The cornea remains in a state of deturgescence, maintained by endothelial cell Na+/K+ ATPase and by tight junctions between endothelial cells that limit entrance of fluid into the stroma. Fuchs’ endothelial corneal dystrophy (FECD) was initially described by Fuchs in 1910 as a combination of epithelial and stromal edema in older patients. It manifests as bilateral, albeit asymmetric, central corneal guttae, corneal edema, and reduced vision. When edema is severe, the corneal epithelium can detach from its basement membrane, creating painful bullae on the anterior surface of the cornea. The course of this dystrophy can be further accelerated after intraocular surgery, specifically cataract extraction. Pseudophakic bullous keratopathy (PBK) is endothelial cell loss caused by surgery in the anterior chamber. If the corneal endothelium is damaged during surgery, the same spectrum of symptoms as found in FECD can develop. In the nineteenth century, penetrating keratoplasty was the only surgical procedure available for isolated endothelial disease. In the 1960s, Dr. José Barraquer described a method of endothelial keratoplasty using an anterior approach via laser-assisted in situ keratomileusis (LASIK) flap. In 1999, Melles and colleague described their technique of posterior lamellar keratoplasty. Later, Melles et al. started to change host dissection using simple “descemetorhexis” in a procedure known as Descemet’s stripping endothelial keratoplasty. Following the widespread adoption of Descemet’s stripping automated endothelial keratoplasty, the Melles group revisited selective Descemet’s membrane transplantation and reported the results of a new procedure, Descemet’s membrane endothelial keratoplasty (DMEK). Recently, some eye banks have experimented with the preparation of DMEK/Descemet’s membrane automated endothelial keratoplasty donor tissue that may help the surgeon avoid the risk of tissue loss during the stromal separation step. Recently, the authors described a new bimanual technique for insertion and positioning of endothelium–Descemet membrane grafts in DMEK.
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