Pathophysiology of Secondary Macular Hole in Rhegmatogenous Retinal Detachment

To describe the pathophysiology of secondary macular hole (MH) in rhegmatogenous retinal detachment (RRD).

A retrospective cohort of 360 consecutive primary fovea-off RRDs presenting to St. Michael's Hospital, Toronto, from January 2012 to September 2022 were included. Preoperative OCT was assessed for bacillary layer detachment (BALAD) abnormalities. Histological sections of normal eyes were assessed to inform OCT interpretations. Primary outcome measure was the progression of BALAD to full-thickness MH (FTMH).

Of the 360 patients, 22.5% (n = 81) had BALAD abnormalities at presentation. Eight percent (29/360) had associated MH, of which 79.3% (23/29) were a BALAD-lamellar hole and 20.7% (6/29) were FTMH. After reattachment, 62% of MHs persisted (18/29), of which 83% (15/18) had BALAD-lamellar holes that subsequently progressed to FTMH in a mean of 8.1 ± 3.2 days. BALAD-lamellar holes had significantly worse postoperative visual acuity (P < 0.001) when compared with other BALAD abnormalities (58/81) or with the rest of the cohort (279/360). OCT spectrum from BALAD to FTMH includes (1) cleavage planes extending from Henle fiber layer into the BALAD; (2) central outer nuclear layer thinning; (3) Müller cell cone loss with tissue remnants at the foveal walls; (4) retinal tissue operculum close to BALAD-MH; and (5) progressive thinning or degradation of the posterior band of BALAD-lamellar hole leading to FTMH. Histological specimens identified foveal regions of low mechanical stability.

BALAD plays a crucial role in the pathophysiology of MH in RRDs, which forms owing to sequential changes in four critical areas: RPE-photoreceptor interface, myoid zone, Henle fiber layer, and Müller cell cone with surrounding tissue. Timely management of fovea-off RRD with BALAD may be prudent to avoid the progression to BALAD-lamellar hole, subsequent FTMH, and worse functional outcomes.