Alterations of the vitreous pathology and anterior chamber angle structures following transscleral cyclophotocoagulation

To describe the alterations of the vitreous pathology and anterior chamber (AC) angle structures following transscleral cyclophotocoagulation (TSCP) and better understand the mechanism of post-laser intraocular pressure (IOP) reduction in angle-closure glaucoma (ACG).

Porcine eyes ex vivo and rabbit eyes in vivo were used. In porcine eyes, permeability rates of the anterior vitreous cortex (AVC) and anterior hyaloid membrane (AHM) were assessed using Schirmer’s strips. Permeability rates in the circumlental space were compared with or without TSCP bursts. Fluorescein diffusion times from the vitreous to the AC were compared between eyes with and without TSCP. In rabbit eyes, changes in IOP and AC angle structures under ultrasound biomicroscopy (UBM) were evaluated at intervals of 30min, 7d, and 14d after TSCP. Vitreous pathology was examined using scanning electron microscopy (SEM) immediately and 14d after TSCP.

In porcine eyes (n=20), the median (range) permeability rates were 10.3 (range 9.8–10.8) mm/min for the AVC and 4.3 (range 3.9–4.9) mm/min for the AHM (P=0.009). Permeability rates in the circumlental space were 4.2 (range 3.8–4.9) mm/min in areas without TSCP, 6.2 (range 5.7–6.8) mm/min in areas with non-burst TSCP, and 11.3 (range 10.9–11.8) mm/min in areas with burst TSCP (P=0.002). The median (range) fluorescein diffusion time was 5 (range 3–8)min in eyes undergoing TSCP, whereas it was 40min (range 35–68) in eyes without TSCP (P<0.001). In rabbit eyes (n=20), SEM showed immediate localized damage to the AHM, AVC, and posterior lens zonules in areas subjected to TSCP bursts, and obvious lens zonule loss with cellular infiltration and possible vitreous liquefaction by post-op day 14. Persistent widening of AC angles was noted at postoperative days 7 and 14, although a significant reduction in IOP was only observed at postoperative day 7.

TSCP-induced damage on the zonules, AHM, and AVC potentially enhances fluid outflow from the vitreous, leading to a widened AC angle and vitreous liquefaction in rabbits. These observations offer insights into mechanisms of TSCP in lowering IOP and pathogenic roles of vitreous in ACG.