Long-Term Endothelial Cell Loss After Ocular Chemical Injuries in Eyes with Resolved Corneal Edema: A Retrospective Paired-Eye Study.
Source: PubMed, NCBI / U.S. National Library of Medicine
To evaluate long-term effects of ocular chemical injuries on corneal-endothelial cells in eyes initially presenting with burn-induced corneal edema that resolved clinically. This retrospective paired-eye study included patients with unilateral chemical burns and corneal edema at presentation, treated between January 2020 and June 2024 at a tertiary ophthalmology center. Patients with bilateral injuries, prior ocular surgery, corneal dystrophies, or less than 3 months of follow-up were excluded. Endothelial parameters as endothelial cell density, coefficient of variation, hexagonality, average cell area, and central corneal thickness were assessed bilaterally using specular microscopy. Injured eyes were compared with contralateral, unaffected eyes. Eight patients (16 eyes) were included (mean follow-up 25.9±17.1 months). Injuries were caused by alkaline (62.5%) or acidic (37.5%) agents. At final follow-up, the mean endothelial cell density was significantly lower in injured eyes compared with contralateral eyes (956.25±137.5 vs. 2740.25±266.94 cells/mm2, P<0.001), representing a 65.1% reduction. No differences were found between acid vs. alkali injuries or saline vs. Diphoterine irrigation. Central corneal thickness did not differ significantly. These analyses should be interpreted with caution due to the small sample size and limited statistical power. Ocular chemical injuries can cause substantial, persistent corneal endothelial cell loss, even after clinical
Abstract
To evaluate long-term effects of ocular chemical injuries on corneal-endothelial cells in eyes initially presenting with burn-induced corneal edema that resolved clinically. This retrospective paired-eye study included patients with unilateral chemical burns and corneal edema at presentation, treated between January 2020 and June 2024 at a tertiary ophthalmology center. Patients with bilateral injuries, prior ocular surgery, corneal dystrophies, or less than 3 months of follow-up were excluded. Endothelial parameters as endothelial cell density, coefficient of variation, hexagonality, average cell area, and central corneal thickness were assessed bilaterally using specular microscopy. Injured eyes were compared with contralateral, unaffected eyes. Eight patients (16 eyes) were included (mean follow-up 25.9±17.1 months). Injuries were caused by alkaline (62.5%) or acidic (37.5%) agents. At final follow-up, the mean endothelial cell density was significantly lower in injured eyes compared with contralateral eyes (956.25±137.5 vs. 2740.25±266.94 cells/mm2, P<0.001), representing a 65.1% reduction. No differences were found between acid vs. alkali injuries or saline vs. Diphoterine irrigation. Central corneal thickness did not differ significantly. These analyses should be interpreted with caution due to the small sample size and limited statistical power. Ocular chemical injuries can cause substantial, persistent corneal endothelial cell loss, even after clinical resolution of corneal edema. Long-term endothelial monitoring and careful surgical planning are recommended in this population.