Abstract

Diseases of the corneal endothelium (Fuchs endothelial dystrophy, bullous keratopathy, and endothelial failure following penetrating keratoplasty) count for the most frequent indications for corneal transplantation. Instead of replacing all five layers of the cornea (epithelium, Bowman layer, stroma, Descemet membrane, endothelium) by penetrating keratoplasty (PK), which has first been performed by Eduard Zirm [1–3] in 1905, nowadays techniques for the selective replacement of the diseased corneal endothelium are preferred. This has first been suggested by Tillet in 1956 [4] to avoid characteristical complications following PK (e.g. high irregular astigmatism and wound healing problems). Although the technical principle of this kind of posterior lamellar keratoplasty or endothelial keratoplasty (EK) could be realised, the visual results were not satisfying for the patients. One important technical step in improving posterior lamellar keratoplasty was the introduction of descemetorhexis by Melles et al. [5], where the stroma of the recipients cornea is not manipulated and only the Descemet membrane including the diseased endothelial cells is removed completely [6]. By avoiding manipulations of the recipient’s posterior stroma the clinical results could be improved as the lamellar graft could be attached to a smooth surface of the posterior stroma. In case of Descemet stripping endothelial keratoplasty (DSEK) the lamellar graft is manually prepared and consists of posterior stroma, Descemet membrane, and endothelium of the donor. It is transferred into the anterior chamber via a corneoscleral or clear cornea incision using special surgical instruments, unfolded and sutureless attached to the posterior stroma of the recipient’s cornea by an air bubble. Regarding DSEK one problem is the manual preparation process of the lamellar graft leading graft preparation failures in some cases [7]. To overcome these problems of complete manual graft preparation the separation of the stromal lamellae can be performed using a microkeratome, by which a 400–500 μm thick layer of the anterior part of the donor cornea can be cut leaving a 80–150 μm thick lamella consisting of posterior stroma, Descemet membrane, and endothelium (Descemet stripping automated endothelial keratoplasty, DSAEK). The characteristic advantages of DSEK/DSAEK compared to PK are a suture-free graft adaptation and a faster improvement of visual acuity without a change of the refractive status. On the other hand, due to more intensive graft manipulations during graft preparation, implantation, and adaptation, the early endothelial cell loss following DSEK/DSAEK seems to be higher than that after PK. Furthermore, patients following DSEK/DSAEK often do not reach the maximum possible visual acuity which may be explained by optical phenomena caused by graft-host-interface reactions [8]. To reach the respective advantages of DSEK/DSAEK but to avoid graft-host-interface problems, Descemet membrane endothelial keratoplasty (DMEK) has been developed where the corneal graft consists only of Descemet membrane and endothelial cells without corneal stroma [9]. For DMEK graft preparation Descemet membrane including the endothelium is manually peeled off the donor’s posterior stroma using fine forceps. Following complete peeling off Descemet membrane forms a roll with the endothelial cells on the exterior. This graft roll can then be implanted into the anterior chamber through a small clear cornea incision and attached to the posterior recipient’s stroma by using an air bubble after the graft has been carefully unfolded. As no stromal tissue of the donor is grafted the primary anatomical situation is restored by DMEK leading to the maximum reachable visual acuity. However, one disadvantage of DMEK is that macroscopically invisible collagen fibres of the donor stroma can insert into Descemet membrane causing tears in the thin graft leading to graft preparation failures [10]. Furthermore, the unfolding of the graft may also be much more difficult than in DSAEK potentially leading to more intraoperative endothelial cell damage and more primary graft failures [3, 11].

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