Late Occlusion of Ciliary Sulcus-placed Ahmed Glaucoma Valve by Proliferative Lens Epithelial Cells: A Case Report

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Dear Editor,

Ahmed glaucoma valve (AGV; New World Medical) implantation is effective in refractive glaucoma, such as uveitic or neovascular glaucoma. However, there is a risk of corneal decompensation associated with a tube in the anterior chamber (AC) [1]. Accordingly, placing the tube in the ciliary sulcus (CS) rather than in the AC in patients with pseudophakic and aphakic eyes has been introduced to prevent corneal decompensation [2].

Besides cornea-related complications, glaucoma drainage device (GDD) implantation can cause tube-related intraocular complications, such as pupil distortion, tube migration, and tube occlusion [3]. Tube occlusion can be caused by iris, fibrovascular membrane, vitreous, silicone oil, fibrin, blood clots, pigmentary debris, or lens capsules [3,4] and occurs mostly in the early postoperative period [5]. Herein, we present a case of late occlusion of an AGV tube placed in the CS by an Elschnig pearl-like mass above the anterior lens capsulotomy. Written informed consent for publication of the research details and clinical images was obtained from the patient.

A 49-year-old Korean man presented with a 2-month history of decreased vision in both eyes. His medical history included only diabetes mellitus. He had a history of uncomplicated phacoemulsification and posterior chamber intraocular lens implantation in the right eye 1 year earlier. His visual acuity was counting fingers at 20 cm in both eyes, and intraocular pressure (IOP) was 46 mmHg in the right eye and 16 mmHg in the left eye. Rubeosis iridis and dense vitreous hemorrhage secondary to proliferative diabetic retinopathy were present in both eyes. He had received intravitreal anti–vascular endothelial growth factor (anti-VEGF) injections (bevacizumab) for both eyes. Despite monthly intravitreal anti-VEGF injections and maximum tolerated medical therapy (bimatoprost, brimonidine–timolol fixed combination, and oral acetazolamide), IOP of the right eye was not controlled. Therefore, an AGV was implanted in the superotemporal quadrant with the tube’s bevel-down end in the CS. Thereafter, IOP was maintained in the mid-teens on the brimonidine–timolol fixed combination.

Four years after AGV implantation, IOP increased to 36.2 mmHg in the right eye. Slit-lamp examination revealed an Elschnig pearl-like mass just below the main incision of the previous cataract surgery and above the anterior capsulotomy, with decreased bleb height. Despite bleb needling, IOP remained high (34.8 mmHg) without change in the bleb height even after applying strong pressure to the eyeball. The mass apparently occluded the CS-placed tip of the AGV (Fig. 1A). Nd:YAG laser to disrupt the mass was unsuccessful. Then, the mass was removed via bimanual vitrectomy through two corneal incisions using a 23-gauge vitrector; an iris retractor was used to expose the CS-placed tip of the AGV tube. On postoperative day 1, IOP was 17.0 mmHg, with an elevated bleb. Slit-lamp examination showed that the AGV tip was fully visible and open (Fig. 1B). One year postoperatively, IOP was controlled with latanoprost and brimonidine–timolol fixed combination.

Fig. 1

Slit-lamp photography of the right eye. (A) An Elschnig pearl-like mass (arrow) blocks the tip of the Ahmed glaucoma valve. (B) The clearly visible tip of the Ahmed glaucoma valve (circle) after successful removal of the mass.

Occlusion of the GDD tubes usually occurs early in the postoperative period and results in IOP elevation. It might be caused by iris, fibrovascular membrane, vitreous, silicone oil, fibrin, blood clots, pigmentary debris, or lens capsule, regardless of the tip positions such as the AC, CS, or vitreous cavity [3,4]. Placing the tip of the GDD tube in the CS has become popular to reduce corneal decompensation risk [2]. However, it may cause novel complications that had not developed when placing tubes in the AC or vitreous cavity. Ertel et al. [4] recently have reported an early occlusion of CS-placed tube by the anterior lens capsule. To our best knowledge, the present case of late occlusion of the CS-placed tube by proliferated lens epithelial cells (LECs) expanding beyond the anterior capsulotomy has not been reported. Interleukin 6 is known to elevate in aqueous humor in patients with neovascular glaucoma [6] and mediate LEC proliferation [7], which might have caused the mass development in our case.

Given that late tube occlusion rarely occurs, the tube occlusion described herein that occurred 4 years after AGV implantation is worth reporting. It might provide novel insights into placing GDD tubes in the CS, as follows. First, when placing a GDD tube in the CS, it may be necessary to polish the LECs underneath the anterior capsulotomy, and the tube length in the CS should exceed at least beyond the anterior capsulotomy. Second, late tube occlusion may occur due to the proliferation of LECs; this is because it takes time for the LECs to accumulate enough mass to block the GDD tube.

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