A Corneal Decompensation Cascade In A Functionally Monocular Eye: Multifactorial Mechanisms Leading To Penetrating Keratoplasty
Published 2026 - 44th Congress of the ESCRS
Reference: POCOR477 | Type: Poster | DOI: 10.82333/0mx8-yn72
Authors: Dr Iulia Mihaela Ivanov* 1 , Dr Alina Gheorghe 2 , Dr Andrei Coleasa 2 , Dr Ana Arghirescu 2 , Dr Laura Dinu 1 , Dr Veronica Toader 1 , Dr Teodora Alexandrescu 1
1Clinical Emergency Eye Institute,Bucharest,Romania, 2Clinical Emergency Eye Institute,Bucharest,Romania;"Carol Davila" University of Medicine and Pharmacy,Bucharest,Romania
Purpose
To illustrate how cumulative anterior and posterior segment risk factors, including prior vitreoretinal surgery, silicone oil–related glaucoma, and impaired corneal nerve status, can synergistically compromise corneal homeostasis, ultimately leading to global corneal decompensation requiring transplantation.
Setting
Tertiary academic ophthalmology referral center managing complex anterior and posterior segment pathology.
Methods
We report the case of a 60-year-old functionally monocular male with high myopia and a complex ocular history, including rhegmatogenous retinal detachment treated with pars plana vitrectomy and silicone oil tamponade. The postoperative course was complicated by secondary glaucoma related to silicone oil, which required silicone oil removal and Ahmed valve implantation.
The patient subsequently developed advanced bullous keratopathy with superimposed corneal ulceration in the context of reduced corneal sensitivity suggestive of neurotrophic keratopathy. Slit-lamp examination and sequential anterior segment imaging were used to document corneal structural changes and postoperative outcomes.
Results
Advanced bullous keratopathy, in conjunction with neurotrophic keratitis, synergistically contributed to the development of secondary infectious keratitis. Infection control was achieved with topical and systemic antimicrobial therapy, followed by amniotic membrane transplantation, which resulted in significant improvement in epithelial integrity. Given the presence of marked stromal fibrosis, thinning, and persistent oedema, penetrating keratoplasty was performed.
Postoperatively, despite prolonged epithelial recovery consistent with impaired corneal nerve regeneration, graft clarity was achieved. Visual acuity improved modestly from hand motion to counting fingers.
Conclusions
In functionally monocular patients with complex ocular history, corneal decompensation is frequently multifactorial and reflects cumulative injury rather than an isolated endothelial event.
In this case, chronic inflammation, corneal nerve damage and endothelial injury collectively accelerated the development of corneal oedema and structural deterioration, ultimately necessitating corneal transplantation.
Penetrating keratoplasty was undertaken to preserve ocular integrity and to maximize residual visual potential in the patient’s sole functional eye.