Treatment and prognosis

TAO is self limiting disease that on average lasts 1 year in nonsmokers and between 2 and 3 years in
smokers, who are also up to 7 times more likely to develop the orbital maniestations of grave
disease. After the active disease plateaus, a quiescent burnt-out phase ensues. Reactivation of
inflammation occurs in approximately 5% - 10% of patients over their lifetime. Most patients with
TAO require only supportive care, including use of topical ocular surface irritation. Eating a reduced-
salt diet limits water retention and orbital edema. Sleeping with the head of bed elevated specifically
reduces fluid retention within the orbit. Wearing wraparound sunglasses relieves symptoms of dry
eye and photopobia. For those with diplopia, use of temporary prims lenses helps maintain binocular
fusion during the active phase of the disease.

If orbital inflammation is severe, intervention may be necessary to prevent or ameliorate corneal

exposure, globe subluxation, or optic neuropathy. Therapy usually is directed toward either
decreasing orbital congestion and inflammation or expanding the orbital bony volume.

Acute phase orbitopathy featuring compressive optic neuropathy is typically treated with oral
corticosteroids. The usual starting is 1 mg/kg of prednisone. This dose is maintained for 2 to 4 weeks
until a clinical response is appreciated. The dose is then reduced as rapidly as can be tolerated by the
patient, based on the clinical response of optic nerve function. Though effective ar reversing optic
nerve compression, prednisone at these levels is poorly tolerated. There is extensive list of potential
systemic adverse effects, and these side effects limit the long-term use of prednisone. The
mechanism for radiotherapy’s effects on the orbit is not well understood, but beyond temporary
lymphocyte sterilization, there is evidence that this dose induces terminal differentiation of
fibroblasts and kills tissue-bound monocytes, which play and important role in antigen presentasion.

Orbital decompression, though historically indicated to treat optic neuropathy, severe orbital
congestion, and advanced proptosis, has been used increasingly in recent years as an elective
prosedure to restore normal globe position in patients without sight-threatening ophtalmopathy.
 Sebagian besar pasien dengan TAO hanya memerlukan perawatan suportif,
termasuk penggunaan iritasi permukaan okular. Makan diet garam rendah membatasi
retensi air dan edema orbital. Tidur dengan kepala tempat tidur ditinggikan secara
khusus mengurangi retensi cairan di dalam orbit. Mengenakan kacamata hitam sampul
mengurangi gejala mata kering dan photopobia. Bagi mereka yang memiliki diplopia,
penggunaan lensa prima biasa membantu mempertahankan fusi binokuler selama fase
aktif penyakit ini.
Jika peradangan orbital parah, intervensi mungkin diperlukan untuk mencegah
atau memperbaiki paparan kornea, subluksasi globe, atau neuropati optik. Terapi
biasanya diarahkan untuk mengurangi kemacetan orbital dan pembengkakan orbital atau
memperluas volume tulang orbital.
Fase akut biasanya diobati dengan kortikosteroid oral yakni prednison 1 mg/kg
sebagai dosis inisial. Dosis ini dipertahankan selama 2 sampai 4 minggu sampai respon
klinis membaik. Dosis ini kemudian di tappering of, berdasarkan respon klinis fungsi
saraf optik. Meskipun efektif mengubah kompresi saraf optik, prednison pada tingkat ini
tidak dapat ditolerir dengan baik. Ada daftar ekstensif efek samping sistemik yang
potensial, dan efek samping ini membatasi penggunaan prednison jangka panjang.
Dekompresi orbital, walaupun secara historis diindikasikan untuk mengobati
neuropati optik, kongesti orbital yang parah, dan proptosis lanjut, telah digunakan
semakin dalam beberapa tahun terakhir sebagai proforma pilihan untuk mengembalikan
posisi bola normal pada pasien tanpa orbitopati yang mengancam mata