Orbit, 2015; 34(1): 6–9 ! Informa Healthcare USA, Inc. ISSN: 0167-6830 print / 1744-5108 online DOI: 10.3109/01676830.2014.950301

ORIGINAL ARTICLE

Reactivation of Thyroid Associated Orbitopathy Following Trauma with Intraorbital Foreign Body Thanos D. Papakostas, Nahyoung Grace Lee, Alison B. Callahan, and Suzanne K. Freitag

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Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts

ABSTRACT A 63-year-old female with mild, bilateral, stable thyroid-associated orbitopathy sustained trauma resulting in glass foreign bodies embedded on the left ocular surface and left lateral orbital extraconal and intraconal space. After 2 orbitotomies including a failed attempt to remove the intraconal foreign body and poor response to oral steroids, she developed severe, progressive left periorbital edema and 9 mm of relative proptosis. Serial, postoperative imaging demonstrated worsening inflammatory changes along the surgical tract, which slowly improved over several months, with simultaneously worsening proptosis and enlargement of the left inferior and medial rectus muscles consistent with worsening thyroid orbitopathy. She subsequently underwent unilateral 3-wall orbital decompression with improvement in her symptoms. Periorbital trauma with orbital foreign bodies and related surgical trauma may result in reactivation of thyroid-associated orbitopathy. Keywords: Reactivation, thyroid-associated orbitopathy, traum

INTRODUCTION

left-sided proptosis. Four years prior to presentation, she was documented to have 3 mm of relative proptosis OS and bilateral eyelid retraction. Neuroimaging at that time showed mild asymmetric extraocular muscle enlargement (Figure 1). She was 19 years status post-radioactive iodine treatment and was currently taking levothyroxine. She was a nonsmoker. She had fallen onto a wine glass 5 months prior to presentation resulting in glass fragments embedded in her left conjunctiva and orbit. Upon surgical exploration at an outside facility, the globe was found to be intact and multiple small fragments of glass were removed from the ocular surface and the anterior lateral orbit. A 6-mm fragment of glass located intraconally between the optic nerve and lateral rectus muscle was not found at the initial surgery (Figure 2). Two days later, a second surgical attempt to remove the glass fragment at the same outside facility was also unsuccessful. Post-operatively she had significant left periorbital edema and increasing proptosis, which was felt to be out of proportion to the surgical trauma.

Thyroid-associated orbitopathy (TAO) was described by Graves in 18351 and by Von Basedow in 1840.2 TAO is associated with hyperthyroidism in 85% of cases3 but may be associated less often with hypothyroidism (5%) or even a euthyroid state (10%).3–7 Genetic predisposition, infection with viruses or Yersinia, stress, smoking, and autoimmune factors have been implicated in the etiology of TAO4. There have been a few case reports in the literature implicating surgical trauma as a causative factor for worsening or reactivation of TAO.8–14 We present herein, a case of TAO reactivation after trauma and surgery to the orbit with intraorbital foreign bodies.

CASE REPORT A 63-year-old Caucasian female with a history of mild, stable, bilateral TAO was referred to the ophthalmic plastic surgery service with worsening

Received 5 April 2014; Revised 4 June 2014; Accepted 28 July 2014; Published online 10 September 2014 Correspondence: Dr. Suzanne K. Freitag, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, MA 02114, USA. Tel: 617-573-5550. Fax: 617-573-5525. E-mail: [email protected]

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FIGURE 1. (A) External photograph 4 years prior to trauma showing baseline TAO with 3 mm proptosis OS and left eyelid retraction. (B) Coronal CT reveals mild enlargement of left inferior and medial rectus muscles.

FIGURE 2. (A) Axial CT immediately after first surgery shows 6 mm intraconal radioopaque foreign body between the optic nerve and lateral rectus muscle. There is soft tissue edema in the lateral canthal area. (B) Coronal CT through the mid-orbit shows minimal enlargement of the left inferior and medial rectus muscles.

FIGURE 3. (A) Magnetic resonance imaging (MRI) axial T1 with contrast and fat saturation performed 1 month after surgery reveals an interval increase in left lateral canthal edema which now extends into the orbit along the surgical tract and spills over into the temporalis fossa. (B) MRI coronal T1 with contrast and fat saturation through the mid-orbit shows significant intraconal enhancement surrounding the foreign body and surgical tract. The left inferior and medial rectus muscles remain minimally enlarged.

Hertel exophthalmometry measured 5 mm of relative left proptosis. Repeat imaging 1 month later showed progression of inflammatory changes along the surgical tract and around the persistent intraconal foreign body (Figure 3). She was treated with an oral steroid !

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taper over several weeks and referred for a second opinion. On examination, her visual acuity was 20/20 OD and 20/25 OS. Pupils were equal and reactive to light with a trace left afferent pupillary defect.

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T. D. Papakostas et al.

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FIGURE 4. (A) and (B) External photographs showing increased proptosis and lid retraction OS 5 months after trauma and surgery.

FIGURE 5. (A) Axial CT at time of presentation 5 months after trauma and surgery showing stable intraconal foreign body, nearly resolved intraconal inflammation and improved lateral canthal edema. (B) Coronal CT at the same time demonstrates significant enlargement of left inferior and medial rectus muscles.

