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Year : 2004  |  Volume : 52  |  Issue : 3  |  Page : 241-4

Posterior scleritis presenting as unilateral secondary angle-closure glaucoma.

Bombay City Eye Institute and Research Centre, Mumbai, India

Date of Submission29-Jan-2003
Date of Acceptance04-Jul-2003

Correspondence Address:
Sunil S Jain
Bombay City Eye Institute and Research Centre, Mumbai
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Source of Support: None, Conflict of Interest: None

PMID: 15510468

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The following is a case report of a 19-year-old male who presented with unilateral acute angle-closure glaucoma. Posterior scleritis was diagnosed based on clinical features and ultrasound B-scan. The acute angle closure attack and exudative retinal detachment completely resolved with use of oral corticosteroids.

Keywords: Angle-closure glaucoma, posterior scleritis, corticosteriod therapy

How to cite this article:
Jain SS, Rao P, Kothari K, Bhatt D, Jain S. Posterior scleritis presenting as unilateral secondary angle-closure glaucoma. Indian J Ophthalmol 2004;52:241

How to cite this URL:
Jain SS, Rao P, Kothari K, Bhatt D, Jain S. Posterior scleritis presenting as unilateral secondary angle-closure glaucoma. Indian J Ophthalmol [serial online] 2004 [cited 2024 Feb 24];52:241. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?2004/52/3/241/14581

Posterior scleritis is a granulomatous inflammation occurring either within the scleral tissue or in the adjacent vascular networks. This inflammatory process can cause fluid to leak from the choroid into the suprachoroidal space, leading to ciliochoroidal effusion, exudative retinal detachment causing secondary angle-closure glaucoma [ACG] without pupillary block.[1]

  Case report Top

A 19-year-old male, earlier diagnosed to have acute non-granulomatous iridocyclitis in the left eye and treated at our institute for 12 days, presented with severe pain, blurred vision, and mild diplopia in downgaze in the left eye of a day's duration. He gave a history of recurrent attacks of redness and pain over the past 2 months. He also had a history of pulmonary tuberculosis and was being treated for the same for the past 2 weeks.

On examination the best-corrected visual acuity in left eye was 6/12. The lids showed mild oedema. Extraocular movements revealed mild restriction of depression in the left eye. Conjunctiva showed conjunctival and ciliary congestion with chemosis localised to the inferior conjunctiva; the anterior chamber [AC] was extremely shallow centrally and peripherally, judged to be grade 1 by van Herick's method [Figure - 1]a. The lens was clear, and the pupil was mid-dilated. The intraocular pressure was 34 mm Hg, and gonioscopy showed total angle closure even on indentation [Figure - 2]a. A fundus examination showed localised subretinal elevation below the inferotemporal arcade with overlying retinal pigment epithelial alteration [Figure - 1]c. The ora serrata was visible by ophthalmoscopy across 360 without scleral depression, suggesting the presence of an annular ciliochoroidal effusion, which was confirmed on ultrasound biomicroscopy (UBM) [Figure - 1]d. Slitlamp biomicroscopy using 90-D lens showed vitreous cells at the posterior vitreous face; the disc was healthy and there were radiating internal limiting folds in the macular area [Figure - 1]c, inset). Fundus fluoroscein angiography showed hypofluorescence in the initial arteriovenous phase and diffuse hyperfluorescence in late phase with no leak. Ultrasound B-scan revealed marked thickening of chorioretinal layer in inferior and temporal quadrant with fluid in Tenon's space. [Figure - 1]e There was no evidence of any orbital mass lesion.

Based on these findings, a diagnosis of posterior scleritis of presumed tuberculous aetiology presenting as secondary angle closure glaucoma (ACG) in the left eye was made. The patient was asked to continue his anti-tuberculosis treatment and was prescribed tablet prednisolone 50 mg daily in consultation with the internist. In addition he was prescribed topical timolol maleate 0.5% eye drops twice daily, brimonidine tartarate 0.2% eye drops thrice daily, atropine sulphate 1% eye drops four times daily, prednisolone acetate 1% eye drops 6 times daily and phenylephrine hydrochloride 10% eye drops four times daily.

One week later the patient improved symptomatically. Unaided vision in left eye was 6/6. Lid oedema had disappeared, extraocular movements were normal, conjunctival, and ciliary congestion and chemosis had completely resolved. The AC was deep and quiet [Figure - 1]b, and the IOP was 10 mmHg. Gonioscopy revealed a completely open angle up to scleral spur without indentation [Figure - 2]b all over without any synechiae formation. Fundus examination revealed persistence of the ILM folds over the macula [Figure - 2]c inset). The localised subretinal elevation had resolved completely [Figure - 2]c. The ora serrata was barely visualised without indentation indicating resolution of the ciliochoroidal detachment. There were no vitreous cells. Topical anti-glaucoma medications were discontinued and patient was advised tapering doses of systemic and topical corticosteroids and cycloplegics. At the last follow-up 4 months later, the patient was off all medications, the unaided vision was 6/6, and the IOP was 14 mmHg in left eye with complete resolution of scleritis.

