内分泌性恶性突眼症一般认为与甲状腺垂体轴的功能失调有关。所有病例都有甲亢病史,眼部表现常在诊断甲亢后几周～35年发生。毒性甲状腺肿患者约有1～2%可发展为恶性突眼症,表现为严重角膜炎、复视、眼球固定和视力减退。其发病机理认为是眶后脂肪中粘多糖量明显增加,由于粘多糖的亲水性和眶内缺乏淋巴引流致脂肪组织张力增加,外眼肌氧气供应减少,可使肌反应性肥大达正常的12倍。眶内压持续增加造成突眼和结膜水肿,当眼睑不能闭合时即成暴露性角膜炎,眼球活动受限亦将随疾病的发展而出现。作者指出,凡恶性突眼经适当内科治疗而视力仍进行性下降和面容畸形者均为手术——眼眶减压术治疗的适应症。Kronlein(1888)用切除眶外侧壁后使眶内脂肪疝入颞窝的方法,但此仅能提供一小的间隙减压。N affziger(1932)采 Endocrine malignant exophthalmos is generally considered to be related to dysfunction of the thyroid pituitary axis. All cases have a history of hyperthyroidism, eye performance often in the diagnosis of hyperthyroidism after a few weeks to 35 years. About 1 ~ 2% of patients with toxic goiter can develop malignant exophthalmos, manifested as severe keratitis, diplopia, fixation of the eye and vision loss. Its pathogenesis is that the amount of mucopolysaccharide in orbital fat increased significantly. Due to the hydrophilicity of mucopolysaccharide and the lack of lymphatic drainage in the orbit, the tension of adipose tissue increased, and the supply of oxygen to the external ophthalmus decreased, which made the reactivity of hypertrophic muscle up to normal 12 times. Orbital pressure continued to increase cause exophthalmos and conjunctival edema, when the eyelids can not be closed when the exposure of keratitis, eye movement will also be limited with the development of the disease. The authors point out that any malignant exophthalmos with proper medical treatment and progressive visual decline and facial deformity are surgical - orbital decompression surgery indications. Kronlein (1888) had herniated orbital fat herniated into the temporal fossa with resection of the orbital wall, but this provided only a small reduction in space. N affziger (1932) mining