Latanoprost-induced cystoid macular oedema (CMO) is well documented, and stopping the drops before or after cataract surgery has been used to reduce this risk.1 What is not clear is whether cataract surgery can increase the risk of prostaglandin-induced CMO, following recovery from cataract surgery. In this context, we report a case of latanoprost-induced CMO developing 30 months after an uneventful cataract surgery.

Case report

An 83-year-old male patient with primary open-angle glaucoma on latanoprost (0.005%) and brinzolamide (1%) eye drops in both eyes underwent phacoemulsification with posterior chamber intraocular lens implanted in the left eye and achieved best-corrected visual acuity of 6/6. Latanoprost eye drops were continued before and after the surgery. After 3 months, the visual acuity in the operated eye dropped to 6/18 and cystoid macular oedema (CMO) was seen clinically. He was in good general health and did not suffer from diabetes mellitus. Latanoprost drops were immediately withdrawn and subtenon's triamcinolone injection was administered. The CMO resolved and the visual acuity improved to 6/9. After 4 months, a trabeculectomy with mitomycin-C (0.4 mg/ml) was carried out in the same eye. The postoperative course was uneventful, and all the antiglaucoma medications in that eye were stopped. After 5 months, needling of the bleb with 5-fluorouracil (5 mg/0.1 ml) was performed. The IOP remained high and the patient was instructed to use brinzolamide eye drops in both eyes and latanoprost eye drops in the right, nonoperated, eye.

Thirty months after the cataract surgery, the patient noticed reduction of visual acuity in the left eye (6/36 now), and CMO was diagnosed that was confirmed on optical coherence tomography (Figure 1). The patient admitted using latanoprost eye drops in both eyes in the preceding 1 month because of an error in the repeat prescription issued by the General Practitioner. Latanoprost eye drops were stopped immediately in the left eye and a repeat posterior subtenon's triamcinolone was given. After 1 week, the CMO started to resolve (Figure 2) and the visual acuity improved to 6/9 over the next 1 month.

Figure 1
figure 1

Optical coherence tomography showing gross CMO.

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Figure 2
figure 2

Reduction in CMO after latanoprost withdrawl.

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Comment

Many antiglaucoma drops have been shown to cause CMO, especially in aphakic and pseudophakic eyes. Latanoprost-associated CMO in pseudophakic patients is thought to occur because of breakdown of the blood–retinal barrier (BRB).

In a retrospective review of 145 patients after an uneventful cataract surgery with lens implant, CMO was identified in four (3%) cases using latanoprost.2 None of the patients who were taken off the latanoprost before surgery developed postoperative CMO in this cohort. Miyake and Nobuhiro3 reported that latanoprost affects the wound healing process of lens epithelial cells, resulting in the biosynthesis of prostaglandins and other mediators that eventually lead to angiographic CMO. Another study by Miyake et al4 suggested that the main cause of CMO induced by various eye drops was the added preservative, benzalkonium chloride. The preservative is thought to cause CMO in the same way as the eye drops themselves do.

Rowe et al5 reported an eye that had undergone uneventful phacoemulsification and developed CMO at an early postoperative stage, and then 1 year after topical latanoprost application. Watanabe et al6 reported a case in which latanoprost use induced CMO 5 years after a complicated phacoemulsification, suggesting that blood–ocular barrier remains fragile.

Our case developed CMO 30 months after an uneventful phacoemulsification. The role of a later trabeculectomy and needling in keeping the BRB fragile is not known and this may have contributed to the development of CMO after a later challenge with latanoprost. Our case raises the possibility that CMO can be induced even many months after the surgery and this possibility should be considered in the management of these patients.