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 des cribe the effects of refractive and intraocular surgery on the corneal endo thelial structure and function. Methods. Significant clinical and experimen tal publications are reviewed and recent experiments conducted in the autho r's laboratory to describe the corneal endothelial stresses. Results. The c orneal epithelium serves as a barrier to topical phenylephrine (2.5-10%). I n a compromised epithelium, topical phenylephrine will cause drug-induced s tromal edema and endothelial vacuolization. Contact lenses are capable of s timulating the epithelial arachidonic acid cascade to release 12(R)hydroxye icosatetraenoic acid (12(R)HETE) and 8(R)hydroxy-hexadecatrienoic acid (8(R )HHDTrE) to cause endothelial Na+/K+ adenosine triphosphatase (ATPase)-inhi bition and polymegethism. Specular microscopy of the corneal endothelial ce lls after refractive surgery (photorefractive keratectomy [PRK], laser in s itu keratomileusis [LASIK], intrastromal rings [INTACs]) has shown that the re is minimal effect. However, laser ablation of the stroma within 200 IJ-m of the corneal endothelium will result in endothelial cell structural chan ges and the formation of the amorphous substance deposited onto Descemet's membrane. Phacoemulsification with a high flow of the irrigation solution c an alter the endothelial surface glycoprotein layer. Lidocaine hydrochlorid e (1%) used as intracameral anesthesia readily diffuses through the corneal endothelium, resulting in stromal uptake and endothelial cell swelling. Wi th phacoemulsification, however, the washout of lidocaine from the cornea ( T1/2, 5 minutes) and iris (T1/2, 9 minutes) occurs quickly. Corneal endothe lial wound healing after keratoplasty occurs in the following sequence: mig ration of endothelial cells, development of tight junctions, and the format ion of Na+/K+ ATPase pump sites. Conclusions. Corneal endothelial resilienc y is due to the increased peripheral endothelial cell number for migration, the ability of endothelial cells to form tight junctions to maintain the e ndothelial barrier, the increase in endothelial Na+/K+ ATPase pump sites un der 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 repai r. All of these factors are important, along with the aqueous humor sodium concentration, which establishes the osmotic gradient for corneal deturgesc ence and transparency.