Fuchs葡萄膜炎综合征是一种主要累及眼前节的慢性前葡萄膜炎。由于病因不明，诊断主要依赖于临床表现，因此眼部结构改变对该病的诊治极为关键。长期慢性炎症致使Fuchs葡萄膜炎综合征患眼从角膜、前房至视网膜及脉络膜，均存在或明显或隐匿的结构改变。本文综述了患眼眼前节的特征性改变：角膜存在特征性的角膜后沉着物以及内皮细胞密度降低、形态改变；前房出现闪辉和细胞，房水中可检测到炎症因子和病毒；虹膜可见特征性萎缩，表现为脱色素和自体荧光改变。三者的结构改变直接反应炎症状态，可为病因机制研究提供线索。白内障和飞蚊症作为常见并发症，与反复的炎症相关，亦伴随着晶状体和玻璃体的结构改变。晶状体-玻璃体界面结构的改变为理解并发症的进展机制与防治方案提供了新思路。Fuchs葡萄膜炎综合征的眼底结构改变隐匿。黄斑区视网膜厚度是否改变尚未定论，另有多项研究认为视网膜血流密度降低。视盘神经节细胞层厚度降低可能与并发性青光眼相关。脉络膜也存在血管层厚度和血流密度改变，也许是慢性炎症的表现。总而言之，关于Fuchs葡萄膜炎综合征的眼部结构改变，尚有诸多疑问有待深入探索。

Fuchs uveitis syndrome is a chronic anterior uveitis that predominantly impacts the anterior segment of the eye. Since its etiology remains unclear, diagnosis largely relies on clinical manifestations.  Consequently, alternations in ocular structure play a pivotal role in both the diagnosis and treatment of this disease. Due to the persistent nature of chronic inflammation, a range of structural changes occur, spanning from the cornea and anterior chamber to retina and choroid. This article provides a detailed account of the characteristic changes in the anterior segment. In the cornea, characteristic keratic precipitates are observable, accompanied by a reduction in endothelial cell density and morphological alterations. The anterior chamber exhibits aqueous flashes and cells, where inflammatory factors and viruses can be detected. Additionally, characteristic iris atrophy is visible, presenting  as depigmentation and altered autofluorescence. These three factors collectively reflect the inflammatory state and progress with the course, potentially offering insights into the etiological mechanism. Concurrent cataract and floates, which are common complications associated with recurrent inflammation, accompanied by structural changes in the lens and vitreous. Structural alterations at the vitreol enticular interface, located between the posterior lens capsule and anterior vitreous, provide valuable clues regarding the pathogenesis of complications and provide new perspectives for therapeutic strategies. The structural changes in the fundus of Fuchs syndrome are often insidious. While it remains undetermined whether the retinal thickness in the macular region undergoes changes, numerous studies suggest a decrease in retinal blood flow density. Thinning of the ganglion cell layer in the optic disc may be linked to concurrent glaucoma. The choroid also experiences changes in the thickness of vascular layer and blood flow density, which could be a manifestation of chronic inflammation. In conclusion, numerous questions regarding the ocular structural changes in Fuchs uveitis syndrome still await further exploration.