Management Of Irvine- Gass Syndrome Following Cataract Surgery

Irvine-Gass Syndrome (Cystoid Macular Edema) is one of the common causes of vision loss in the postoperative period of cataract surgery. It can occur even after an uncomplicated surgical intervention. The mechanisms underlying the syndrome are not yet fully understood, and there are no universal guidelines for its management. The aim of this case report presentation is to present an effective treatment option for Irvine-Gass Syndrome.

Department of Ophthalmology, Yerevan Scientific Medical Center.
Professional and Continuing Education Center, Yerevan State Medical University after Mkhitar Heratsi.

A 58-year-old Caucasian male was admitted to the hospital complaining of a gradual decrease in vision in both eyes. At the time of presentation, VA was OU=0.1 and IOP was 14mmHg. Clinical and instrumental exams revealed OU-age-related nuclear cataract, nuclear grade 2-3. There were no associated systemic or ocular diseases. The Amsler test was negative. On 08.02.2024, the patient underwent surgery on the left eye Phaco with posterior chamber IOL implantation. The surgery and postoperative period were uneventful. Postoperatively, VA was OS=0.9 ph=1.0 on day 1 and OS=1.0 at discharge, with preserved ophthalmoscopic macular reflex and no edema. P (iCare) was 13 mmHg. Postoperative treatment was administered according to guidelines. Two months later, the patient complained of gradual vision loss in the left eye. VA was OS=0.1, and P₀=12mmHg. Examination showed an unchanged anterior segment and an in-position IOL but macular edema was detected. OCT of the macula revealed significant retinal edema (567 microns) with intraretinal fluid. The patient was diagnosed with Irvine-Gass syndrome. Treatment with topical NSAID (nepafenac 3 times a day for 3 months) and carbonic anhydrase inhibitor (dorzolamide 2 times a day for 3 months) was prescribed. After 2 weeks, VA improved to OS=0.3; after 1.5 months, OS=0.6; and after 3 months, OS=1.0. OCT showed a reduction in macular thickness to 308 µm in 1.5 months and 221 µm in 3 months. Throughout follow-up, IOP remained stable at 12-14 mmHg.

We believe the combination of NSAIDs and topical CAIs in our clinical case gave a positive result. In the prescribed treatment regimen, NSAIDs inhibit the COX enzyme, which promotes prostaglandin production, thereby blocking the arachidonic acid cascade. CAIs enhance the cellular pump function, facilitate fluid outflow from the retina, and improve perfusion and oxygenation. As a result of combined treatment, visual acuity was restored due to the resolution of macular edema.Considering this case, we suggest this treatment approach for managing Irvine-Gass Syndrome. However, to further clarification of the pathophysiological mechanisms of above-mentioned syndrome, detailed cellular and subcellular studies should be conducted.