[Endothelial protection in surgical interventions and corneal donor tissue]

Perioperative iatrogenic lesions due to physico chemical trauma may worsen a primary endotheliopathy or lead to a secondary endotheliopathy with subsequent decompensation and corneal opacification. The incisions in anterior segment surgery induce permanent vertical cellular disparity, considering the peripheral endothelium in an area that may correspond to its germinative zone. Cells are lost by corneal folding, e.g., during nuclear expression or sutureinduced distortion. Floating nuclear particles and a high perfusion volume, e.g., during phacoemulsification or vitrectomy in aphakic eyes, create diffuse cellular necrosis. The same thing happens with chemically or osmotically inadequate perfusion media or extraocular solutions applied to the open eye during surgical interventions, e.g., to maintain mydriasis. Large areas of cell erosion are encountered after direct contact with instruments and PMMA. This has been one of the reasons for the development of new IOL materials like Poly-Hema or silicone that are less traumatizing for the endothelium. Long-lasting endothelial lesions result from direct contact with IOL haptics or mobile iris- or angle-supported lenses. The effect of a short post-operative rise in IOP on the endothelium is not clear. For all lens styles and materials, it still remains unclear whether there is chronic subclinical inflammation due to the IOL plastic material itself or not. To protect the endothelium, e.g., during cataract surgery, several techniques have been developed: preoperative hypotony; nuclear expression respecting corneal topography; the use of small amounts of mostly physiological rinsing solutions warmed to body temperature; endocapsular irrigation-aspiration; posterior chamber phacoemulsification; posterior chamber IOL implantation with an anterior chamber deepened by air and/or viscoelastics; postoperative reduction of the IOP.(ABSTRACT TRUNCATED AT 250 WORDS)