Abstract
We evaluate the surgical outcomes and surgical responses of medial rectus muscle (MR) recession patients with thyroid eye disease (TED)-related esotropia (ET). The surgical dose-response curves 1 week postoperatively and at the final visit were analyzed. Univariable and multivariable linear regression analyses were applied to investigate factors influencing surgical dose-response. A total of 43 patients with TED-related ET that underwent MR recession were included. The final success rate was 86.0% and the rate of undercorrection was 14.0%. The surgical dose-response curves of TED-related ET showed a gentle slope compared with those of standard surgical tables. In the univariable model, simultaneous vertical rectus muscle recession was the only significant factor influencing surgical dose-response of MR recession in TED-related ET (β = -0.397, P = 0.044). In a model adjusted for age, sex, type of surgery, and preoperative horizontal angle of deviation, simultaneous vertical rectus muscle recession showed marginal significance (β = -0.389, P = 0.064). The surgical dose-response curve of TED-related ET was unique. Simultaneous vertical rectus muscle recession was associated with increased surgical dose-response in TED-related ET.
Highlights
Thyroid eye disease (TED) is an autoimmune disorder characterized by inflammation and expansion of orbital fat and extraocular muscles (EOMs) [1]
One previous study reported that there was lesser surgical response compared to the expected surgical response based on a standard surgical table in patients with TED-related esotropia [16]
Orbital decompression can alter the orbital structure and may influence developing strabismus, and surgical response. Another possible explanation is that pathologic changes in vertical rectus muscles in TED could play a role in the reduced response to MR recession, since adduction is the secondary action of the vertical rectus muscles [33, 34]
Summary
Thyroid eye disease (TED) is an autoimmune disorder characterized by inflammation and expansion of orbital fat and extraocular muscles (EOMs) [1]. Type I disease is predominantly caused by orbital fat enlargement and accumulation of glycosaminoglycan and hyaluronic acid, which are produced by orbital fibroblasts. These patients show noninflammatory enlargement of retrobulbar fat with normal extraocular motility. Type II TED is associated with muscle enlargement and orbital inflammation, which result in limitation of extraocular motility and diplopia [2,3,4,5].
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