Refractory Open-Angle Glaucoma After Neodymium–Yttrium-Aluminum-Garnet Laser Lysis of Vitreous Floaters




Purpose


To illustrate 3 cases of chronic open-angle glaucoma secondary to the neodymium–yttrium-aluminum-garnet (Nd:YAG) laser vitreolysis procedure for symptomatic vitreous floaters.


Design


Observational case series.


Methods


Location of the study was the Doheny Eye Institute. Three eyes of 2 patients who developed chronic open-angle glaucoma after Nd:YAG vitreolysis for symptomatic floaters presenting with very high intraocular pressure (IOP >40 mm Hg) were selected. The time from the laser treatment to the onset of elevated pressure ranges from 1 week to 8 months. There was no associated inflammation, steroid use, or other identifiable cause of chronic IOP elevation.


Results


All eyes were treated initially with glaucoma medication, followed by selective laser trabeculoplasty (SLT) and eventually glaucoma surgery (Trabectome) in 2 eyes for disease management. In all eyes, intraocular pressures were eventually stabilized within a normal pressure range from 18 to 38 months following Nd:YAG vitreolysis. At the latest follow-up post surgery, all eyes had intraocular pressures of 22 mm Hg or less with or without medications.


Conclusions


Secondary open-angle glaucoma is a complication of Nd:YAG vitreolysis for symptomatic floaters that may present with an increase in intraocular pressure immediately, or many months after the surgery. Furthermore this complication may be permanent and require chronic medical therapy or glaucoma surgery.


Lysis of visually symptomatic vitreous floaters with the neodymium–yttrium-aluminum-garnet (Nd:YAG) laser has been described by several case series in the literature. The procedure has not been widely accepted by the ophthalmic community in part because the procedure lacks US Food & Drug Administration (FDA) approval. Existing studies show a modest overall success rate in resolution of symptoms of floaters after laser. While the procedure has been regarded as safe, with only transient increases in intraocular pressure (IOP) being reported, in our experience a permanent increase in IOP can be seen as a complication. We discuss the published data on Nd:YAG vitreolysis for floaters and present the cases of 3 eyes of 2 patients that were treated with Nd:YAG vitreolysis for the photodisruption of floaters and subsequently developed open-angle glaucoma that was refractory to maximal medical and glaucoma laser management. To our knowledge, this is the first report of intractable IOP elevation and secondary open-angle glaucoma following laser vitreous floater disruption.


Methods


We retrospectively reviewed the charts of 2 patients from July 2009 to May 2011 who developed glaucoma after Nd:YAG vitreolysis for floater disruption. Both patients were referred for treatment to the glaucoma service of the Doheny Eye Institute, and had chronic elevations in intraocular pressure despite antiglaucoma medication. Both patients failed conservative therapy including medical and laser trabeculoplasty treatment, and 1 eventually required glaucoma surgery with the Trabectome (trabeculotomy by internal approach; Neomedix, Inc, Tustin California, USA). The indications for the procedure were intraocular pressures above the level desired for the level of optic nerve cupping, defects in the retinal nerve fiber layer, or visual field progression on maximally tolerated medical therapy. This study was approved by the Institutional Review Board of the University of Southern California and met with the tenets of the Declaration of Helsinki and the Health Insurance Portability and Accountability Act (HIPAA).




Results


Case 1


A 50-year-old male patient was treated OD with Nd:YAG vitreolysis floater disruption at an outside institution (6 procedures, total laser energy dose >10 J). One week after the procedure, he had an unspecified elevated IOP and all topical steroids were tapered, and fixed combination brimonidine tartrate 0.2%/timolol maleate 0.5% twice daily (BID) was begun. Seven months after the last laser procedure, his IOP reached a peak of 40 mm Hg and bimatoprost 0.03% daily was added. However, the patient was unable to tolerate bimatoprost owing to development of side effects with eyelid swelling. Ten months after the last vitreolysis procedure, while using brimonidine tartrate 0.2%/timolol maleate 0.5% BID and latanoprost nightly at bedtime (qHS), visual acuity was 20/30 with improvement to 20/20 on pinhole OD and 20/15 OS. IOPs were 19 mm Hg OD and 16 mm Hg OS by Goldmann applanation. There was no history of elevated IOP OS.


