Graves' orbitopathy is part of an autoimmune systemic disease which compiles hyperthyroidism, orbitopathy, dermopathy and acropachy. Stimulating antibodies against the TSH receptor play the central pathogenetic role. Main symptoms of Graves' orbitopathy comprise soft tissue inflammation, proptosis impairment of ocular motility and lid retraction. Inflammatory reactions of orbital fibroblasts are responsible for the symptoms. To restrict damage anti-inflammatory therapy (mainly systemic steroids, orbital irradiation) is indicated in moderate to severe active disease stages, and surgical orbital decompression in sight threatening states. In mild cases expectant strategy and selenium administration is sufficient. In inactive disease stages surgery is performed to improve appearance and function. Restoring euthyroidism leads to improvement of Graves' orbitopathy in about 60% of the patients. Radioiodine therapy without glucocorticoids is associated with a small but significant risk (15%) of deterioration or relapse. Thyroidectomy is neutral in later stages but may improve Graves' orbitopathy in early active stages.