Prechoroidal Cleft in Type 3 Neovascularization: Incidence, Timing, and Its Association with Visual Outcome

Abstract

Purpose: To investigate the incidence and timing of prechoroidal cleft development and its association with visual prognosis in type 3 neovascularization.

Methods: This retrospective study included 166 eyes that were diagnosed with type 3 neovascularization. All eyes were treated with antivascular endothelial growth factor therapy. The incidence and timing of prechoroidal cleft development were evaluated. Best-corrected visual acuity (BCVA) at diagnosis and at final follow-up was compared between eyes with (cleft group) and without (no-cleft group) prechoroidal cleft. The incidence of retinal pigment epithelium (RPE) tear and subretinal hemorrhage was also compared between the two groups.

Results: During the mean 39.7 ± 18.5 months of follow-up, prechoroidal cleft developed in 37 eyes (22.3%) at an average of 14.6 ± 10.4 months. The BCVA at final follow-up was significantly worse in the cleft group than in the no-cleft group (P=0.024), whereas the difference was not significant at diagnosis (P=0.969). The incidence of RPE tear (P=0.002) and subretinal hemorrhage (P < 0.001) was significantly higher in the cleft group.

Conclusions: Prechoroidal cleft is a frequently observed finding during the treatment course of type 3 neovascularization. Eyes with prechoroidal cleft are at high risk of RPE tear or subretinal hemorrhage and subsequently associated with poor prognosis.

Figures

Figure 1

Representative images showing prechoroidal cleft (arrowheads), which developed during the treatment course of type 3 neovascularization. Note that the subretinal pigment epithelial tissue attaches to the Bruch's membrane at the edge of the cleft (arrows).

Figure 2

A Kaplan–Meier graph showing the cumulative incidence of prechoroidal cleft.

Figure 3

Fundus photography (a, e), indocyanine green angiography (b), and optical coherence tomography (c, d, f) images of a patient diagnosed with type 3 neovascularization. The images were taken at diagnosis (a–c), at 29 months (d), and at 35 months (e, f). The patient was treated with antivascular endothelial growth factor monotherapy during the follow-up period. Development of prechoroidal cleft was identified at 29 months (d) (arrowheads). Six months later, retinal pigment epithelium tear developed (e, f, arrows). Sixteen antivascular endothelial growth factor injections were performed during the follow-up period.

Figure 4

Fundus photography (a, f), indocyanine green angiography (b), and optical coherence tomography (c, d, e) images of a patient diagnosed with type 3 neovascularization. The images were taken at diagnosis (a–c), at 3 months (d), at 16 months (e), and at 17 months (f). After 3 monthly antivascular endothelial growth factor injections, the fluid was completely resolved (d). The patient was treated with anti-VEGF monotherapy during the follow-up period. Development of prechoroidal cleft was identified at 16 months (e) (arrowheads). One month later, subretinal hemorrhage developed (f). Nine antivascular endothelial growth factor injections were performed during the follow-up period.

Figure 5

A schematic drawing showing the postulated developmental mechanism of prechoroidal cleft. (a) The subretinal pigment epithelial (RPE) fibrovascular tissue (asterisk) and Bruch's membrane may not attach or may be only weakly attached in some regions (arrowheads). However, around these regions, the two tissues attach firmly (arrows). (b) When sub-RPE tissue becomes contracted or leaks, prechoroidal cleft develops in the area of weak adhesion between tissues. The firmly attached area impedes further extension of the cleft.

Figure 6

A schematic drawing showing the postulated developmental mechanism of subretinal hemorrhage in eyes with prechoroidal cleft. (a) The subretinal pigment epithelial (RPE) fibrovascular tissue (asterisk) firmly attaches to the Bruch's membrane in some regions (black arrows). In these regions, new vessels in the fibrovascular tissue may also firmly attach to the Bruch's membrane (red circles). (b) Strong sub-RPE tissue contraction or high-pressure exudation from the tissue (blue arrows) makes a force separating the sub-RPE tissue from the Bruch's membrane, resulting in rupture of vasculature, sub-RPE hemorrhage (area filled with red dots), and subretinal hemorrhage (area filled with light red).