Thyroid-associated orbitopathy: a clinicopathologic and therapeutic review.

PURPOSE OF REVIEW

To review the literature related to thyroid-associated orbitopathy and to emphasize recent developments in its pathophysiology, diagnosis, and therapy. Current therapeutic trends and controversies are discussed.

RECENT FINDINGS

Expression of thyroid stimulating hormone receptor is highest in the fat and connective tissue of patients with thyroid-associated orbitopathy, where fibroblasts have the potential for adipogenesis. Electrophysiology can now detect subclinical optic neuropathy, and somatostatin-receptor scintigraphy can help justify immunomodulation. Other than steroids, radiotherapy can control inflammation, but its use is controversial. Current trends in orbital decompression are to camouflage incisions and to limit strabismus with balanced decompression, deep lateral wall techniques, fat removal, and onlay implants. Proptosis reductions of 0.9 to 12.5mm are possible by the use of various algorithms. Before or after decompression, botulinum toxin can correct strabismus, intraocular pressure elevation, and retraction. The latter is now also treated with full-thickness blepharotomy.

SUMMARY

As knowledge of the pathophysiology of thyroid-associated orbitopathy grows, there is a slow movement from nonspecific and invasive measures to more directed treatments causing less morbidity.