DELAYED POST-CATARACT EXTRACTION ANTERIOR ISCHAEMIC OPTIC NEUROPATHY IN A PRIMARY OPEN ANGLE GLAUCOMA PATIENT, WITH SEVERELY ELEVATED REFRACTORY EYE PRESSURE FOLLOWING ROUTINE CATARACT EXTRACTION

To present a case of delayed post-cataract extraction anterior ischaemic optic neuropathy in a primary open angle glaucoma (POAG) patient, with severely elevated refractory intraocular pressure (IOP) following routine cataract extraction.

James Paget University Hospital NHS Foundation Trust, United Kingdom

Retrospective case report

A 78-year-old Caucasian male was seen in clinic in January 2024, two weeks after uncomplicated right eye (RE) cataract surgery with an IOP of 40mmHg, and a visual acuity (VA) of 6/20 unaided and 6/15 with pinhole. He was known to have bilateral POAG on Lumigan, Alphagan, and Cosopt. His past ophthalmic history included bilateral Selective Laser Trabeculoplasty as well as uneventful left cataract surgery in October 2023. His eye pressures were well controlled on four topical agents prior to the cataract surgery.

Following the RE post-phacoemulsification IOP rise he was started on Diamox and Iopidine, whilst post-operative Dexamethasone was stopped due to the suspected steroid response. A complex timeline of refractory elevated IOP ensued. By six weeks post-operatively, his RE VA was Counting Fingers (CF) and IOP was 56mmHg. He was urgently referred and reviewed by a glaucoma consultant on the same day; the impression was of optic nerve oedema on a cupped disc.

He underwent urgent RE trans-scleral Cyclodiode laser two days later, with a pre-procedure vision of Hand Movements (HM) and IOP of 60mmg despite maximum tolerated treatment. The laser procedure itself was uncomplicated. Post-cyclodiode, his RE IOP initially improved but rose again within six weeks on maximal treatment (five agents including Diamox).

Five weeks following this, he subsequently had a RE PAUL glaucoma implant inserted with scleral application of Mitomycin C. Pre-operatively, IOP had reached 55mmHg. VA day one post-operatively remained as HM, but IOP reduced to 14mmHg without IOP-lowering agents.

His IOP continued to fluctuate, and regular review with alterations to his glaucoma medication, and removal of the stent, proved crucial. He had uncomplicated removal of the stent four months after the PAUL implant. In his most recent review in October 2024 (ten months post-RE cataract surgery), RE VA was CF and IOP was 13mmHg on two agents. He remains under frequent follow-up.

A post-cataract surgery rise in IOP is not uncommon and can be due to many factors including a steroid response. However, patients with known glaucomatous optic neuropathy are particularly vulnerable to an increase in IOP, which could lead to superimposed ischaemic optic neuropathy and irreversible visual loss. Unfortunately, visual outcomes in the RE for this patient have remained poor. This case emphasizes the importance of stringent IOP control post-operatively.