The anterior chamber was found to be deep and quiet with no transillumination defects of the iris or pseudoexfoliation material present. On gonioscopy, the angles were open 4+ to ciliary body OU with normal 2+ pigment. The dilated fundus examination showed a cup-to-disc ratio of 0.5 OD and 0.35 OS. Corneal pachymetry indicated that corneal thickness was 395 μm OD, and 516 μm OS, with a history of laser in situ keratomileusis procedure OD. There was a superior thinning of the retinal nerve fiber layer OD on ocular coherence tomography measurements. The visual field done 3 months prior revealed both eyes to be essentially normal. The posterior capsule was not intact as he had history of central Nd:YAG capsulotomy for posterior capsule opacification OD.


Owing to irritation from the medications and the patient’s desire to reduce the number of medications, selective laser trabeculoplasty (SLT) was performed with 2 sessions of 180 degrees treatment at 11 and 12 months after last Nd:YAG procedure. The SLT reduced the IOP from a baseline of 20–23 mm Hg OD preoperatively to a new baseline of 17–18 mm Hg postoperatively.


After SLT, a trial off of latanoprost resulted in IOP elevation to 23 mm Hg, and the medicine was reinstituted. The IOP reduced to 16 mm Hg OU with visual acuity (VA) of 20/40 pinhole to 20/25+2 OD, 20/15 OS while taking brimonidine 0.2%/timolol maleate 0.5% 1 drop (gtt) BID OD, latanoprost 1 gtt qHS OD, and cyclosporine ophthalmic solution 0.05% 1 gtt BID OU. Sixteen months after SLT, the cup-to-disc ratio was 0.7 OD and 0.5 OS. The visual field revealed no specific glaucomatous defect OU. A trial discontinuation of brimonidine/timolol was performed 18 months after laser, and the IOP has remained in the 18–22 mm Hg range on latanoprost monotherapy. The patient was not interested in further surgery or medications and the patient was observed on latanoprost monotherapy.


Cases 2 and 3


A 59-year-old white female patient with a history of Nd:YAG laser vitreolysis floater disruption OU performed at an outside institution presented with complaints of intermittent visual blurring 8 months following the procedure. The amount of laser energy used was not known. Uncorrected visual acuity was 20/40 OU with improvement on pinhole to 20/30. IOP measured 48 OD and 46 OS by Goldmann applanation on no medications. The anterior segment examination showed pseudophakia OU with accommodative intraocular lenses in good position. The patient had a history of posterior capsulotomy OU for posterior capsule opacification. There was no evidence of iris transillumination defects or pseudoexfoliation material or evidence of current pigment dispersion, but the possibility of prior undiagnosed pigmentary dispersion cannot be ruled out entirely. The optic nerves appeared healthy with a cup-to-disc ratio of 0.35 OU. On gonioscopy, the angles were 4+ open to ciliary body band with 3+ pigment OU.


Left eye


After 3 weeks on maximum medications (latanoprost 0.005% qHS OU, brimonidine tartrate 0.2%/timolol maleate 0.5% BID OU, and oral acetazolamide 500 mg BID) with reported good compliance, the IOP OS was 38 mm Hg with VA of 20/40. Trabectome surgery OS was performed. Loteprednol etabonate 0.05% 4 times daily (QID), moxifloxacin QID, and pilocarpine 1% BID were started postoperatively. On postoperative day 1, visual acuity was 20/hand motions left eye. The IOP measured 9 mm Hg OS. A diffuse microhyphema was present OS and pilocarpine was discontinued. At this time, acetazolamide 500 mg dosing was reduced from BID to every morning (qAM). At 1-week follow-up, visual acuity improved to 20/60 OS with an IOP of 14 mm Hg. Acetazolamide and moxifloxacin drops were discontinued at this time point. Two weeks after Trabectome OS, vision further recovered to 20/40 with an IOP of 16 mm Hg OS. At this time, loteprednol etabonate 0.05% QID was tapered to thrice daily (TID), BID, and daily (QD) by weekly intervals.


