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Anders Ivarsen, Jesper Hjortdal, Nicolaj Aagaard, J.Christian Hedegaard, Henrik Sejersen, Christina Møller; Corneal thickness after posterior lamellar keratoplasty. Invest. Ophthalmol. Vis. Sci. 2013;54(15):3101.
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© ARVO (1962-2015); The Authors (2016-present)
Descemet’s stripping automated keratoplasty (DSAEK) has become the most frequently performed treatment for visually significant endothelial dystrophy. The surgery causes a transient increase in recipient corneal hydration; however, it remains unknown whether structural changes in the recipient cornea also occur.
Seventy-six patients treated for endothelial dystrophy were followed with routine clinical examination for at least one year after DSAEK. At all visits, central corneal thickness (CCT) was determined with a Haag-Streit optical pachymeter. The difference in CCT from 3 days to 1 year after sugery (ΔCCT = CCT3days - CCT1year) was calculated as a crude measure of postoperative corneal edema. At their latest visit, patients were examined with spectral domain OCT (SD-OCT; Heidelberg Spectralis with anterior segment module) to determine the central thickness of the recipient cornea (recipient corneal thickness; RCT). SD-OCT was also used to determine CCT in a group of normal corneas.
From 1 to 6 years after DSAEK, RCT averaged 490 ± 29 μm, which was significantly less than the CCT of 531 ± 18 μm that was observed with SD-OCT in normal corneas (p < 0.001). RCT measured 487 ± 28 μm after one year (n = 43), 491 ± 29 μm after 2 years (n = 24), and 505 ± 26 μm after 3 to 6 years (n = 9), with a slight but significant increase over time (Pearson’s corr; r2 = 0.06; p = 0.03). Correlating RCT with ΔCCT also showed a significant correlation between postoperative corneal edema and RCT, with more edema causing the recipient cornea to become thinner over time (r2 = 0.11; p = 0.006).
In patients treated with DSAEK for endothelial dystrophy we found corneas to be thinner than normal once the postoperative edema had resolved.The correlation between post-operative edema and RCT may suggest that wash-out of stromal ground substances induce the thinning, with the subsequent gradual increase in thickness being caused by resynthesis of extracellular material. However, the long-lasting nature of the observed changes could also suggest underlying structural abnormalities in endothelial dystrophy.
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