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1 retinal artery occlusion, macular hole, and corneal decompensation).
2 f 1, meaning no increased risk of developing corneal decompensation.
3 ausing displacement of the IOL and secondary corneal decompensation.
4 retained nuclear material, vitreous loss and corneal decompensation.
5 ial cell damage leading to stromal edema and corneal decompensation.
6 rosion, diplopia, motility disturbances, and corneal decompensation.
9 t pachymetry, leads to an increased risk for corneal decompensation after phacoemulsification in pati
10 rect myopia and myopic astigmatism, although corneal decompensation can occur after implantation.
11 other complications (eg, retinal detachment, corneal decompensation, dislocated intraocular lens [IOL
12 trabismus, proptosis, tube erosion, failure, corneal decompensation, endophthalmitis, and visual loss
13 ur, but there is a low probability of severe corneal decompensation, even in patients with a low endo
14 s that underwent DMEK for graft failure with corneal decompensation following DSAEK were analyzed; 15
15 As the fibrosis can cause IOL dislocation, corneal decompensation, hypotony, and retinal detachment
16 s (4.7%) lost >/= 3 Snellen lines because of corneal decompensation in one and angle-closure glaucoma
19 ent selection is crucial, because unexpected corneal decompensation leads to dissatisfied patients.
20 l acuities of 1/60 OD and 6/18 OS, bilateral corneal decompensation, lens opacities and raised intrao
24 at may be valuable in treating patients with corneal decompensation secondary to endothelial dysfunct
25 rvention to minimize the duration of central corneal decompensation, the visual outcomes with seconda
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