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Tangential vitreous traction: a possible mechanism of development of cystoid macular edema in retinitis pigmentosa

机译:玻璃体切向牵引:色素性视网膜炎囊状黄斑水肿发展的可能机制

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摘要

We report the possible mechanism of development of cystoid macular edema (CME) in retinitis pigmentosa (RP) in the case of a 68-year-old woman with RP and CME in the right eye and resolving CME in the left eye. Spectral domain optical coherence tomography showed CME and posterior vitreoschisis in the nasal quadrant of the fundus without a posterior vitreous detachment (PVD). This vitreous pathology suggested bilateral thickening and shrinkage of the posterior vitreous cortex. In the right eye, CME was evident with no vitreofoveal separation. However, in the left eye, minimal change was seen in the CME associated with a focal shallow PVD over the fovea. The best-corrected visual acuity (BCVA) in the left eye increased to 0.3 from 0.15 7 years after the first visit. Tangential vitreous traction on the macula may have caused the CME in the right eye. The shallow PVD over the fovea might have released the tangential vitreous traction from the fovea, induced spontaneous resolution of the CME, and improved the BCVA in the left eye.
机译:我们报道了68岁的右眼RP和CME左眼CME患者的视网膜色素变性(RP)发生囊性黄斑水肿(CME)的可能机制。光谱域光学相干断层扫描显示CME和眼底鼻象限后玻璃体切开术,无玻璃体后脱离(PVD)。这种玻璃体病理提示玻璃体后皮质双侧增厚和缩小。在右眼中,CME很明显,没有玻璃体腔分离。然而,在左眼中,与中央凹上浅局灶性PVD相关的CME几乎没有变化。第一次就诊后7年,左眼的最佳矫正视力(BCVA)从0.15增加到0.3。黄斑上的切向玻璃体牵引可能导致右眼的CME。中央凹上方的浅层PVD可能从中央凹处释放了切向的玻璃体牵引力,诱发了CME的自发分辨率,并改善了左眼的BCVA。

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