Cystoid macular edema (CME) is the leading cause of visual loss in patients with uveitis; however, development of a full-thickness macular hole in this setting is rare. We report a post-uveitis macular hole, which persisted after vitrectomy, but was successfully closed with periocular corticosteroid injection.
A 43-year-old lady presented with blurring of vision for several months; best-corrected visual acuity (BCVA) was 20/40 in right eye (RE) and 20/30 in left eye (LE). Past ocular and systemic history was unremarkable. On examination, anterior segment was quiet in right eye; LE showed iridolenticular synechiae. Fundus examination revealed 2+ vitreous cells, pars plana exudates suggestive of intermediate uveitis, and macular edema in both eyes (BE). Optical coherence tomography (OCT) revealed serous detachment rather than edema at macula in BE [Figs. 1a and b]. Physician examination and laboratory investigations revealed no evidence of any systemic infective or rheumatic inflammatory disease affecting skin, joints or organ systems. She was started on oral prednisolone (1mg/kg/day). Re-evaluation two months later showed resolved uveitis and total posterior vitreous detachment (PVD) in BE. However, BCVA had declined to 20/160 in RE, with a full-thickness macular hole [Figs. 1c and d]; LE showed resolved macular detachment with visual recovery to 20/20. With informed consent of the patient, vitrectomy with internal limiting membrane peeling and sulphur hexafluoride 20% tamponade was performed in RE. Postoperatively, the macular hole flattened marginally, but remained open [Fig. 1e]. When no change occurred in macular contours over the next two months, triamcinolone acetonide (40 mg/mL) was injected by posterior sub-Tenon's route in RE, with a course of topical corticosteroids. One week postinjection, BCVA improved to 20/60, with closure of the macular hole [Fig. 1f]. Ten months later, macular hole remained closed with no recurrence of edema/detachment [Figs. 1g and 1h].
Since macular hole is a rare sequel to intraocular inflammation, its pathogenesis is speculative: de-roofing of CME, inflammation-induced PVD, or traction by vitreous membranes.[2–6] Macular edema probably has significant role in formation as well as reopening of macular hole. We are aware of only one report in the literature describing non-surgical closure of a uveitic macular hole with periocular corticosteroids. Unlike that case, uveitis had already resolved in our patient when we observed a macular hole along with PVD, prompting the surgical decision. Others too have described macular hole formation after resolution of uveitis with concomitant vitreomacular separation. The macular hole in our patient remained open despite the relief of vitreomacular traction. The possibility of delayed spontaneous closure of macular hole could not be ruled out, but was remote in our case. Anti-inflammatory pharmacotherapy successfully closed a surgically refractory macular hole. Bhatnagar et al., reported re-opening of a postvitrectomy macular hole in the presence of CME, and suggested preventive aggressive treatment with corticosteroids. Our experience suggests that there still remains hope for successfully closing a persisting or re-opened macular hole with anti-inflammatory measures, especially in a background of uveitis.
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