To analyze longitudinal changes in the thicknesses of the macula, ganglion cell–inner plexiform layer (GC-IPL), and peripapillary retinal nerve fiber layer (RNFL) after vitrectomy.
Thirty-eight patients diagnosed with intraocular lens (IOL) dislocation without evidence of other vitreoretinal diseases were included. They underwent conventional vitrectomy and IOL transscleral fixation, with a follow-up of 12 months. Using spectral domain optical coherence tomography, the thicknesses of the macula, GC-IPL, and peripapillary RNFL in the vitrectomized and fellow control eyes were measured. Various optic nerve head parameters were also determined.
Optical coherence tomography showed that there were no significant differences in postoperative central macular thickness compared with baseline values. The average GC-IPL thickness increased 1 month after surgery from baseline (P = 0.038). The average RNFL thickness increased from baseline at 1 month (P = 0.001) and 3 months (P = 0.011) after vitrectomy. The mean foveal, GC-IPL, and RNFL thicknesses of the study eyes compared with the fellow control eyes increased at 1 month (P = 0.034), 1 month (P = 0.048), and 1 month (P = 0.013) to 3 months (P = 0.038), respectively, after surgery. However, no significant differences were found in intraocular pressure or optic nerve head parameters between the study and fellow control eyes at 12 months after surgery.
Transient increases in the thickness of the macula and GC-IPL were observed at 1 month after vitrectomy, and the postoperative RNFL thickness increased until 3 months after surgery, after which it returned to preoperative levels. There was no significant change in intraocular pressure or optic nerve head parameters before and after surgery.
A transient increase in the macula, ganglion cell–inner plexiform layer, and peripapillary retinal nerve fiber layer thicknesses was observed from 1 to 3 months in patients without vitreoretinal disease after vitrectomy. The authors' findings during a follow-up of 12 months did not show glaucoma development after changes in disk parameters, intraocular pressure, and ganglion cell–inner plexiform layer and retinal nerve fiber layer thicknesses.
*Department of Ophthalmology, Chungnam National University College of Medicine, Daejeon, Republic of Korea;
†Department of Ophthalmology, Armed Forces Capital Hospital, Seongnam, Republic of Korea;
‡Department of Computer Engineering, San Jose State University, San Jose, California; and
§Research Institute for Medical Science, Chungnam National University College of Medicine, Daejeon, Republic of Korea.
Reprint requests: Jung-Yeul Kim, MD, PhD, Department of Ophthalmology, Chungnam National University Hospital, #640 Daesa-dong, Jung-gu, Daejeon 301-721, Korea; e-mail: firstname.lastname@example.org
This research was supported by Chungnam National University Hospital Research Fund, 2015. None of the authors have any conflicting interests to disclose.
Design and conduct of the study (H.B.L., B.S.K., and J.Y.K.); Collection of data (H.B.L. and M.W.L.); Analysis and interpretation of data (H.B.L., Y.J.J., and J.Y.K.); Writing the article (H.B.L. and J.Y.K.); Critical revision of the article (Y.J.J. and J.Y.K.); Final approval of the article (H.B.L., M.W.L., B.S.K., Y.J.J., and J.Y.K.).
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