The resiliency of the corneal endothelium to refractive and intraocular surgery

Purpose. To describe stress factors (phenylephrine and contact lenses) from the corneal epithelium that can affect the corneal endothelium, and to describe the effects of refractive and intraocular surgery on the corneal endothelial structure and function. Methods. Significant clinical and experimental publications are reviewed and recent experiments conducted in the author's laboratory to describe the corneal endothelial stresses. Results. The corneal epithelium serves as a barrier to topical phenylephrine (2.5-10%). In a compromised epithelium, topical phenylephrine will cause drug-induced stromal edema and endothelial vacuolization. Contact lenses are capable of stimulating the epithelial arachidonic acid cascade to release 12(R)hydroxyeicosatetraenoic acid (12(R)HETE) and 8(R)hydroxy-hexadecatrienoic acid (8(R)HHDTrE) to cause endothelial Na+/K+ adenosine triphosphatase (ATPase)-inhibition and polymegethism. Specular microscopy of the corneal endothelial cells after refractive surgery (photorefractive keratectomy [PRK], laser in situ keratomileusis [LASIK], intrastromal rings [INTACs]) has shown that there is minimal effect. However, laser ablation of the stroma within 200 IJ-m of the corneal endothelium will result in endothelial cell structural changes and the formation of the amorphous substance deposited onto Descemet's membrane. Phacoemulsification with a high flow of the irrigation solution can alter the endothelial surface glycoprotein layer. Lidocaine hydrochloride (1%) used as intracameral anesthesia readily diffuses through the corneal endothelium, resulting in stromal uptake and endothelial cell swelling. With phacoemulsification, however, the washout of lidocaine from the cornea (T1/2, 5 minutes) and iris (T1/2, 9 minutes) occurs quickly. Corneal endothelial wound healing after keratoplasty occurs in the following sequence: migration of endothelial cells, development of tight junctions, and the formation of Na+/K+ ATPase pump sites. Conclusions. Corneal endothelial resiliency is due to the increased peripheral endothelial cell number for migration, the ability of endothelial cells to form tight junctions to maintain the endothelial barrier, the increase in endothelial Na+/K+ ATPase pump sites under stress, and the ability of the corneal endothelial cells to shift their metabolism of glucose to the hexose monophosphate shunt for the production of nicotinamide adenine dinnucleotide phosphate (NADPH) and membrane repair. All of these factors are important, along with the aqueous humor sodium concentration, which establishes the osmotic gradient for corneal deturgescence and transparency.