The diagnosis of TAO was based on orbital computed tomography scan findings of EOM enlargement or muscle proliferation, in addition to serological results, a history of endocrine findings, and one or more clinical findings, including upper eyelid retraction, proptosis, and EOM restriction. This study was approved by the Chung-Ang University Hospital Institutional Review Board and adhered to the tenets of Declaration of Helsinki. We completed a retrospective chart review of patients undergoing orbital decompression for stable proptosis secondary to TAO from 7 October 2012 to 21 September 2014. In this study, we assessed the biometrics of the eyeball, including axial length (AL), anterior chamber depth (ACD), lens thickness (LT), refraction, keratometry, and aberration, before and after orbital decompression in order to estimate the correlation between proptosis progression and biometric changes.
Although there have been studies reporting the effect of orbital decompression on refraction, 8, 9, 10 whether or not refractive error is induced or not remains uncertain. For patients undergoing successful decompression, we can estimate ophthalmic status prior to the start of proptosis. Orbital decompression is a useful procedure to alleviate proptosis in TAO patients. However, in TAO patients, the correlations between proptosis progression, biometric changes, and refractive error have not yet been investigated. This mechanism may induce changes in ocular biometrics and alter the refractive error. Therefore, the direction of the final vector on the eyeball results in a compressive force parallel to the visual axis, increasing the amplitude of the vector. 6, 7 Proliferative retrobulbar tissue pushes the eyeball forward and elongates the four rectus muscles, causing them to pull the eyeball more strongly posterior. The contractile force of the extraocular muscles (EOMs) is positively correlated to the EOM length. Complications due to eyeball compression, such as increased intraocular pressure, primary open angle glaucoma, 3, 4 and optic neuropathy, 5 are clinically significant problems.Īs proptosis progresses, the four rectus muscles, the medial, superior, inferior, and lateral rectus muscles, elongate. 2 Proliferated fatty tissue and engorged muscles occupy the retrobulbar space and push the eyeball forward, often resulting in proptosis. Longstanding inflammation induces adipogenesis, hyaluronic acid deposition, secondary hydration, and finally, ocular muscle thickening and proliferation of fatty tissue.
Pathological changes in TAO are related to T and B lymphocytes, along with various cytokines and chemokines. The prevalence of thyroid-associated ophthalmopathy (TAO) is >30% in Asian and Caucasian patients with Graves' disease, 1 and TAO is one of the most common cause of orbital inflammatory disorders in adults.
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