Cystoid Macular Edema

Cystoid macular edema (CME) is the accumulation of fluid within the outer plexiform and inner nuclear layers of the macula, producing a characteristic petaloid pattern on OCT and fluorescein angiography. Pseudophakic CME (Irvine-Gass syndrome) — occurring after cataract surgery — is the most common cause of suboptimal vision after an otherwise uncomplicated procedure. The pathophysiology involves prostaglandin-mediated breakdown of the blood-retinal barrier. Topical NSAIDs and corticosteroids are the primary treatment; most cases resolve within 3–6 months with appropriate therapy. Chronic or refractory CME may require intravitreal anti-VEGF or corticosteroid injection.

Clinical pseudophakic CME (visually significant, symptomatic) occurs in approximately 1–2% of uncomplicated cataract surgeries. Angiographic CME (detectable on FA without significant visual symptoms) occurs in up to 20%. Risk is significantly higher with surgical complications (vitreous loss, iris trauma, retained lens fragments) and in patients with pre-existing risk factors (uveitis, diabetic retinopathy, epiretinal membrane, prior CME).

The dominant mechanism in pseudophakic CME is prostaglandin-mediated breakdown of the inner blood-retinal barrier (BRB). Surgical trauma to the iris and ciliary body releases arachidonic acid, which is metabolized via the cyclooxygenase (COX) pathway to prostaglandins. Prostaglandins increase vascular permeability of the perifoveal capillaries, causing fluid accumulation in the outer plexiform and inner nuclear layers. The radial arrangement of Henle's fiber layer in the outer plexiform layer produces the characteristic petaloid pattern. VEGF also contributes to BRB breakdown, particularly in diabetic and vascular CME.

Reduced visual acuity — typically presenting 4–12 weeks after cataract surgery (the classic window for Irvine-Gass syndrome). Metamorphopsia. The patient may describe vision as "blurry" or "wavy" despite an otherwise successful surgery. Fundoscopy: subtle macular thickening — often not visible without OCT. OCT: petaloid cystic spaces in the outer plexiform and inner nuclear layers with foveal thickening. FA: petaloid hyperfluorescence with late leakage at the fovea (the gold standard for diagnosis but rarely required when OCT is available).

First-line: topical NSAID (ketorolac, bromfenac, nepafenac) + topical corticosteroid (prednisolone acetate 1%, loteprednol 0.5%) — combination therapy is more effective than either agent alone. Duration: typically 4–8 weeks, with taper guided by OCT response. Discontinue prostaglandin analogues if present. Refractory CME (persistent > 3 months despite topical therapy): sub-Tenon's triamcinolone acetonide injection; intravitreal anti-VEGF (bevacizumab, ranibizumab); intravitreal triamcinolone; dexamethasone implant (Ozurdex). Surgical: pars plana vitrectomy for CME associated with vitreous incarceration in the wound.

OCT macula at every visit during active treatment — macular central subfield thickness (CST) is the primary endpoint. BCVA at every visit. Taper topical therapy based on OCT resolution, not just visual acuity.