Posterior chamber intraocular lens (PC-IOL) subluxation is uncommon but represents one of the most serious complications following phacoemulsification. Late spontaneous IOL-capsular bag complex dislocation is defined as occurring three months or later following cataract surgery. Unlike early IOL dislocation, late spontaneous IOL dislocation is due to a progressive zonular dehiscence and contraction of the capsular bag many years what seemed to be uneventful surgery. In recent years, late in-the-bag IOL subluxation or dislocation has been reported with increasing frequency, having a cumulative risk of IOL dislocation following cataract extraction of 0.1% after 10 years and 1.7% after 25 years. A predisposition to zonular insufficiency and capsular contraction is identified in 90% of reviewed cases. Multiple conditions likely play a role in contributing to this zonular weakness and capsular contraction. Pseudoexfoliation is the most common risk factor, accounting for more than 50% of cases. Other associated conditions predisposing to zonular dehiscence are aging, high myopia, uveitis, trauma, previous vitreoretinal surgery, retinitis pigmentosa, diabetes mellitus, atopic dermatitis, previous acute angle-closure glaucoma attack, and connective tissue disorders. The recognition of these predisposing factors suggests a modified approach in cases at risk. We review certain measures to prevent IOL-bag complex luxation that have been proposed.

Purpose. To investigate the effects of Fuchs’ corneal dystrophy (FCD) on corneal biomechanical properties and the results of IOP readings in relation to changes in corneal hysteresis (CH) and central corneal thickness (CCT). methods. Corneal biomechanical properties, including CH, corneal resistance factor (CRF), and CCT, were measured with the ocular response analyzer (ORA) in 11 eyes of 11 patients with clinically confirmed FCD and 12 eyes of 12 healthy subjects. The ORA was also used to determine the values of intraocular pressure (IOP_g) and corneal compensated IOP (IOP_cc). Goldmann applanation tonometry (GAT) was also measured. results. CH measured 10.3 ± 1.6 mm Hg (range, 8.7–13.8) in normal eyes and 6.9 ± 1.8 mm Hg (range, 4.6–11.7) in FCD eyes (P = 0.001). CRF in the normal and FCD eyes was 10.5 ± 1.5 mm Hg (range, 8.5–13.3) and 8.1 ± 1.9 (range, 4.5–11.2), respectively (P = 0.005). CCT was higher in FCD eyes (606 ± 20 μm; range, 578–635) than in normal eyes (538.4 ± 24.9 μm; range, 495–575; P = 0.0001). IOP_g was 16.2 ± 2.2 mm Hg (range, 13.5–18.7) in control eyes compared with 17.6 ± 2.7 mm Hg (range, 12.8–18.6) in FCD eyes (P = 0.201). However, IOP_cc in the FCD group (21.8 ± 4.6 mm Hg; range, 12.8–29.0) was higher than in the control group (16.5 ± 3.4 mm Hg; range, 11.9–23.9; P = 0.006). GAT in the normal and FCD eyes was 16.7 ± 2.1 mm Hg (range, 12.8–18.6) and 16.9 ± 2.3 mm Hg (range, 13.1–19.0), respectively (P = 0.205). conclusions. FCD led to a change of corneal biomechanical properties. CH and CRF were significantly lower in FCD eyes than in normal eyes. IOP_cc was significantly higher in FCD eyes than in control eyes. These values may be useful in addition to CCT when assessing corneal rigidity. Thus, FCD may cause an underestimation error in IOP measurement.

Diabetes mellitus is one of the most prevalent chronic diseases worldwide. Diabetic patients are at risk of developing cataract and present for surgery at an earlier age than non-diabetics. The aim of this study was to review the problems associated with cataract surgery in a diabetic patient. Corneal complications in diabetic patients include delayed wound healing, risk of developing epithelial defects or recurrent erosions due to the impairment of epithelial basement membranes and epithelial–stromal interactions. Diabetic patients present lower endothelial cell density and their endothelium is more susceptible to trauma associated with cataract surgery. A small pupil is common in diabetic patients making cataract surgery technically challenging. Finally diabetic patients have an increased risk for developing postoperative pseudophakic cystoid macular edema, posterior capsule opacification or endophthalmitis. In patients with pre-proliferative or proliferative diabetic retinopathy, diabetic macular edema or iris neovascularization adjunctive therapy such as an intravitreal anti-vascular endothelial growth factor injection, can inhibit exacerbation related to cataract surgery.

Macular edema (ME) is a nonspecific sign of numerous retinal vascular diseases. This paper is an updated overview about the role of inflammatory processes in the genesis of both diabetic macular edema (DME) and ME secondary to retinal vein occlusion (RVO). We focus on the inflammatory mediators implicated, the effect of the different intravitreal therapies, the recruitment of leukocytes mediated by adhesion molecules, and the role of retinal Müller glial (RMG) cells.

In the last decade, we have witnessed substantial progress in our understanding of corneal biomechanics and architecture. It is well known that diabetes is a systemic metabolic disease that causes chronic progressive damage in the main organs of the human body, including the eyeball. Although the main and most widely recognized ocular effect of diabetes is on the retina, the structure of the cornea (the outermost and transparent tissue of the eye) can also be affected by the poor glycemic control characterizing diabetes. The different corneal structures (epithelium, stroma, and endothelium) are affected by specific complications of diabetes. The development of new noninvasive diagnostic technologies has provided a better understanding of corneal tissue modifications. The objective of this review is to describe the advances in the knowledge of the corneal alterations that diabetes can induce.