucoma secondary to posterior scleritis. Br J Ophthalmol 1978;62:330-5.
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6Bashir H, Sridhar U, Mazumdar S, Tripathy K. Panscleritis masquerading as an attack of primary acute angle closure glaucoma. GMS Ophthalmol Cases 2019;9:Doc31.