The evolving fate of the corneal endothelium in cataract surgery

Cataract surgery, the most commonly performed ophthalmic procedure, can result in corneal endothelial cell loss (ECL), which can have a lasting impact due to the endothelium's limited regenerative capacity. This review highlights surgical technologies and considerations that can provide protection of the corneal endothelium.

Endothelial cell density (ECD) at birth is about 3,000-5,000 cells/mm 2 and decreases 0.3-0.6% per year, with the adult eye endothelial cell density being approximately 2000-3000 cells/mm 2 . Most ECL occurs within the first three months after surgery, with attributing factors including shallow anterior chamber depth (ACD), low baseline ECD, and high cumulative dissipated energy (CDE), as well as patient-specific comorbidities. Diabetes has been shown to play a role in corneal endothelium recovery, as central corneal thickness (CCT) was found to be significantly higher in diabetic patients after cataract surgery at one month compared to nondiabetic patients, although not at six months in a meta-analysis. Modern fluidics platforms enhance chamber stability and minimize turbulence, and low-perfusion phacoemulsification has decreased ECL rates in high-risk eyes. Corneal tunnel length has been identified as an intraoperative factor; in eyes with short anterior chamber depth, longer tunnel lengths are associated with greater ECL. Microincision surgery, ultrasound energy modulation, and femtosecond laser use provide additional benefits. Hydrogen-enriched irrigating solutions were found to potentially significantly reduce early ECL, and chondroitin sulfate-hyaluronic acid ophthalmic viscosurgical devices (OVDs) further lowered both cell loss and corneal edema.

Advances in surgical technology, combined with individualized planning based on risk factors and anterior segment anatomy, enable minimization of ECL and optimize visual outcomes.