Abstract
The corneal endothelium has a crucial role in maintaining a clear and healthy cornea. Corneal endothelial cell loss occurs naturally with age; however, a diagnosis of glaucoma and surgical intervention for glaucoma can exacerbate a decline in cell number and impairment in morphology. In glaucoma, the mechanisms for this are not well understood and this accelerated cell loss can result in corneal decompensation. Given the high prevalence of glaucoma worldwide, this review aims to explore the abnormalities observed in the corneal endothelium in differing glaucoma phenotypes and glaucoma therapies (medical or surgical including with new generation microinvasive glaucoma surgeries). Descemet membrane endothelial keratoplasty (DMEK) is increasingly being used to manage corneal endothelial failure for glaucoma patients and we aim to review the recent literature evaluating the use of this technique in this clinical scenario.
Highlights
Glaucoma is a group of conditions with varying pathophysiological processes, which cause a progressive optic neuropathy associated with characteristic structural damage to the optic nerve and associated visual field loss [1]. e condition can be caused by various pathophysiological processes
Descemet membrane endothelial keratoplasty (DMEK) is increasingly being used to manage corneal endothelial failure for glaucoma patients, and we aim to review the recent literature evaluating the use of this technique in this clinical scenario
Corneal endothelial abnormalities, including a reduction in cell count and morphology, have been detected in glaucoma patients [3]. e corneal endothelium is a monolayer of hexagonal cells, which plays a critical role in regulating corneal hydration and transparency [4]. e cells are highly interdigitated and possess apical junctional complexes that, together with abundant cytoplasmic organelles e.g., mitochondria, are indicative of their crucial role in active fluid transport [5]. e abnormal endothelial changes observed in glaucoma are due to multiple influences, including intraocular pressure (IOP), aqueous humour abnormalities, medication use, and surgical interventions [3]. is review article aims to describe the endothelial changes seen in glaucoma and the role Descemet membrane endothelial keratoplasty (DMEK) has in managing corneal endothelial cell loss in glaucoma patients
Summary
Glaucoma is a group of conditions with varying pathophysiological processes, which cause a progressive optic neuropathy associated with characteristic structural damage to the optic nerve and associated visual field loss [1]. e condition can be caused by various pathophysiological processes. Carlson et al reported in a study of corneas aged 5–79 years that the number of hexagonal cells significantly decreased with age, but the number of pentagonal and heptagonal cells increased simultaneously [16] They observed a 23% increase in endothelial permeability to fluorescein with age but found no differences in corneal thickness or pump rate. Additional levels of inflammatory cytokines within the aqueous humour, such as tumour necrosis factor (TNF), interleukin-1, and interferons (IFNs), are known to increase with age [25] In vitro, they have been shown to induce apoptosis in corneal endothelial cells [25]. Cataract surgery can lead to long-term alterations of the intraocular microenvironment in normal, glaucomatous [28], and FECD eyes [29]
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