EFFECTIVENESS OF THE INTRAVITREAL DEXAMETHASONE IMPLANT IN THE MANAGEMENT OF REFRACTORY UVEITIC MACULAR OEDEMA: A SYSTEMATIC REVIEW OF RANDOMISED CONTROLLED TRIALS AND PRIMARY STUDIES

Abstract

Introduction. Macular oedema is the single most important structural cause of irreversible central visual loss in non-infectious uveitis, and a substantial proportion of eyes remain oedematous despite topical, periocular, systemic corticosteroid, immunomodulatory, or anti-VEGF therapy. The biodegradable 0.7 mg intravitreal dexamethasone implant (Ozurdex®) delivers sustained intravitreal corticosteroid over approximately six months and has become a widely used option for refractory disease, yet the magnitude, durability, and safety of its effect specifically in refractory uveitic macular oedema have never been quantified across the entire primary evidence base.

Methods. The study strictly adhered to the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) 2020 guidelines. Eligible: RCTs, prospective and retrospective cohorts, case-control, cross-sectional, and observational interventional series with ≥5 eyes. Risk of bias assessed with RoB 2 and ROBINS-I; GRADE for certainty.

Results. Thirty-five reports from 33 independent study populations comprising 1,871 eyes. Central macular thickness fell by −156.8 µm at month 1 (95%CI −184.9 to −128.7; P<0.0001; I²=74.8%), −146.2 µm at month 3, and −101.1 µm at month 6. Best-corrected visual acuity improved by 0.160 logMAR at month 1 (95%CI −0.195 to −0.125; P<0.0001; I²=0%), 0.186 logMAR at month 3, and 0.141 logMAR at month 6, equivalent to gains of 8, 9, and 7 ETDRS letters. Complete resolution of macular oedema was achieved in 79.0% (95%CI 65.9–89.8), a gain of ≥15 letters in 33.8% (95%CI 25.7–42.3), and vitreous haze score of 0 in 72.2% (95%CI 56.0–86.0). In the sham-controlled RCT, DEX-I quadrupled vitreous clearing (RR 3.95; 95%CI 2.04–7.62) and more than trebled 15-letter gain (RR 3.26; 95%CI 1.73–6.13). Median time to recurrence clustered between 6 and 9 months and 49.1% of eyes (95%CI 37.6–60.6) required re-implantation within six months. Clinically significant IOP elevation occurred in 20.7% (95%CI 14.4–27.7) and cataract progression in 23.0% of phakic eyes (95%CI 12.5–35.4); glaucoma surgery (≈1.1%) and endophthalmitis (0.11%) were rare. Meta-regression showed greater baseline CMT predicted larger absolute reduction (β=−0.71 µm per µm; R²=68.2%; P=0.006). An exploratory multivariable prognostic model achieved AUC 0.734.

Discussion. The pooled effect sizes confirm that a single dexamethasone implant reverses the great majority of retinal thickening in refractory uveitic macular oedema within one month, with maximal anatomical and functional benefit between months 1–3, and approximately one third lost by month 6—consistent with the six-month pharmacokinetic profile of PLGA matrix degradation. Heterogeneity was substantial for anatomical but negligible for functional outcomes, indicating variability lies principally in baseline oedema severity.

Conclusion. In refractory uveitic macular oedema, the 0.7 mg intravitreal dexamethasone implant produces clinically substantial improvement in macular thickness, visual acuity, and intraocular inflammation with a predictable and manageable safety profile. Because approximately half of treated eyes recur within six months, DEX-I should be planned as a repeatable component of a structured long-term strategy, with pre-emptive re-treatment around month 4–5, mandatory IOP surveillance, and consideration of a longer-acting fluocinolone acetonide implant in eyes with repeated early recurrence.