A STUDY ON ENDOTHELIAL CELL LOSS AFTER OPTICAL KERATOPLASTY- A RETROSPECTIVE STUDY IN A TERTIARY EYE CARE CENTRE IN CHENNA

2021 ◽  
pp. 19-21
Author(s):  
Rohini K ◽  
Padmapriya R ◽  
Niranjan Karthik Senthil Kumar

Aim: a study of endothelial cell loss after optical keratoplasty in 50 patients in a tertiary care centre in Chennai. Materials and Methods: A retrospective study was carried out on 50 patients who underwent optical keratoplasty in a tertiary care centre in Chennai. 50 patients in the age group 11-80 were included in this study. Postoperatively they were periodically followed up regarding graft clarity, presence of vascularisation, vision and endothelial cell count. During follow up presence of any complications were assessed and recorded. At the end of 6 months, there was an average of 37.5% loss of endothelial ce Observation And Results: lls in PKP and 44.5% in LKPs and 38.6% in Triple procedure. At the end of one month, patients who had repeat Keratoplasty for failed graft had more loss (20.1%) whereas at the end of 6 months, Pseudophakic Bullous Keratopathy patients showed more loss (49.4%). These indicate migration of endothelial cells along a density gradient after keratoplasty. Overall there is continuous loss of endothel Conclusion: ial cells in all cases of Keratoplasty regardless of the indication for keratoplasty and the type of keratoplasty. Even in cases of clear grafts, there is a continuous loss of endothelial cells. It has been reported that chronic subclinical rejection, chronic low-level inammation or continued interaction between the donor endothelium and a healthy recipient endothelium could explain the greater cell loss

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Guojian Jiang ◽  
Tingjun Fan

The introduction of intracameral anaesthesia by injection of lidocaine has become popular in cataract surgery for its inherent potency, rapid onset, tissue penetration, and efficiency. However, intracameral lidocaine causes corneal thickening, opacification, and corneal endothelial cell loss. Herein, we investigated the effects of lidocaine combined with sodium ferulate, an antioxidant with antiapoptotic and anti-inflammatory properties, on lidocaine-induced damage of corneal endothelia with in vitro experiment of morphological changes and cell viability of cultured human corneal endothelial cells and in vivo investigation of corneal endothelial cell density and central corneal thickness of cat eyes. Our finding indicates that sodium ferulate from 25 to 200 mg/L significantly reduced 2 g/L lidocaine-induced toxicity to human corneal endothelial cells, and 50 mg/L sodium ferulate recovered the damaged human corneal endothelial cells to normal growth status. Furthermore, 100 mg/L sodium ferulate significantly inhibited lidocaine-induced corneal endothelial cell loss and corneal thickening in cat eyes. In conclusion, sodium ferulate protects human corneal endothelial cells from lidocaine-induced cytotoxicity and attenuates corneal endothelial cell loss and central corneal thickening of cat eyes after intracameral injection with lidocaine. It is likely that the antioxidant effect of sodium ferulate reduces the cytotoxic and inflammatory corneal reaction during intracameral anaesthesia.


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