Dataset Information

Effect of Myopic Femtosecond Laser-Assisted LASIK on Anterior Chamber Inflammation (Flare Values) and Corneal Endothelium: A Prospective before and after Study.

ABSTRACT:

Purpose

This study aimed to investigate whether femtosecond laser-assisted LASIK (FS-LASIK) surgery causes inflammation in the anterior chamber and to analyze its effect on endothelial cells.

Methods

This prospective, longitudinal study included left eyes of 30 patients (19 females) who had undergone FS-LASIK surgery due to myopia and myopic astigmatism. Endothelial cell density (ECD) and morphological measurements were performed using a specular microscopy, and laser flare photometry was used to measure the anterior chamber flare values on the day of surgery. iFS™ Advanced FS and VISX STAR S4-IR Wavescan Excimer Laser platforms were used. Flare measurements were repeated on the postoperative 1^st day and 7^th day and the 1^st and 3^rd months. The endothelial measurements were repeated in the 3^rd month.

Results

Preoperatively, the mean flare was 5.59 ± 1.24 photons/ms; it was 6.49 ± 2.42 on the postoperative 1^st day, 5.87 ± 2.27 on the 7^th day, 5.68 ± 1.66 on the 1^st month, and 5.35 ± 1.24 on the 3^rd month. A significant difference was observed only between the preoperative and postoperative 1^st day flare values (p=0.047). The decrease in the ECD was clinically insignificant but statistically significant, with an average of 97.0 ± 209.9 cell count/mm² (3.3%, p=0.017). However, there was no significant change in the coefficient of variation (p=0.448) and hexagonality (p=0.096). No significant correlation was found between the increase in the flare value on the postoperative 1^st day and variables. A significant correlation was found between the decrease in ECD and the preoperative ECD (r = 0.356, p=0.027).

Conclusion

FS-LASIK caused minimal inflammation in the anterior chamber on only the 1^st postoperative day; additionally, a minimal decrease of cell count with no morphological changes were noted in the endothelial cells on postoperative 3^rd month. This trial is registered with NCT04899258.

SUBMITTER: Ozbilen KT

PROVIDER: S-EPMC8642012 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:PurposeTo investigate the relationship between early post-operative anterior chamber inflammation (aqueous flare) and central corneal thickness (CCT) after cataract surgery and to evaluate the effect of anti-inflammatory prophylaxis on CCT.SettingDepartment of Ophthalmology, Rigshospitalet-Glostrup, University Hospital Copenhagen, Denmark.DesignPost-hoc analysis of a prospective randomized controlled trial.Patients and methodsA total of 470 participants who underwent standard cataract surgery were randomly allocated to prophylactic treatment with nonsteroidal anti-inflammatory drug (NSAID, groups C and D) or a combination of NSAID and steroid eye drops (groups A and B), commenced either pre-operatively (A and C) or post-operatively on the day of surgery (B and D), or "drop-less surgery" (peri-operative subtenon depot of dexamethasone, group E). Aqueous flare was measured before and three days after surgery. CCT was measured before surgery, three days, three weeks, and three months after surgery. Data were analyzed according to the intention-to-treat method.ResultsDoubling of aqueous flare increased mean CCT by 15.6 microns (95% CI 9.8; 21.3, P<0.001) three days after surgery. Mean CCT increased from 549 microns (95% CI 545; 552) at baseline to 594 microns (95% CI 585; 602) three days after surgery and returned to 551 microns (95% CI 545; 557) three months after surgery. Mean CCT was thinner in group C compared to group A three days after surgery. No difference was found for any other groups or time points.ConclusionIncreased anterior chamber inflammation was associated with significant corneal thickening three days after cataract surgery. Choice of anti-inflammatory regimen seemed to be of no or minimal importance on CCT when the effect of inflammation was accounted for. Corneal thickening is possibly mediated by underlying deterioration of the blood-aqueous barrier and corneal endothelium pump function caused by a post-operative inflammatory response.