Ocular Hypertension After Phakic Intraocular Collamer Lens Implantation: The Lens Is Not Always To Blame
Published 2026 - 44th Congress of the ESCRS
Reference: CC02.13 | Type: Case Report | DOI: 10.82333/3xkr-hv63
Authors: Dr Clara Heredia-Pastor* 1 , Javier García-Bardera 1 , Pilar Pérez-García 1 , Laura Morales-Fernández 1 , Julián García-Feijoo 1
1Glaucoma,Hospital Clínico San Carlos,Madrid,Spain
Purpose
To report the case of a patient who underwent bilateral Intraocular Collamer Lens (ICL) implantation and developed ocular hypertension (OHT) refractory to medical treatment, in whom secondary glaucoma due to pigment dispersion or angle closure was ruled out. Adequate ICL positioning (vault and angle configuration) allowed glaucoma surgery to be performed without lens explantation, achieving good intraocular pressure (IOP) control.
Setting
ICL implantation is widely used to correct high myopia. Reported complications include elevated IOP, which is most commonly attributed to mechanisms such as angle closure, pigment dispersion, or pupillary block. In such cases, ICL explantation may be considered. However, not all cases of OHT are related to lens-induced anatomical alterations. This case highlights the importance of a detailed anatomical evaluation of the anterior segment before making surgical decisions.
Report of case
A 36-year-old man with high myopia (−8.00 −1.00 × 50° OD; −8.00 −1.00 × 115° OS) underwent bilateral phakic ICL implantation. Fourteen months later, ocular hypertension was detected (IOP ~24 mmHg), and latanoprost was started OU. Control was poor, especially OS, with intolerance to dorzolamide and latanoprost–netarsudil. After two years of medical therapy, SLT was performed OS without effect, and he was referred to our center.
At presentation, BCVA was 0.0 LogMAR OU. Central corneal thickness was 529 µm OD and 532 µm OS. Endothelial cell density was 2322 cells/mm² OD and 2291 cells/mm² OS. Visual fields and optic nerve OCT were normal (RNFL 96 µm OD, 95 µm OS).
Slit-lamp examination showed pigment on the ICL surface OU, without iris transillumination defects or significant trabecular pigmentation. IOP was 20 mmHg OD and 29 mmHg OS despite latanoprost OU and brinzolamide–brimonidine OS.
AS-OCT demonstrated a wide-open angle, adequate vault, flat iris, and no significant irido-lenticular contact, excluding an ICL-related mechanism.
Preserflo MicroShunt implantation was performed OS without ICL explantation. Surgery was uneventful, with 0.04% mitomycin C applied for three minutes.
Postoperatively, a functional bleb formed with sustained IOP reduction. At two months, IOP OS was 8–9 mmHg, with stable OCT and visual fields. In the right eye, intensified topical therapy reduced IOP from 22 to ~13 mmHg, and surgery was not planned.
Conclusion/Take home message
In patients with ocular hypertension and phakic ICLs, elevated IOP should not be automatically attributed to pigment dispersion or ICL-induced angle closure. Careful evaluation of the anterior segment is essential to identify the underlying pathophysiological mechanism and guide appropriate management.
The use of anterior segment OCT allows objective exclusion of an ICL-induced angle mechanism, thereby avoiding unnecessary lens explantation in patients with a good refractive outcome after ICL implantation.