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 Table of Contents  
Year : 2021  |  Volume : 1  |  Issue : 3  |  Page : 503-505

Unilateral acute secondary angle-closure glaucoma in active thyroid eye disease

Department of Glaucoma, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, Madurai, Tamil Nadu, India

Date of Submission15-Oct-2020
Date of Acceptance04-Feb-2021
Date of Web Publication02-Jul-2021

Correspondence Address:
Dr. Vijayalakshmi A Senthilkumar
Glaucoma Consultant, Department of Glaucoma, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, Madurai - 625 020, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_3260_20

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Thyroid eye disease (TED) is the most common and disfiguring orbital disease in adults. This complex condition is characterized by autoimmune-mediated inflammation of the orbital soft tissues, extraocular muscles, and eyelids. Majority of those with TED have autoimmune hyperthyroidism (Graves disease), but rarely patients can have hypothyroidism or normal thyroid function. Association of TED with open-angle glaucoma has been reported widely, whereas its association with angle-closure glaucoma has been sparsely reported as case reports. We report two instances of secondary angle-closure glaucoma (SACG) in patients with active TED, with focus on clinical presentation, diagnostic challenges, and presumed mechanisms of angle closure.

Keywords: Acute angle-closure glaucoma, aqueous misdirection syndrome, graves ophthalmopathy, pupillary block glaucoma, thyroid eye disease

How to cite this article:
Senthilkumar VA, Pradhan C, Dosapati S, Krishnadas R. Unilateral acute secondary angle-closure glaucoma in active thyroid eye disease. Indian J Ophthalmol Case Rep 2021;1:503-5

How to cite this URL:
Senthilkumar VA, Pradhan C, Dosapati S, Krishnadas R. Unilateral acute secondary angle-closure glaucoma in active thyroid eye disease. Indian J Ophthalmol Case Rep [serial online] 2021 [cited 2021 Jul 29];1:503-5. Available from: https://www.ijoreports.in/text.asp?2021/1/3/503/320095

TED is a self-limiting disease and may present in one of two stages: active or quiescent.[1] In active stage, there is active inflammation, which can lead to orbital muscle enlargement, conjunctival injection and chemosis, ocular pain, and swelling of the periocular tissues & eyelids. Orbital fibroblasts are stimulated in active TED and synthesize glycosaminoglycans & hyaluronic acid, overproduction of which leads to orbital edema and congestion.[2],[3] Secondary angle-closure glaucoma in TED has been sparsely reported in the literature.

  Case Reports Top

Case 1

A 49-year-old man with known h/o hyperthyroidism since 5 years, on irregular treatment with oral Methylcarbimazole (10 mg), presented with defective vision of acute onset in right eye (OD) of two weeks duration. At presentation, his thyroid profile values were free T3––4.89 pg/mL, free T4––1.40 ng/mL, TSH––0.001 μIU/mL. Elsewhere, he had been diagnosed as TED and glaucoma a week prior to presentation & treated with oral corticosteroids & topical timolol. Best-corrected-visual-acuity (BCVA) was 6/18 and 6/9 in the right (OD) and left eyes (OS). Intraocular pressure (IOP) was 28 mmHg OD and 20 mmHg OS. Clinical evaluation OD was remarkable for axial proptosis (29 mm OD on Hertel's exophthalmometry), circumcorneal congestion, shallow anterior chamber (AC) depth, restricted ocular movements, 4 mm mid-dilated pupil & occludable angles on gonioscopy [Figure 1]. Fundus was characteristic for disc edema and splinter hemorrhage. Clinical evaluation OS was unremarkable with open angles on gonioscopy except for axial proptosis (27 mm on exophthalmometry) [Figure 1].
Figure 1: (a)- Clinical photography showing bilateral proptosis OD>OS. (b)- CT Brain showing bilateral thickened extraocular muscles ( white arrowheads). (c)- Slit lamp photograph OD at presentation showing circumcorneal congestion, shallow anterior chamber depth, mid dilated pupil, insert showing diffuse illumination of the same. (d)- Slit lamp photograph OS at presentation showing quiet eye with normal anterior chamber depth. (e)- Slit lamp photograph OD after YAG PI showing patent YAG PI (white arrowhead) and deep anterior chamber depth (insert). (f)- Gonioimage OD taken after YAG PI showing open angles with pigment dispersion in the angles due to appositional angle closure. (g and h)- ASOCT images taken before and after YAG PI showing increased ACA after YAG PI. (i and j)- Fundus photographs OD& OS taken at 1 month follow up showing resolving retinal hemorrhage in OD (white arrowhead)

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B scan OU revealed thickened extraocular muscles without any choroidal effusion or posterior segment pathology. ASOCT OD revealed ACA (Anterior-Chamber-Angle) of 0 degrees & UBM certainly excluded aqueous misdirection in this patient [Figure 1]. CT Orbit revealed bilateral thickened & crowded muscles in orbital apex (OD>OS) [Figure 1]. The patient was diagnosed to have active TED based on clinical activity score (CAS>3) [Table 1] and started on intravenous pulse therapy of methylprednisolone 1 g/day for 3 days & topical aqueous suppressants was stepped up with dorzolamide eyedrops 2% twice daily in OD. The next day there was further significant increase in IOP to 70 mmHg in OD, and laser peripheral iridotomy (PI) was performed. After half an hour of PI, IOP decreased to 24 mmHg with deepening of AC confirmed by ASOCT with ACA of 24 degrees. We arrived at a presumptive diagnosis of unilateral acute onset pupillary block glaucoma secondary to TED. To the best knowledge of the authors, this is the first report of possible association of acute onset pupillary block with active TED managed by Laser PI and aqueous suppressants. He has been advised to continue oral steroids, topical aqueous suppressants & periodical review to exclude progressive angle closure glaucoma.
Table 1: Disease activity

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Case 2

A 47-year-old man was referred for glaucoma consultation in view of raised IOP and shallow AC depth in OD. The patient had been on thyroid medications intermittently for the past 2 years. A thyroid-function-test showed hyperthyroid status. His thyroid profile values were free T3––5.22 pg/mL, free T4––1.86 ng/mL, TSH––0.008 μIU/mL. BCVA was 20/20 OU and IOP was 38 mm Hg OD, 20 mm Hg OS. Examination OD was characteristic of axial proptosis of 27 mm on Hertel's exophthalmometry with ocular motility restriction, whereas OS had a axial proptosis of 25 mm with full ocular movements [Figure 2]. Slit-lamp examination OD revealed shallow peripheral ACD with normal pupillary reaction and gonioscopy revealed appositional angle closure over 270 degrees. Fundus evaluation revealed edematous disc with blurred margins. OS examination was within normal limits and open angles on gonioscopy [Figure 2]. Imaging of orbits showed thickened extraocular muscle bellies in both eyes suggestive of TED. UBM OD showed anteriorly rotated ciliary body with increased thickness of ciliary body and loss of ciliary sulcus [Figure 2], suggestive of aqueous misdirection syndrome. Hence, a diagnosis of aqueous misdirection secondary to active TED was made. The patient was started with combination therapy of topical aqueous suppressants consisting of Timolol 0.5% & Brimonidine 0.2% twice a day in OD. In view of dysthyroid optic neuropathy patient was given intravenous Methylprednisolone 500 mg BD dosage for 3 days followed by oral steroids in tapering doses. A laser PI was done in OD to exclude any pupillary block component.
Figure 2: (a)- Clinical photography showing bilateral proptosis OD>OS, lateral view showing moderate-severe proptosis (insert). (b)- CT Brain showing bilateral thickened extraocular muscles (black arrowheads). (c)- Slit lamp photograph OD at presentation showing circumcorneal congestion, shallow anterior chamber depth. (d)- ASOCT OD showing shallow anterior chamber with ACA of 17 degrees. (e)- Slit lamp photograph OD after cycloplegics & steroids showing deep anterior chamber depth and quiet eye on insert. (f)- Gonio image OD taken after cycloplegics & steroids showing open angles. (g)- UBM image at presentation showing thickened, congested & anteriorly rotated ciliary body (white arrowheads). (h)- UBM image after cycloplegics and steroids showing normally placed ciliary body (white arrowhead)

