Pournaras C J, Kapetanios A D, Donati G
University Eye Department, University Hospitals of Geneva, Switzerland.
Doc Ophthalmol. 1999;97(3-4):439-47. doi: 10.1023/a:1002408206561.
Traction macular edema may develop through contraction of macular epiretinal membranes (ERM), or due to persistent vitreomacular traction during the evolution of vitreomacular traction syndrome (VMS). The purpose of this retrospective study was to determine the effect of vitreous surgery and the release of the vitreomacular traction or the removal of epiretinal membranes, on the evolution of traction induced macular edema.
Fourteen eyes from 14 patients presenting with idiopathic or secondary epiretinal membranes, and 11 eyes from 10 patients presenting with vitreomacular traction syndrome, underwent vitrectomy for reduced vision and cystoid macular edema, identified by slit-lamp examination and fluorescein angiography. No coexistent ocular conditions that might have caused macular traction were present. History, preoperative eye examination, operative findings, postoperative course and final examination as well as pre- and postoperative fluorescein angiography were reviewed.
In the ERM group, cystoid macular edema disappeared in all cases during the postoperative period and the mean visual acuity (VA) at the end of the follow-up (0.48 +/- 0.23) significantly increased compared to the preoperative one (0.29 +/- 0.2) (p=0.004). In the group of patients suffering from VMS, the posterior vitreous traction on the macula was released and macular edema disappeared in all cases but one. The mean v.a. at the end of the follow-up (0.42 +/- 0.24) significantly increased compared to the preoperative one (0.18 +/- 0.1) (p=0.01). Complications included intraoperative small petechias and postoperative progressive nuclear sclerosis, retinal detachment and retinal pigment epitheliopathy.
Cystoid macular edema may develop secondary to vitreomacular traction syndrome or epiretinal membrane contraction. Vitrectomy is effective in releasing macular traction which, in turn, may induce a decrease of the macular edema with improvement of visual acuity.
牵引性黄斑水肿可能通过黄斑视网膜前膜(ERM)收缩而发生,或由于玻璃体黄斑牵引综合征(VMS)演变过程中持续的玻璃体黄斑牵引所致。这项回顾性研究的目的是确定玻璃体手术以及解除玻璃体黄斑牵引或切除视网膜前膜对牵引性黄斑水肿演变的影响。
14例患有特发性或继发性视网膜前膜患者的14只眼,以及10例患有玻璃体黄斑牵引综合征患者的11只眼,因视力下降和裂隙灯检查及荧光素血管造影确诊的黄斑囊样水肿而接受了玻璃体切除术。不存在可能导致黄斑牵引的并存眼部疾病。回顾了病史、术前眼部检查、手术发现、术后病程和最终检查以及术前和术后荧光素血管造影。
在ERM组中,所有病例术后黄斑囊样水肿均消失,随访结束时的平均视力(VA)(0.48±0.23)与术前(0.29±0.2)相比显著提高(p = 0.004)。在患有VMS的患者组中,黄斑上的玻璃体后牵引被解除,除1例患者外所有病例黄斑水肿均消失。随访结束时的平均视力(0.42±0.24)与术前(0.18±0.1)相比显著提高(p = 0.01)。并发症包括术中小瘀点以及术后进行性核硬化、视网膜脱离和视网膜色素上皮病变。
黄斑囊样水肿可能继发于玻璃体黄斑牵引综合征或视网膜前膜收缩。玻璃体切除术可有效解除黄斑牵引,进而可能导致黄斑水肿减轻和视力改善。