A case report of central toxic keratopathy in a patient post TransPRK (followed by corneal collagen cross-linking)
| Autor: | Ioannis M Aslanides, Nicholas Davey, Vasilis D Selimis |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
medicine.medical_specialty
Keratoconus Stromal cell laser refractive surgery complications genetic structures PRK medicine.medical_treatment Corneal collagen cross-linking Case Report 03 medical and health sciences 0302 clinical medicine Ophthalmology Refractive surgery medicine Corneal Haze business.industry Proteolytic enzymes TransPRK General Medicine medicine.disease eye diseases Photorefractive keratectomy central toxic keratopathy Surgery Contact lens 030221 ophthalmology & optometry sense organs business 030217 neurology & neurosurgery |
| Zdroj: | International Medical Case Reports Journal |
| ISSN: | 1179-142X |
| DOI: | 10.2147/imcrj.s123327 |
| Popis: | Purpose The purpose of this article is to report a case of central toxic keratopathy in a patient post transepithelial photorefractive keratectomy (TransPRK), followed immediately by corneal collagen cross-linking. Methods This article describes the case of a 26-year-old male after bilateral aberration-free, TransPRK laser (Schwind Amaris 750S). The procedure was performed for compound myopic astigmatism in November 2015, followed immediately by accelerated corneal collagen cross-linking for early keratoconus. Results From day 3 post-op, tear film debris underneath both contact lenses with corneal haze and early, progressive central anterior stromal opacity formation only in the left eye were noted. At 2 weeks post-op, the left eye was noted to have a significant hyperopic shift with central corneal thinning in the anterior stroma. A central anterior stromal dense opacity had formed in the left eye with the surrounding superficial stromal haze. As of month 2, the opacity gradually started to improve in size and density. The hyperopic shift peaked at 2 months and continued to improve, largely due to epithelial compensation with a gradual recovery of stromal thickness. Conclusion The question remains as to what provokes the typical central corneal necrosis/thinning in central toxic keratopathy. We hypothesize that the space between the contact lens and the corneal surface post TransPRK is prone to a "pseudo-interface pathology" that could mimic diffuse lamellar keratitis-like pathology. Suboptimal lid hygiene, resulting in tear film combinations of bacteria, inflammatory cells, matrix metalloproteinases and other proteolytic enzymes, contributes to the degradation of vulnerable, exposed collagen stromal tissue post TransPRK or any surface corneal ablation. Refractive surgeons should maintain a healthy lid margin and tear film, especially in contact lens wearers, to prevent potential complications in refractive surgery procedures. |
| Databáze: | OpenAIRE |
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