Severe Graves' Ophthalmopathy After Retrobulbar Anesthesia for Cataract Extraction in a Patient With Mild Stable Thyroid Eye Disease

Daniel Chun-Hang Wai, Su-Chin Ho, Lay-Leng Seah, Kee-Siew Fong, Daphne Hsu-Chin Khoo


Thyroid. 2003;13(8) 

In This Article

Abstract and Introduction

It has been hypothesized that the distinct anatomic localization of the Graves' triad may be partially explained by pressure and trauma. While there are reports of local trauma clearly contributing to the pathogenesis of pretibial myxedema, direct evidence for a similar mechanism in Graves' ophthalmopathy (GO) has been lacking. We describe a 65-year-old male patient with stable mild Graves' ophthalmopathy of 24 years' duration in whom a retrobulbar block was administered prior to cataract removal. Three weeks after the procedure, he complained of rapidly progressive bilateral diplopia. In 6 months, there was moderate exophthalmos, exposure keratitis, almost complete ophthalmoplegia, and decreasing visual acuity requiring surgical decompression. Postdecompression, inflammatory signs and vision improved but there was complete ophthalmoplegia. The eye signs remained unchanged for the next 4 months but there was exacerbation of the disease within a week of receiving radioiodine despite concomitant steroid administration. Orbital irradiation was finally administered with rapid improvement in extraocular eye muscle function. We hypothesize that local inflammatory and immune responses stimulated by trauma and/or pressure in the retrobulbar compartment, triggered the development of severe ophthalmopathy in this patient. Thyroid-stimulating immunoglobulin (TSI) levels remained markedly elevated despite the clinical improvement suggesting that the beneficial effects of radiotherapy in this case were not mediated by suppressing TSI production.

The pathogenesis of Graves' ophthalmopathy (GO) remains an area of controversy. Autoimmune reactions directed against one or more shared antigens located in the thyroid and orbit are hypothesized to be the cause. While thyroglobulin[1] has recently been detected in the eye, current evidence favors the thyrotropin receptor (TSH-R) as the autoantigen.[2,3] Although it appears that environmental factors as well as systemic immune responses may contribute to GO, the fact that the disease is not infrequently unilateral suggests that local factors are also likely to play a role. We report a patient with mild thyroid eye disease who developed a severe, atypical form of GO after retrobulbar anesthesia for cataract surgery.


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as: