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Predović, J; Bosnar, D; Marković, L; Ćurić, A; Bračić, J; Georgi, T; List, W; Glatz, W; Ivastinovic, D.
Vitreous hyper-reflective dots and the macular thickness after cataract surgery.
PLoS One. 2024; 19(4): e0300148 Doi: 10.1371/journal.pone.0300148 [OPEN ACCESS]
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Leading authors Med Uni Graz
Ivastinovic Domagoj
Co-authors Med Uni Graz
Georgi Thomas Patrick
Glatz Wilfried Maximilian
List Wolfgang Michael
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Abstract:
PURPOSE: To assess the association between vitreous hyper-reflective dots (VHD) and the macular thickness changes following uneventful phacoemulsification. METHODS: In this prospective cohort study optical coherence tomography (OCT) examinations were performed preoperatively and 1 week, 1 month and 3 months postoperatively in patients undergoing cataract surgery. OCT images were analyzed for retinal central subfield thickness (CST) and preretinal VHDs. Surgeries were recorded for the assessment of lens fragments in the space of Berger. RESULTS: 111 eyes of 97 patient were enrolled of whom 69 (62.2%) were female. VHDs were seen in 25 eyes (22.5%) at week 1; in 21 eyes (18.9%) at month 1 and in 3 eyes (2.7%) at month 3. In all eyes with VHDs retro-capsular lens fragments were visible immediately after phacoemulsification. The number of VHDs significantly decreased over the postoperative period. There was a moderate correlation between the number of VHDs and CST at 1 month (r = 0.426, p<0.001). In eyes with VHD the CST averaged 238.8±17.6 μm (214-266) at 1 week; 276.1±63.5 μm (231-481) at 1 month and 285.1±122.3 μm (227-785) at 3 months. In eyes with no detectable VHDs CST averaged 235.9±23.3 μm (192-311) at 1 week; 240.1±21.6 μm (200-288) at 1 month and 242.2±21.3 μm (205-289) at 3 months. Although the differences among the assessment points were relatively low, there was a significant difference in general (p<0.001, Friedman test). CONCLUSION: In conclusion, VHDs seem to cause macular thickening throughout the postoperative course. The origin of VHDs is still unknown; however, they presumably represent lens fragments that provoke subclinical inflammation.

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