Abstract
Purpose :
To explore the pathophysiology of secondary macular hole(MH) formation in rhegmatogenous retinal detachment(RRD) by assessing bacillary layer detachment(BALAD) and associated foveal abnormalities using optical coherence tomography(OCT).
Methods :
Single-centered retrospective cohort including 360 consecutive primary fovea-off RRDs referred to St. Michael’s Hospital, Toronto, between January 2012-September 2022. Pre-operative OCTs were assessed for BALAD and structural abnormalities of the fovea, including associated lamellar and full-thickness MH(FTMH).
Results :
22.5%(81/360) of patients had evidence of BALAD or associated abnormalities. 8%(29/360) had a MH associated with the RRD, of which 79.3%(23/29) were lamellar holes with only the posterior border of BALAD intact(BALAD-MH) and 20.6%(6/29) were FTMH. Immediately following reattachment, 62%(18/29) of MHs persisted and 38%(11/29) closed with RRD repair. Of those that persisted, 83%(15/18) had a BALAD-MH, all of which had subsequent loss of photoreceptor remnants in a mean of 8.1(±3.2SD) days, progressing to FTMH. A detailed analysis of OCT imaging demonstrated the spectrum of morphological changes from BALAD to FTMH (Figure 1). Salient features included (1)cleavage planes at Henle fiber layer(HFL)-outer plexiform interface extending into the BALAD cavity, between the Müller cell cone(MCC) and foveal walls; (2)significant thinning of central outer nuclear layer(ONL); (3)loss of MCC and residual medium reflectivity tissue remnants at the inner edges of the foveal walls; (4)retinal tissue operculum attached to vitreous strands in close proximity to BALAD-MH; and (5)progressive thinning/degradation of the posterior border of BALAD-MH leading to FTMH.
Conclusions :
BALAD is associated with MH formation in RRD, and likely plays a crucial role in its pathophysiology. This large retrospective study and previous histological data provide novel insights into the progression from BALAD to FTMH in RRD. Specific OCT morphological features suggest that cystic/cellular degeneration, hydration and tractional forces are key factors. This pathophysiological process occurs with sequential structural changes in three known areas of low mechanical stability in the fovea: RPE-photoreceptor interface, myoid zone, foveal wall HFL-MCC culminating in photoreceptor-MCC disjunction and subsequent degradation of photoreceptor remnants leading to FTMH.
This abstract was presented at the 2023 ARVO Annual Meeting, held in New Orleans, LA, April 23-27, 2023.