Viscocanalostomy for Refractory Glaucoma Secondary to Intravitreal Triamcinolone Acetonide Injection

Intravitreal injection of triamcinolone acetonide (IVTA) has gained widespread use in the treatment of a variety of neovascular and inflammatory intraocular conditions, including proliferative diabetic retinopathy, chronic cystoid macular edema, and chronic uveitis. Intraocular pressure (IOP) greater than 21 mm Hg occurs in approximately 42% of eyes following IVTA. Most of these patients are successfully treated with medical therapy, while a small percentage (1%) require glaucoma surgery for pressure management.¹ We report a series of 3 patients who developed refractory glaucoma secondary to IVTA. All 3 were successfully treated with viscocanalostomy.

Patient 1 was a 54-year-old man with a previous central retinal vein occlusion. Patient 2 was a 51-year-old woman with a history of a superotemporal branch retinal vein occlusion. Both had undergone IVTA for treatment of macular edema associated with the vein occlusions. Patient 3 was a 77-year-old woman who had received IVTA for exudative age-related macular degeneration. All 3 patients developed raised IOPs following a single IVTA (20 mg/0.1 mL) that were not controlled despite maximal medical therapy. Preoperative IOPs were 38 mm Hg, 40 mm Hg, and 40 mm Hg and preoperative visual acuities were 20/200, 20/125, and 20/40 for patients 1, 2, and 3, respectively.

All patients underwent viscocanalostomy by P.K.W. after informed consent was obtained. Details of the procedure in all cases are as follows. A corneal traction suture was inserted and a fornix-based conjunctival flap was constructed superiorly. A superficial scleral flap measuring 5 mm × 5 mm × 250 μm was created with the base at the limbus (Figure 1). The corner of the scleral flap was elevated and dissected forward with a crescent blade kept parallel to the scleral surface advancing 2 mm into the clear cornea (Figure 2).

A deep scleral flap was constructed just within the first flap, deep enough to reveal only a thin translucent layer of sclera overlying the choroid. The deep flap was dissected forward in the same plane to reach the scleral spur, which was incised to reveal Schlemm's canal. The lateral edges of the deep flap were then extended 1 mm into the clear cornea. As the deep flap was dissected forward, the posterior then anterior trabecular meshwork were exposed before the flap was extended into the clear cornea, stripping off 1 to 2 mm of the Descemet membrane, creating a trabeculo-descemetic window. The endothelial lining of Schlemm's canal and the underlying juxtacanicular tissue were removed with a cellulose sponge until aqueous was seen seeping from the anterior chamber. The deep flap was excised with the roof of Schlemm's canal (Figure 3).

An ophthalmic viscoelastic device (Viscoat, Alcon Laboratories Inc, Fort Worth, Texas) was injected into the deep scleral lake and toward the cut ends of Schlemm's canal. Four 10.0 Vicryl sutures (Ethicon Inc, Somerville, New Jersey) closed the superficial scleral flap; the conjunctiva was also closed with 10.0 Vicryl sutures (Figure 4). Prednisolone, 1%, drops were used 4 times a day for 4 weeks followed by ketorolac, 0.5%, drops 4 times a day for 4 weeks. No perioperative or postoperative complications occurred, except for a small perforation of the trabeculo-descemetic window in patient 2. No antimetabolites, suture lysis, or postoperative needling were necessary.

Patients 1 and 3 had 6 months of follow-up and patient 2 completed 1 year. At 1 month, IOPs were 14 mm Hg in patient 1, 26 mm Hg in patient 2, and 10 mm Hg in patient 3. At 6 months postoperatively, IOPs were 10 mm Hg in patient 1, 16 mm Hg in patient 2, and 10 mm Hg in patient 3. Patient 2 had an IOP of 14 mm Hg at 1 year of follow-up. No antiglaucoma medication was necessary at any time postoperatively. Visual acuities at 6 months were 20/125, counting fingers, and 20/40 in patients 1, 2, and 3, respectively.

A few options have been suggested for the successful management of persistently elevated IOP following IVTA. These include trabeculectomy,¹ laser trabeculoplasty,² and pars plana vitrectomy.³

Viscocanalostomy has been shown to be effective in treating open-angle glaucoma with a reduced risk of the potentially sight-threatening complications, such as hypotony and endophthalmitis, compared with trabeculectomy.⁴ We report a series of 3 patients who were treated successfully with viscocanalostomy for refractory glaucoma secondary to IVTA.

Steroids induce glaucoma by lowering outflow facility through an unknown mechanism. Theories include the deposition of extracellular matrix in the trabecular meshwork.⁵ The complete success of viscocanalostomy in lowering IOP to acceptable levels without using antiglaucoma medication suggests that stripping the juxtacanalicular tissue and the inner waterproof endothelial lining of Schlemm's canal relieves the steroid-induced resistance to aqueous outflow. We feel this case series illustrates that the obstruction to aqueous outflow in IVTA-induced secondary glaucoma may lie predominantly in the juxtacanalicular tissue and the endothelium of Schlemm's canal. These structures are removed in viscocanalostomy as opposed to the corneoscleral or uveal trabecular meshwork, which are retained. This technique therefore sheds light on the possible biological mechanisms involved in the development of steroid-induced glaucoma and offers a safe and effective treatment option for such patients.

Correspondence: Dr Krishnan, St Paul's Eye Unit, Royal Liverpool University Hospital, Prescot Street, Liverpool L7 8XP, England (radhikrishnan2004@yahoo.co.uk).

Author Contributions: Dr Krishnan, had full access to all the data in the study and takes responsibility for the integrity of this data.

Financial Disclosure: None reported.

Additional Contributions: Carl Groenwald, FRCOphth, provided the diagrams illustrating the technique of viscocanalostomy.