Corneal edema caused by undiagnosed iridocorneal endothelial syndrome after SMILE

• Published in: Acta biomedica scientifica Vol. 8; no. 4; pp. 165 - 169
• Main Authors: Iureva, T. N., Pisarevskaya, O. V.
• Format: Journal Article
• Language: English
• Published: Scientific Сentre for Family Health and Human Reproduction Problems 04.10.2023
• Subjects: corneal edema; iridocorneal endothelial syndrome; keratorefractive surgery; postoperative complications
• ISSN: 2541-9420; 2587-9596
• DOI: 10.29413/ABS.2023-8.4.18

The aim . To present a clinical case of a patient with corneal edema caused by undiagnosed iridocorneal endothelial syndrome after SMILE surgery. Iridocorneal endothelial syndrome is characterized by abnormal proliferation of the corneal endothelium beyond the Schwalbe line, blockade of the iridocorneal angle, specific changes in the shape of the pupil and the formation of synechiae between adjacent structures of the anterior chamber angle of the eye, which is accompanied by the development of pretrabecular retention of intraocular aqueous humour, increased intraocular pressure (IOP) and subsequent development of glaucoma in 46–82 % of patients. One of the forms of the disease is Chandler’s syndrome, which clinically in the initial stages may be accompanied by the formation of only moderate ectropion. At the same time, endothelial dysfunction is characterized by a significant decrease in the number of cells, a change in their shape and the appearance of epithelioid cells with a hyper-reflective nucleus (the so-called “ICE (iridocorneal endothelial) cells”), with a violation of their natural pumping function. The article presents a clinical case of a patient who underwent a standard examination and symptomatic treatment after laser keratorefractive surgery for myopia correction. Low visual acuity, diffuse corneal edema, IOP decompensation of unclear genesis were observed in one operated eye. Conclusion . Keratorefractive operations can act as a trigger that stimulates the transition of the latent form into a clinically developed pathological process, which causes a decrease in corrected visual acuity due to the formation of corneal edema and glaucoma optic neuropathy.