Abstract
Glaucoma is the leading cause of irreversible blindness worldwide. The only proven factor in slowing the progression of glaucomatous neuropathy is lower intraocular pressure (IOP), which can be achieved with pharmacology, laser therapy, or surgery. However, these treatments are associated with various adverse effects, including corneal endothelial cell loss (CECL). In recent years, several novel surgeries for reducing the IOP, collectively referred to as minimally invasive glaucoma surgery (MIGS), have been developed, one of which is the iStent. However, the long-term effects of such surgeries remain unknown. We compared a group of patients with open-angle glaucoma and cataract who underwent phacoemulsification alone with a group of patients with similar demographic and clinical characteristics who underwent simultaneous phacoemulsification and iStent implantation. Overall, 26 eyes of 22 subjects who underwent a combined phacoemulsification-iStent procedure and 26 eyes of 24 subjects who underwent cataract surgery were included. Before surgery, endothelial cells accounted to 2228.65 ± 474.99 in iStent group and 2253.96 ± 404.76 in the control group (p = 0.836). After surgery, their number declined to 1389.77 ± 433.26 and 1475.31 ± 556.45, respectively (p = 0.509). There was no statistically significant difference in CECL between the two groups 18–24 months after surgery, despite increased manipulation in the anterior chamber and the presence of an implant in the trabecular meshwork in those with an iStent implant. Thus, iStent bypass implantation is a safe treatment in terms of CECL for mild-to-moderate open-angle glaucoma.
Highlights
Glaucoma is the leading cause of irreversible blindness worldwide
The only proven intervention in slowing the progression of glaucomatous neuropathy is to lower intraocular pressure (IOP), which can be achieved with pharmacotherapy, laser therapy, or surgery [1]
These treatments are associated with various adverse effects, including corneal endothelial cell loss (CECL) [2,3]
Summary
Glaucoma is the leading cause of irreversible blindness worldwide. The only proven intervention in slowing the progression of glaucomatous neuropathy is to lower intraocular pressure (IOP), which can be achieved with pharmacotherapy, laser therapy, or surgery [1].These treatments are associated with various adverse effects, including corneal endothelial cell loss (CECL) [2,3].The corneal endothelium is a single layer of hexagonal-shaped cells found on the posterior surface of the cornea; its most important function is maintaining corneal transparency. Glaucoma is the leading cause of irreversible blindness worldwide. The only proven intervention in slowing the progression of glaucomatous neuropathy is to lower intraocular pressure (IOP), which can be achieved with pharmacotherapy, laser therapy, or surgery [1]. These treatments are associated with various adverse effects, including corneal endothelial cell loss (CECL) [2,3]. Endothelial cells do not proliferate, and their numbers gradually decrease with age at 0.56% per year [3]. Endothelial cell density (ECD) is affected by glaucoma
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