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


In 1840, Basedow first described the association of pretibial myxedema with orbital abnormalities and features of hyperthyroidism.[4] The term Graves' disease triad is currently used to describe this constellation of features although the original Merseburg triad in fact referred to exophthalmos, goiter, and palpitations.[4] The distinct anatomic distribution of the extrathyroidal manifestations remains unexplained. It has long been assumed that a common autoantigen must be present, and presumably restricted, to the three sites.[5] Indeed, the TSH-R, the putative autoantigen, has been demonstrated in orbital[3,6,7] and pretibial[8,9,10,11] tissues. However, TSH-R have been detected in normal skin,[9] adrenal,[12] kidney,[12] thymus,[12] cardiac,[13] and adipose tissue[14] as well as the pituitary gland[15] without evidence that these sites are targeted in Graves' disease. An alternative explanation proposed has been that fibroblast heterogeneity may explain the distribution of extrathyroidal manifestations.[16,17] Trauma and pressure may, at least in part, explain the Graves' triad with an interesting description by Rapoport et al.[9] of a case where these factors clearly were associated with the development of pretibial myxedema. While it has been proposed that a similar mechanism may explain GO, there have been, to our knowledge, no reports in the thyroid literature to support this.

Strabismus after cataract surgery is an infrequent but well-documented event. It develops in 0.23%-1% of cases given retrobulbar[18] or peribulbar[19] anesthesia but rarely, if ever, in cases in whom general or topical anesthesia[18] were administered. These findings reinforce the theory that direct injection of orbital tissue is likely to be the causative factor. The left eye is more frequently involved as in our case, and this is thought to be related to the technique used by righthanded individuals addressing the left eye.[18] In a series of 58 patients developing strabismus after cataract surgery, Hamed and Lingua[20] reported 8 cases of thyroid eye disease. In 7 of these cases local retrobulbar blocks had been given as in our patient. In at least some cases, it appears that the diplopia may have been masked preoperatively by the impaired vision. In other cases, however, there was clear progression of thyroid eye disease in the following months suggesting that the procedure may have, in some way, aggravated the disease.

It has been hypothesized that strabismus in such cases may result from surgical trauma or anesthetic myotoxicity.[21] The most commonly affected muscle is in the inferior rectus presumably because of its proximity to the area of needle entry, although the superior rectus is also at risk because of traction in extracapsular cataract extraction. Myotoxicity of local anesthetics may also play a role, with evidence at least in rat models, that these agents can cause massive necrosis of extraocular muscles.[21,22] It would be attractive to hypothesize that the initiating event then led to inflammatory responses and ultimately, the features of severe ophthalmopathy. Interestingly, in contrast to Rapoport's pretibial myxedema case,[9] in which the response appeared to be limited to the traumatized area, our patient developed bilateral disease. The findings were similar in Hamed's study in which patients who developed thyroid eye disease after cataract surgery in one eye invariably had bilateral eye involvement.[20]

While progression of eye disease after 131I is a well described phenomenon,[23] the rapidity of the reaction is unusual, with only one previous reported case occurring within a week.[24] The acuteness of the reaction could possibly be the result of intense response against an increase in release of shared thyroidal/orbital antigens from the inflamed thyroid gland caused by an immune system already primed against orbital antigens by the previous two surgeries. The possibility that the deterioration of the eye disease and radioiodine were unrelated events cannot be definitively excluded. Finally, this patient illustrates the effectiveness of orbital irradiation under certain circumstances. Our patient had almost complete ophthalmoplegia for 3 months prior to decompression, which had worsened after surgery and did not respond to oral steroids, even at doses of 120 mg. In all, there was complete or near-complete ophthalmoplegia for 9 months. Yet improvements in motility were clear 3 weeks after initiation of irradiation. The exact modulatory effects of radiation on GO pathophysiology are not known but are thought to act either by suppressing orbital lymphocytes or to reduce GAG production by orbital fibroblasts.[27] Radiotherapy has been shown to induce interleukin1 receptor antagonist (IL-1RA), an inhibitor of the proinflammatory activities of interleukin1.[28] We[29,30] and others,[31,32] have shown associations between TSI and GO suggesting that these antibodies may play a role in disease pathogenesis. In this patient, improvements were seen despite TSI values remaining markedly elevated. This does not exclude a role for TSI in disease pathogenesis but suggests that orbital irradiation does not appear to significantly affect TSI production despite the putative effects of radiotherapy on suppressing lymphocyte activity.


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