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| CLINICAL IMAGES |
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| Year : 2008 | Volume
: 1
| Issue : 1 | Page : 32-33 |
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Isolated, unilateral inferior rectus involvement in euthyroid orbitopathy
Abdullah Al-Mujaini, Anuradha Ganesh, Pascale Cooymans
Department of Ophthalmology, Sultan Qaboos University Hospital, Muscat, Oman
Correspondence Address:
Abdullah Al-Mujaini
Department of Ophthalmology, Sultan Qaboos University Hospital, 123 Al Khod / Muscat
Oman
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0974-620X.43319
How to cite this article:
Al-Mujaini A, Ganesh A, Cooymans P. Isolated, unilateral inferior rectus involvement in euthyroid orbitopathy. Oman J Ophthalmol 2008;1:32-3 |
How to cite this URL:
Al-Mujaini A, Ganesh A, Cooymans P. Isolated, unilateral inferior rectus involvement in euthyroid orbitopathy. Oman J Ophthalmol [serial online] 2008 [cited 2021 Jun 14];1:32-3. Available from: https://www.ojoonline.org/text.asp?2008/1/1/32/43319 |
A 37-year-old male presented with binocular vertical diplopia of six months duration.
The diplopia was gradual in onset, slowly progressive, and was greatest in upgaze. The patient had a history of hyperthyroidism which was diagnosed three years ago, and had been managed medically. He was pronounced clinically euthyroid in his last examination six months ago. At the time of presentation, he was not on any medications and was systemically asymptomatic. There was no history of orbital trauma or surgery.
Examination revealed a well-appearing male patient in no acute distress. Visual acuity was normal at 20/20 bilaterally. A right hypotropia and mild proptosis was observed in primary position [Figure 1]. Hertel's exophthalmometry showed a bar reading of 100 mm and values of 20 mm right eye (OD ) and 19 mm left eye (OS ). Findings on orthoptic examination are shown in [Table 1] and [Figure 2]. The patient's symptoms and motility examination were consistent with right inferior rectus restriction. Anterior segment and fundus examination, pupils and intraocular pressure were normal. In particular, no anterior inflammatory signs such as conjunctival injection and chemosis were observed. Computed tomography (CT) scan of the orbits showed fusiform enlargement of the right inferior rectus muscle [Figure 3A, B].
A diagnosis of thyroid related orbitopathy (TRO) was made based on history, clinical examination, forced duction testing, and radiographic findings. A variety of orbital disorders, including infectious, inflammatory, and neoplastic, may present with findings suggestive of TRO; these entities should be considered when evaluating patients with presumed TRO. In our patient, a diagnosis of orbital pseudotumor was considered, especially due to the unilateral nature of the findings and the fact that the patient was euthyroid at the time of presentation. This was ruled out due to absence of orbital pain and lack of compressive effect on orbital structures especially at level of the optic nerve. Acquired Brown syndrome also may result in hypotropia with restricted elevation, but the restriction in elevation in Brown syndrome is limited to adduction, and does not affect elevation in primary position and abduction. Our patient had severe limitation of elevation in all positions of gaze. Further, proptosis is not a feature of Brown syndrome.
TRO, the most common cause of proptosis and diplopia in adults, varies widely in its pattern of clinical presentation. During the course of the disease, fibrosis can develop around the extraocular muscles, and excess extracellular matrix (glycosaminogycan) and fat accumulate in the periorbital space. [1] This dramatic remodeling results in protrusion of the eye, also known as exophthalmos and restrictive motility. The active phase of the disease typically lasts one year, following which most cases improve. Residual stigmata of the disease persist in most, but only few patients require surgical rehabilitation. Stabilization of the motility measurements in patients with TRO is extremely important before planning surgery for strabismus. It is advisable to wait 6 months or more after motility measurements stabilize before proceeding with strabismus surgery. Recession of the involved extraocular muscle, on adjustable sutures, is the surgical method of choice. [2],[3]
 References | |  |
| 1. | Lehmann GM, Feldon SE, Smith TJ, Phipps RP. Immune mechanisms in thyroid eye disease. Thyroid 2008;18:959-65.  [PUBMED] [FULLTEXT] |
| 2. | Metz HS. Strabismus related to Graves' Ophthalmopathy. In: Rosenbaum AL, Santiago AP, editors. Clinical Strabismus Management, Principles and Surgical Techniques. Philadelphia: W. B. Saunders; 1999. p. 285-95. |
| 3. | Schotthoefer EO, Wallace DK. Strabismus associated with thyroid eye disease. Curr Opin Ophthalmol 2007;18:361-5. [PUBMED] [FULLTEXT] |
[Figure 1], [Figure 2], [Figure 3A, B]
[Table 1]
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