Treatment of Graves' Orbitopathy in 1990.

Abstract

In a mechanical sense, we understand how the orbital changes and the symptoms of endocrine ophthalmopathy develop. Expansion of the retrobulbar tissues results in forward displacement of the globe beyond the protective cover of the eyelids. Lymphocytic infiltration, followed by fibrosis of the extraocular muscles and the eyelid retractors, leads to diplopia and corneal exposure. Glycosaminoglycans, which are water binding molecules, accumulate in the retrobulbar tissues of patients with orbitopathy and add to the bulk to the retrobulbar tissues. Proptosis at first serves to relieve retrobulbar pressure but eventually the restrictive action of the extraocular muscles and the orbital septum limits protrusion of the globe. As forward motion is restricted, pressure from the expanded tissues rises in the confined retrobulbar space, and the optic nerve may be compressed and functionally impaired. If one thinks of the central problem in orbitopathy as being a discrepancy between the volume of the bony orbit and the bulk of the tissues it is supposed to contain, then it follows that effective treatment must either shrink the swollen tissues or make more space available for them. Medical therapy attempts to shrink the swollen tissues by steroids, radiotherapy or cyclosporin. Surgery relies on making more space available for the swollen tissues and can be modified for each patient. Further rehabilitation for diplopia can be managed with prisms or extraocular muscle surgery. Non-urgent eyelid surgery follows completion of extraocular muscle surgery. Close collaboration with an interested endocrinologist is essential.