<![CDATA[Background: Thyroid Eye Disease (TED) is an autoimmune inflammatory disorder affecting the orbital tissues and may cause increased intraocular pressure (IOP) through structural, inflammatory, and hemodynamic changes. Persistent IOP elevation may increase the risk of optic nerve damage and glaucoma. Objective: This literature review aims to examine the pathophysiological mechanisms underlying increased IOP in patients with TED and evaluate current management approaches. Methods: A literature review was conducted by identifying and analyzing scientific publications addressing the mechanisms, contributing factors, clinical evaluation, and management of IOP elevation in TED. The reviewed literature included studies investigating orbital tissue expansion, extraocular muscle enlargement, episcleral venous pressure, aqueous humor outflow abnormalities, and therapeutic interventions. Results: Increased IOP in TED is multifactorial. Orbital inflammation, glycosaminoglycan accumulation, adipose tissue expansion, and extraocular muscle enlargement may increase intraorbital pressure and impair orbital venous drainage, consequently elevating episcleral venous pressure and reducing aqueous humor outflow. Structural alterations in the trabecular meshwork and Schlemm’s canal may also contribute. IOP measurements may vary with gaze direction, particularly in patients with extraocular muscle restriction. Management includes regular IOP monitoring, control of thyroid dysfunction and orbital inflammation, appropriate IOP-lowering medication, selected targeted therapies, and orbital decompression when clinically indicated. Conclusion: Understanding the mechanisms underlying IOP elevation in TED is essential for individualized management and early detection of ocular complications. Comprehensive evaluation of IOP, optic nerve structure, visual function, and orbital involvement may help reduce the risk of glaucoma and vision loss.]]>