  Discussion Top

Posterior scleritis due to its protean manifestations is one of the most commonly misdiagnosed conditions in ophthalmology.[2] Such misdiagnosis occurs due to its variable presentations, and also the relative non-familiarity of the general ophthalmologists with this condition.[3] The most common presentation is acute loss of vision associated with a moderate to severe degree of pain and redness. Proptosis, eyelid oedema, and restriction of ocular movements[3] can also be seen with intense periscleral inflammation spreading to orbit and extraocular muscles, as in this patient. Some anterior scleral involvement is often associated with posterior scleritis. In the acute stage mild non-granulomatous anterior uveitis can also be seen as in our patient. In the absence of specific diagnostic signs in posterior scleritis, ancillary tests are very useful for diagnosis. The B-scan ultrasonographic findings, provided the strongest evidence for diagnosis in a case series of Biswas et al.[3] Ultrasound should be done where choroidal folds are seen and diagnosis is uncertain. The characteristic findings include flattening and thickening of posterior coats of the eye, retrobulbar oedema and the "T" sign.

Posterior scleritis is associated with increased IOP in 12-46% of cases.[4] This occurs through a variety of mechanisms, including increased viscosity of the aqueous humor, inflammation of the outflow channels, obstruction of the trabecular meshwork by inflammatory cells and debris, peripheral anterior synechiae, neovascularisation, and elevated episcleral venous pressure.[5] Posterior scleritis can also be associated with choroidal effusion and secondary ACG without pupillary block.[1] The pathophysiology for the development of the secondary ACG is initiated by posterior scleritis which can cause accumulation of suprachoroidal and supraciliary fluid due to inflammation and vascular congestion. This causes narrowing of the ciliary ring and anterior rotation of the ciliary body and iris root into the angle. This reduces tension on the zonules, permits the forward movement of the lens and displaces the peripheral iris.

The management is directed at two events, i.e., treating the uveal inflammation and pulling the lens-diaphragm back so as to open the angles of the AC. Systemic corticosteroids are essential to treat the uveal inflammation and reduce the choroidal effusion. The anterior chamber deepens spontaneously when the inflammation and the effusion subside. By the time the corticosteroids act and the inflammation gets under control, cycloplegics and IOP lowering agents such as topical β -adrenergic antagonists, a2- adrenergic agonists and oral carbonic anyhydrase inhibitors are added. Treatment with pilocarpine is contraindicated. Apart from not working, it actually makes the anterior chamber shallower.[6] Cycloplegics by their action tighten the zonules thus pulling the lens-iris diaphragm posteriorly, deepen the AC and open the angles. However, the scleritis can produce extensive peripheral anterior synechiae and chronic angle-closure glaucoma. If the cause is not recognised, the patient may be given inappropriate treatment and even submitted to unnecessary surgery.[7],[8] In these patients, peripheral iridotomies are ineffective. Early diagnosis is important because prompt treatment often leads to complete resolution with excellent visual recovery.

  References Top

Dodds EM, Lowder CY, Barnhorst DA, Lavertu P, Caravella LP, White DE. Posterior scleritis with Annular Ciliochoroidal Detachment. Am J Ophthalmol 1995;120:677.  Back to cited text no. 1
Benson WE, Shields JA, Tasman W, Crandall AS. Posterior scleritis: A cause of diagnostic confusion. Arch Ophthalmol 1979;97:1482-86.   Back to cited text no. 2
Biswas J, Mittal S, Ganesh SK, Shetty N, Gopal L. Posterior Scleritis: Clinical Profile and Imaging Characteristics. Indian J Ophthalmol 1998;46:195-202.  Back to cited text no. 3
Watson PG, Hayreh SS. Scleritis and episcleritis. Br J Ophthalmol 1976;60:163.  Back to cited text no. 4
Chen CJ, Harisdangkul V, Parker L. Transient glaucoma associated with anterior diffuse scleritis in relapsing polychondritis. Glaucoma 1982;4:109.  Back to cited text no. 5
Poinooswamy D, Nagasubramanian S, Brown NAP. The effects of pilocarpine on the visual acuity and on the dimensions of the cornea and anterior chambers. Br J Ophthalmol 1976;60:678.  Back to cited text no. 6
Philips CD. Angle-closure glaucoma secondary to ciliary body swelling. Arch Ophthalmol 1974;92:287.  Back to cited text no. 7
Quinlan MP, Hitchings RA. Angle closure glaucoma secondary to posterior scleritis. Br J Ophthalmol 1978;62:330.  Back to cited text no. 8


  [Figure - 1], [Figure - 2]

This article has been cited by
1 Acute angle-closure glaucoma in a teenage girl [10]
Utman, S.A.K., Menon, G.J., Nabi, N.U.
Canadian Journal of Ophthalmology. 2007; 42(6): 881-882
2 Progression in diagnosis and differential diagnosis of posterior scleritis
Liu, Q.
Chinese Ophthalmic Research. 2007; 25(10): 789-792


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