Risk Factors for Endothelial Decompensation after Penetrating Keratoplasty and Its Novel Therapeutic Strategies

Abstract

Purpose To review the risk factors and pathogenesis of endothelial decompensation after penetrating keratoplasty (PKP) and its novel therapeutic strategies. Methods Literature review. Results As the major cause of graft failure in PKP, endothelial decompensation of corneal allograft is considered an irreversible decrease in endothelial cell density and endothelial dysfunction. Various risk factors, including donor status and operative and recipient factors, have been found to be associated with this pathological process. Operative factors like graft size and recipient factors such as indications, glaucoma, or glaucoma surgery history are highly associated with the occurrence of endothelial decompensation, while others are still under investigation. Although the mechanism of these risk factors remains unclear, pathogenesis can be summarized as an acute and chronic loss of endothelium, and cell exchange between donor and recipient is at the core of chronic cell loss. Endothelial keratoplasty has been a useful alternative to repeat standard PKP in eyes with failed grafts. Descemet stripping automated endothelial keratoplasty (DSAEK) and Descemet's membrane endothelial keratoplasty (DMEK) following failed PKP provide more rapid visual recovery and achieve better rates of graft survival than those of a second PKP. Conclusions Any direct or indirect damage to the endothelium could cause the loss, morphological changes, and dysfunction of endothelial cells. Graft size, indications, and recipient glaucoma or glaucoma surgery history are risk factors for endothelial decompensation. DSAEK and DMEK are novel therapeutic strategies for failed PKP grafts and have potential superiorities compared with repeat PKP.

Identification of the preoperative and perioperative factors that predict postoperative endothelial cell density after Descemet membrane endothelial keratoplasty: A retrospective cohort study

“…A common concern regarding all keratoplasty techniques is that they induce a steep short-term decrease in endothelial cell density (ECD) that eventually slows to low rates [ 16 – 20 ]. For example, in DMEK, 30–40% of endothelial cells are lost in the first 12 months, after which there is a stable annual loss of 7% [ 21 ].…”

Corneae from body donors in anatomy department: valuable use for clinical transplantation and experimental research

“…6). This difference in mean ECN could translate into higher rates of functional decompensation of the grafts, since according to the linear model of endothelial cell loss, a lower ECN at the time of surgery is associated with a higher speed of endothelial cell loss over time [15]. Although, endothelial cell number of the donor was identified in many studies as a risk factor for endothelial decompensation, it is by far not the only one.…”

Clinical Outcomes in Maximum Tolerated Medical Therapy in Penetrating Keratoplasty for Bullous Keratopathy

“…Glaucoma is a well-known risk factor for corneal endothelial decompensation after penetrating keratoplasty (1)(2)(3)(4). Both uncontrolled intraocular pressure (IOP) and Ahmed glaucoma valve (AGV) implantation may affect the endothelial cell decompensation of the graft (1,5).…”

“…Glaucoma is a well-known risk factor for corneal endothelial decompensation after penetrating keratoplasty (1)(2)(3)(4). Both uncontrolled intraocular pressure (IOP) and Ahmed glaucoma valve (AGV) implantation may affect the endothelial cell decompensation of the graft (1,5). To avoid endothelial damage associated with AGV implantation, maximum tolerated medical therapy (MTMT) can be maintained in patients with glaucoma after penetrating keratoplasty (PKP).…”