ABSTRACT
Graves’ orbitopathy features variable expansion of the soft tissue contents within the fixed bony orbital volume. During the acute phase of the disease, the extraocular muscles, lacrimal gland, and orbital fat become infiltrated with lymphocytes and are subject to volumetric expansion due to fibroblast deposition of glycosaminoglycans, fibrous tissue, and as yet unexplained expansion of the orbital fat compartment (1-3). The persistent increase in soft tissue volume results in the constellation of signs and symptoms associated with the chronic phase of Graves’ orbitopathy. Axial proptosis is often the most obvious feature to the patient. It can be the cause of significant cosmetic disfigurement and in turn give rise to lid position abnormalities and corneal exposure. It has also been postulated that ventral displacement of the globe places the recti muscles in a state of permanent tension, significantly contributing to reduced ocular motility (4). Compression of the orbital contents can produce a sensation of deep orbital pain and, in the extreme, cause optic neuropathy (5). The goal of decompressive surgery is to alleviate this set of signs and symptoms.
