Reabsorption of vitreomacular traction syndrome-related acquired vitelliform lesions after pars plana vitrectomy.

Abstract

Purpose: Acquired vitelliform lesions are mainly progressive retinal pigment epithelium alterations and lipofuscin accumulation in the macular region. They may occur due to many different etiologies including vitreoretinal interface disorders. While vitreomacular traction can cause vitelliform lesions, the lesions then may also cause photoreceptor atrophy. We aimed to demonstrate the reabsorption of acquired vitelliform lesions after 25-gauge pars plana vitrectomy to treat patients with vitreomacular traction syndrome.

Methods: Nine eyes of eight patients, who were diagnosed with vitreomacular traction syndrome accompanied by acquired vitelliform lesions, were included in this institutional study. Patients with symptoms such as metamorphopsia, distorted vision of any kind or a decrease in visual acuity underwent 3-port 25-gauge pars plana vitrectomy and internal limiting membrane peeling with air or sulphur hexafluoride used as the endotamponade agent. During each preoperative and postoperative visit, the patients underwent a detailed ophthalmological examination. The differences in the median best-corrected visual acuity (BCVA) between the preoperative, postoperative second week, first,third and sixth months, first year and last follow-up were statistically compared using the Wilcoxon signed-rank test.

Results: The median (interquartile range IQR) preoperative BCVA was 0.40 0.30-0.45 LogMAR. During the second postoperative week, when intravitreal gas reabsorption occurred, the size of the vitelliform deposits decreased, and a median BCVA of 0.30 0.20-0.35 LogMAR was observed (p = 0.014). During the first month control vitelliform lesions were completely reabsorbed, and the BCVA was 0.20 0.15-0.35 LogMAR (p = 0.016).

Conclusion: The presence of vitelliform lesions alongside vitreoretinal interface problems may indicate the need for early surgical intervention to address potential photoreceptor damage due to additive photoreceptor stress results of traction and deposit accumulation.