Culprit and cure: Spontaneous closure of an inflammation-induced macular hole

A 59-year-old female presented with blurring of vision in OS for 1 year. She had been diagnosed to have intermediate uveitis due to sarcoidosis and received two doses of posterior subtenon injection of triamcinolone. On presentation to us, the best corrected visual acuity (BCVA) was 6/7.5 in OD and 2/60 in OS. Anterior segment examination revealed occasional cells and flare 1+ in and cells in anterior vitreous bilaterally. Fundus examination showed media haze due to vitritis [Fig. 1a and b], hyperemic disc, macular edema (CME) in OU with full thickness macular hole (MH) with a base diameter of 1023 µm, apex diameter 179 µm, and hole height 570 µm was observed in OS [Fig. 1b] by optical coherence tomography (OCT) [Fig. 1c]. Investigations showed alarmingly poor glycemic control. Intravitreal dexamethasone implant was administered in the left eye, and oral methotrexate (15 mg/week) was initiated. After 2 months, the visual acuity in OD improved to 6/6 and OS to 6/60 with improvement in inflammation in OU. Macular edema in OD resolved, while OS showed gradual anatomical improvement in OCT [Fig. 1d]. At 5 months, the MH had closed [Fig. 1e] and BCVA improved to 6/18. There was complete resolution of inflammation with immunosuppression, and oral methotrexate was continued. OCT at 10 months showing closure of hole with loss of ellipsoid zone layer and external limiting membrane [Fig. 1f].Figure 1: (a, b): Fundus photograph of right eye showing normal disc with cystic macula and left eye showing macular hole at presentation. (c): Left eye OCT at presentation showing full thickness macular hole with cystoid macular edema. (d): OCT at 2 months showing approximation of inner retinal layers with inner retinal cystic spaces. (e): OCT at 3 months showing inner layer closure with persistent outer layer defect. (f): OCT at 10 months showing closure of hole with loss of ellipsoid zone layer and external limiting membraneDiscussion The index case highlights that clinicians should exercise caution when managing MH in uveitis patients as those secondary to inflammatory CME may not always require surgical intervention.[1] The retinal thickening and increased volume caused by CME, which brings the edges of the MH closer together, result in closure due to primary intention. This proximity may facilitate the natural formation of a tissue “bridge” (often via glial or Müller cell proliferation) across the defect, allowing MH to close without surgical intervention.[2] According to a study by Wang et al., holes under 200 µm size have a substantial chance of MH closure with medical therapy. In the absence of anteroposterior traction, macular dehydration occurs and hole edges reoppose.[3,4] Authors’ contributions Dr. RK prepared the draft, Dr. SP collected the data, and images Dr. PDM was involved in patient management, provided additional inputs and finalized the manuscript. All the authors reviewed the final manuscript. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published, and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship: Nil. Conflicts of interest: There are no conflicts of interest.