Superficial Lasik Corneal Flap Necrosis As A Complication In A Patient Undergoing Epikeratophakia. A Case Report.
Published 2025 - 43rd Congress of the ESCRS
Reference: PO249 | Type: Case Report | DOI: 10.82333/wzmk-wm06
Authors: Ana Miró Sánchez 1 , Sara Rodrigo Rey 2 , Behidy Héctor Díaz* 1
1Ophthalmology,Hospital General Universitario Dr. Balmis,Alicante,Spain, 2Cornea Unit, Ophthalmology,Hospital General Universitario Dr. Balmis,Alicante,Spain
Purpose
Reporting and Describing a Rare and Late Complication of Corneal Refractive Surgery, Along with Its Approach and Treatment.
Setting
Case report.
Report of case
A clinical case is presented of a 45-year-old male patient referred for a persistent corneal ulcer in the left eye, resistant to medical treatment after the removal of a foreign body. Regarding ophthalmologic history, the patient had amblyopia in the same eye and had undergone LASIK surgery and epikeratophakia in 1999.
On examination, visual acuity (VA) was 0.05. Biomicroscopy revealed a peripheral LASIK flap and a central epikeratophakia of approximately 5 mm, along with superficial flap necrosis in the superior paracentral area, about 3 mm in size. OCT-SA supported these findings.
Given this situation, it was decided to explant the intrastromal implant through the flap, achieving epithelialization of the defect. Subsequently, due to the resulting astigmatism, the patient was offered the adaptation of rigid gas permeable (RGP) contact lenses, with which a VA of 0.7 with a pinhole was achieved. However, the patient did not tolerate their use, so it was decided to perform a deep anterior lamellar keratoplasty (DALK), which had to be converted to a penetrating keratoplasty (PKP) due to an intraoperative perforation.
Currently, the patient has a VA of 0.2 and remains stable.
Conclusion/Take home message
This clinical case demonstrates a late complication of epikeratophakia, a refractive surgery technique that has been replaced by more advanced and safer procedures. The necrosis of the flap with persistent ulceration is likely a result of an alteration in corneal homeostasis and structural changes in the underlying basal lamina, Bowman’s layer, and stroma, caused by the intrastromal lenticule, which prevented proper epithelial regeneration and favored the persistence of the defect. The extraction of this lenticule halted the ulcerative process and allowed reepithelialization.