Spontaneous development of cystoid macula edema in the ICE syndrome is rare. A literature review on ICE syndrome includes 87 references from 1978 to 2002 showed that there were no reports of association with macular or papillary edema. The common causes of cystoid macular edema include diabetic retinopathy, uveitis, post-surgery macular edema, vitreo-macular traction, and usage of prostaglandin analogues. None of the above-mentioned causes was found.
Fourmaux et al [4] have speculated the development of CME in ICE can be due to the abnormal contracture endothelial cells, which causing the breach of the inner blood-retinal barrier.
In our case, the patient’s macular edema has subsided in the subsequent examination. This can be due the effectiveness of the NSAIDs eyedrops in inhibiting the inflammatory process and thus treating macular edema. A similar finding was reported by Suzuki et al [3], where the CME resolved after the topical nepafenac 0.1% was used for 4 weeks. It was postulated that the prostaglandin-like material from the abnormal endothelial cells can possibly disturbed the inner blood-retinal barrier. The NSAIDs appeared effectively eliminated the macular edema.
A similar case was first reported by E. Fourmax of a 44-year-old woman who was treated with acetazolamide 325 mg/day. It was not successful and subsequently a subtenon injection of 40 mg triamcinolone in 2002. A rapid recovery and stabilization of macular was noted.[4]
However, in another case reported by Kocaoglan H et al, a similar condition was found in a 38-year-old woman and she was treated with topical prednisolone acetate 1% and ketorolac tromethamine 0.5% QID for 3 months, but the CME persisted. [5]
Both Nepafenac and Ketorolac belonged to the same group but they differ structurally and pharmacologically. Ketorolac is a not prodrug and it exerts its effect by inhibiting prostaglandin biosynthesis after it penetrates the cornea. Nepafenac, on the other hand, is a prodrug which is less polarized and penetrates the cornea easier. In the anterior chamber, it converts into Amfenac by intraocular hydrolases, and distribute rapidly to ciliary body, cornea, iris, retina and choroid. [6]
Furthermore, topical NSAIDs and topical steroids have become a standard preoperative treatment regimen for preventing CME. It appeared that topical NSAIDs is more effective in re-establishing the blood aqueous barrier, as quantitatively measured with anterior ocular fluorophotometry [7]. In a study by Miyake et al, Nepafenac was found to me more effective in preventing angiographic CME and blood aqueous barrier disruption.[8].
In reference to the above cases, we may conclude that Nepafenac 0.1% is more superior in treating cystoid macular edema in patients with iridocorneal endothelial syndrome.