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However, after 3 days of patent YAG PI, IOP in OD was persistently high (34 mmHg) with shallow ACD. The patient was started on strong cycloplegics ( atropine 1% drops) and continued with topical glaucoma therapy. After two weeks of conservative treatment, IOP OD reduced to 18 mm Hg, AC deepened, UBM showed normal positioned ciliary body with presence of iridociliary sulcus [Figure 2]. Aqueous misdirection being a diagnosis of exclusion was confirmed in this patient based on persistent shallow ACD despite patent PI, characteristic finding on UBM and favorable response to cycloplegics. The patient was advised to continue topical cycloplegics twice daily and a single aqueous suppressant (Timolol 0.5% BD) and oral steroids.

  Discussion Top

Tripathy et al. reported a case of aqueous misdirection during inactive stage of TED, managed conservatively with steroids and cycloplegics.[4] Kurtz et al. & Bernardino et al. reported cases of orbital pseudotumor presenting as acute ACG with choroidal and retinal detachment.[5],[6] They hypothesized that generalized orbital venous engorgement resulted in uveal engorgement and compression of anterior segment.

We presumed that orbital congestion due to enlargement of extraocular muscles & adipose tissue in TED could have raised intraorbital pressure with consequent compression of compliant structures such as ophthalmic veins leading to elevated episcleral venous pressure and vortex veins. Hence, the resulting venous stasis probably resulted in congestion of ciliary body & choroid causing forward shift of lens-iris diaphragm and SACG with or without a pupillary block component.[7]

  Conclusion Top

Acute onset SACG due to TED although rare is crucial to diagnose this clinical entity by meticulous clinical evaluation including gonioscopy and anterior segment imaging modalities like AS-OCT & UBM. Treatment must aim to reduce the activity of thyroid-associated orbitopathy as well as glaucomatous damage with ocular hypotensive medications, steroids & cycloplegics. Laser iridotomy may be indicated in instances where SACG comprises pupillary block components.


Photographer Mr. Rajkumar, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, Madurai, Tamil Nadu, India.

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.

  References Top

Douglas RS, Gupta S. The pathophysiology of thyroid eye disease: Implications for immunotherapy. Curr Opin Ophthalmol 2011;22:385-90.  Back to cited text no. 1
Smith TJ, Koumas L, Gagnon A, Bell A, Sempowski GD, Phipps RP, et al. Orbital fibroblast heterogeneity may determine the clinical presentation of thyroid-associated ophthalmopathy. J Clin Endocrinol Metab 2002;87:385-92.  Back to cited text no. 2
Tsui S, Naik V, Hoa N, Hwang CJ, Afifiyan NF, Sinha Hikim A, et al. Evidence for an association between thyroid-stimulating hormone and insulin-like growth factor 1 receptors: A tale of two antigens implicated in Graves' disease. J Immunol 2008;181:4397-4405.  Back to cited text no. 3
Tripathy D, Rao A, Banerjee A, Padhy D. Aqueous misdirection in thyroid eye disease. BMJ Case Rep 2014;2014:bcr2014205824.  Back to cited text no. 4
Kurtz S, Moisseiev J, Gutman I, Blumenthal M. Orbital pseudotumor presenting as acute glaucoma with choroidal and retinal detachment. Ger J Ophthalmol 1993;2:61-2.  Back to cited text no. 5
Bernardino CR, Davidson RS, Maus M, Spaeth GL. Angle-closure glaucoma in association with orbital pseudotumor. Ophthalmology 2001;108:1603-6.  Back to cited text no. 6
Nassr MA, Morris CL, Netland PA, Karcioglu ZA. Intraocular pressure change in orbital disease. Surv Ophthalmol 2009;54:519-44.  Back to cited text no. 7


  [Figure 1], [Figure 2]

  [Table 1]


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