Marmor M F
Stanford University, Calif., USA.
Doc Ophthalmol. 1999;97(3-4):239-49. doi: 10.1023/a:1002192829817.
This paper reviews the anatomic and physiologic conditions which predispose to fluid accumulation within the retina. Retinal edema has its inception in disease that causes a breakdown of the blood-retinal barrier in retinal capillaries and/or the retinal pigment epithelium (RPE). Edema develops not only because protein and fluid enter the extracellular space, but because the external limiting membrane and the convoluted extracellular pathway within the retina limit the clearance of albumin and other large osmotically-active molecules. These molecules bind water to cause edema. Recognition of edema clinically is complicated by the facts that angiographic markers (fluorescein and ICG) do not match albumin in size, and that clinical leakage does not always correlate closely with tissue swelling or functional loss. Active water transport across the RPE is efficient at removing subretinal water, but the flow resistance of the retina limits RPE access to the water of retinal edema. Consideration of the pathophysiology of retinal edema may aid in the development of better strategies for managing retinal edema.
本文综述了易导致视网膜内液体蓄积的解剖学和生理学状况。视网膜水肿始于导致视网膜毛细血管和/或视网膜色素上皮（RPE）血视网膜屏障破坏的疾病。水肿的发生不仅是因为蛋白质和液体进入细胞外间隙，还因为视网膜内的外界膜和盘曲的细胞外通道限制了白蛋白和其他具有较大渗透活性分子的清除。这些分子结合水分从而导致水肿。临床上对水肿的识别较为复杂，原因在于血管造影标记物（荧光素和吲哚菁绿）在大小上与白蛋白不匹配，且临床渗漏并不总是与组织肿胀或功能丧失密切相关。RPE上的主动水转运在清除视网膜下水分方面效率很高，但视网膜的流动阻力限制了RPE对视网膜水肿水分的接触。对视网膜水肿病理生理学的思考可能有助于制定更好的视网膜水肿管理策略。