She correctly identified 8 of 8 Ishihara color plates OU. Extraocular motility showed slight horizontal restriction OD and severe restriction in all directions OS. There was moderate resistance to retropulsion of her right orbit and severe resistance to retropulsion of the left orbit, with 9 mm of relative proptosis OS. There was upper and lower eyelid retraction bilaterally, significantly worse on the left than the right (Figure 4). Slit-lamp biomicroscopy revealed conjunctival injection along the horizontal rectus muscle insertions and superficial punctate keratitis OS. Dilated funduscopic examination was normal with no optic nerve pallor or edema. Her thyroid function tests and Humphrey automated perimetry remained normal throughout the course of events. Serial computed tomography (CT) showed interval improvement in the orbital changes along the surgical pathway from the lateral orbit toward the intraconal foreign body. However, there was significant progression of TAO of the left orbit with worsening left proptosis and significant enlargement of the left inferior and medial rectus muscles when compared

to scans obtained immediately following the trauma as well as 5 years earlier. The glass fragment position remained unchanged (Figure 5). The patient’s diagnosis was felt to be reactivation of previously stable TAO attributed to orbital trauma with a retained intraconal foreign body and subsequent surgery. Because of severe proptosis with a trace afferent papillary defect and exposure keratopathy, she was started on a slow taper of oral prednisone and underwent a 3-wall left orbital decompression resulting in a 7-mm improvement in proptosis and resolution of the corneal exposure and afferent pupillary defect.

DISCUSSION There are a few reports in the literature associating surgical trauma with reactivation of TAO. Baldeschi et al.8 reported reactivation of TAO after orbital decompression surgery. Kim et al.9 described a series of 9 patients in which TAO occurred after periocular Orbit

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Thyroid Orbitopathy Reactivated after Trauma and ocular surgery. The procedures included botulinum toxin injection, cataract surgery, LASIK, and injectable fillers as well as facelift, blepharoplasty and laser resurfacing. Yi et al.11 reported a series of 5 patients who had initial presentation or exacerbation of TAO following cataract surgery in an Asian eye center. Hamed and Lingua10 reported their findings in a series of 58 patients with strabismus presenting after cataract surgery. Eight patients (14%) were found to have previously unsuspected thyroid eye disease. Three of the eight patients had past histories of systemic dysthyroidism, but none reported diplopia prior to cataract extraction. Wai et al.14 reported a 65-year-old male with stable mild Graves’ ophthalmopathy of 24 years’ duration in whom a retrobulbar block was thought to reactivate the disease. Most recently, Xu, Glass, and Kazim15 reported a 60-yearold man with stable thyroid eye disease who developed reactivation 1 month following contralateral strabismus surgery and then again after 6 months of inactivity when re-challenged with bilateral strabismus surgery. To our knowledge, this is the first reported case of TAO reactivation after trauma to the orbit with intraorbital foreign bodies and subsequent orbital surgery. It had not been clear to her treating physicians in the immediate post-operative period that TAO was the reason for her persistent, massive periorbital edema. The etiology eventually became obvious radiographically as the surgical tract inflammatory changes improved and the extraocular muscles became significantly enlarged. In this case, trauma with intraorbital foreign bodies in addition to surgical trauma likely perpetuated the previously stable orbit to undergo a dramatic, unilateral inflammatory response.

ACKNOWLEDGMENTS Dr. N. Grace Lee is a recipient of the Heed Ophthalmic Foundation Fellowship.

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DECLARATION OF INTEREST The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

REFERENCES 1. Graves RJ. Graves disease. Lond Med Surg J 1835;7:516. 2. Von Basedow C. Exophthalmos durch hyperetrophie des Zellgewebes in der augenhohle. Wehnscher ges Heilk 1840;6: 197–204, 220–228. 3. Rootman J. Diseases of the Orbit; A multidisciplinary Approach, vol. 1, 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2003. chap. 8. 4. Sergott RC, Glaser JS. Graves ophthalmopathy. A clinical and immunologic review. Surv Ophthalmol 1981;26:1–21. 5. Glaser JS. Graves’ ophthalmopathy. Arch Ophthalmol 1984; 102:1448–1449. 6. Felberg NT, Sergott RC, Savino PJ, et al. Lymphocyte subpopulations in Graves Ophthalmopathy. Arch Ophthalmol 1985;103:656–659. 7. Solomon DH, Green DE, Snuder NJ, et al. Clinical significance of the long acting thyroid stimulator of Graves disease. Clin Res 1964;12:119. 8. Baldeschi L, Lupetti A, Vu P, et al. Reactivation of Graves’ orbitopathy after rehabilitative orbital decompression. Ophthalmology 2007;114:1395–1402. 9. Kim SJ, Kim BJ, Lee HB, et al. Thyroid associated orbitopathy following periocular surgery. Kor J Ophthalmol 2006; 20:82–86. 10. Hamed LM, Lingua RW. Thyroid eye disease presenting after cataract surgery. J Pediatr Ophthalmol Strabis 1990;27: 10–15. 11. Yi BP, Leng SL, Kwang LB, Rootman J. Development of thyroid-related orbitopathy following cataract surgery. Orbit 2009;28:383–387. 12. Gupta OP, Boynton JR, Sabini P, et al. Proptosis after retrobulbar corticosteroids injections. Ophthalmology 2003; 110:443–447. 13. Korn BS, Seo SW, Levi L, et al. Optic neuropathy associated with botulinum A toxin in thyroid related orbitopathy. Ophthal Plast Reconstr Surg 2007;23:109–114. 14. Wai DC, Ho SC, Seah LL, et al. Severe Graves’ ophthalmopathy after retrobulbar anesthesia for cataract extraction in a patient with mild stable thyroid eye disease. Thyroid 2003;13:823–826. 15. Xu L, Glass LR, Kazim M. Reactivation of thyroid eye disease following extraocular muscle surgery. Ophthal Plast Reconstr Surg 2014;30(1):e5–e6.

Reactivation of thyroid associated orbitopathy following trauma with intraorbital foreign body.

A 63-year-old female with mild, bilateral, stable thyroid-associated orbitopathy sustained trauma resulting in glass foreign bodies embedded on the le...
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