Iridocorneal contact as a potential cause of corneal decompensation following laser peripheral iridotomy

This study aimed to investigate the relationship between corneal decompensation following laser peripheral iridotomy (LPI) and iridocorneal endothelial contact.

Retrospective observational case series.

Specular microscopy images of LPI recipients with narrow angles were taken at the central cornea and the 8 midperipheral corneal regions at approximately 3 mm from the center. Eleven eyes of 11 patients had a minimum of  ≤ 1600 cells/mm² among 8 midperipheral corneal endothelial cell densities (ECDs). Radial scans of the angles in the 8 directions were taken with ultrasound biomicroscopy (UBM) in the supine and face-down positions. The minimum and maximum angle opening distance at 750 μm from the scleral spur of the 8 directions were defined as the narrowest and widest angles, respectively. The ECD of the narrowest angle direction was compared with the ECD of the widest angle direction.

When UBM was performed with the subject in the supine position, the iris and cornea at the narrowest angle were in contact in only 4 of 11 eyes, while in the face-down position, the iris and the cornea at the narrowest angle were in contact in 10 of the 11 eyes. In the face-down UBM, the midperipheral ECD of the narrowest angle direction was significantly smaller than the midperipheral ECD of the widest angle direction (P = 0.006).

The ECD of the narrow angle direction can decrease after LPI. This suggests that corneal endothelial cell damage following LPI may be due to mechanical damage from iridocorneal endothelial contact.