At the last follow-up, the IOP OS was 21 mm Hg, 24 months after glaucoma surgery. Cup-to-disc ratio was 0.7 and OCT revealed full peripapillary retinal nerve fiber layer. The Humphrey visual fields (SITA standard 24-2) at this time showed no specific glaucoma defect, but indicated a questionable artifact in the peripheral inferior field.


Right eye


At 12 months following Trabectome OS, and 20 months following laser vitreolysis, the patient was noncompliant with her medications (latanoprost, brimonidine tartrate 0.2%/timolol maleate 0.5%) for a period of 2 weeks and her IOP increased to 45 OD with a VA of 20/20-2. She complained of side effects of brimonidine/timolol as well as topical carbonic anhydrase inhibitors. The medical regimen was simplified to latanoprost OD qHS; however, while the patient was being compliant with medications, the IOP increased to 48 mm Hg. The patient elected to have SLT OD (101 spots at 0.6–0.7 mJ, treating 360 degrees) and was prescribed oral acetazolamide 250 mg BID in addition to latanoprost qHS OD. One week after SLT OD, visual acuity was 20/20 and IOP measured 23 mm Hg. At the 2-month interval following SLT, the IOP was 20 mm Hg and acetazolamide was reduced from 250 mg BID to QD. However, when the acetazolamide was discontinued, the IOP rose to 26 mm Hg and the patient desired surgery in order to be able to discontinue the oral carbonic anhydrase inhibitor.


Five months after SLT, the patient underwent Trabectome procedure OD and continued latanoprost qHS OD, acetazolamide 250 mg BID, with the additional postoperative medications: loteprednol etabonate 0.05% QID OD and moxifloxacin QID OD. On postoperative day 1, the patient’s VA was 20/80 and IOP was 9 mm Hg OD. At 1-week-postoperative follow-up, the patient’s VA was 20/25-2 with an IOP of 36 mm Hg OD. A steroid-induced rise in IOP was suspected; therefore, the loteprednol etabonate 0.05% drops were discontinued and replaced with fluorometholone 0.1%, taper from BID for 2 days to QD for 2 days, then discontinued. Two weeks after Trabectome procedure OD, the IOP was 18 mm Hg OD, the acetazolamide was reduced to 250 mg qAM, and the moxifloxacin was discontinued. One month status post Trabectome OD, the IOP was 17 mm Hg, and the acetazolamide dosing was reduced to every other day. Ten weeks after the surgery, IOP was 20 mm Hg, and the acetazolamide was stopped completely. Five months after Trabectome OD, IOP was controlled at 20 mm Hg and latanoprost was discontinued. At follow-up 18 months after Trabectome OD, the IOP was 19 mm Hg, with cup-to-disc ratio of 0.4 and a full OCT peripapillary retinal nerve fiber layer. The Humphrey visual fields (SITA standard 24-2) at this time showed no specific glaucoma defect.




Results


Case 1


A 50-year-old male patient was treated OD with Nd:YAG vitreolysis floater disruption at an outside institution (6 procedures, total laser energy dose >10 J). One week after the procedure, he had an unspecified elevated IOP and all topical steroids were tapered, and fixed combination brimonidine tartrate 0.2%/timolol maleate 0.5% twice daily (BID) was begun. Seven months after the last laser procedure, his IOP reached a peak of 40 mm Hg and bimatoprost 0.03% daily was added. However, the patient was unable to tolerate bimatoprost owing to development of side effects with eyelid swelling. Ten months after the last vitreolysis procedure, while using brimonidine tartrate 0.2%/timolol maleate 0.5% BID and latanoprost nightly at bedtime (qHS), visual acuity was 20/30 with improvement to 20/20 on pinhole OD and 20/15 OS. IOPs were 19 mm Hg OD and 16 mm Hg OS by Goldmann applanation. There was no history of elevated IOP OS.


The anterior chamber was found to be deep and quiet with no transillumination defects of the iris or pseudoexfoliation material present. On gonioscopy, the angles were open 4+ to ciliary body OU with normal 2+ pigment. The dilated fundus examination showed a cup-to-disc ratio of 0.5 OD and 0.35 OS. Corneal pachymetry indicated that corneal thickness was 395 μm OD, and 516 μm OS, with a history of laser in situ keratomileusis procedure OD. There was a superior thinning of the retinal nerve fiber layer OD on ocular coherence tomography measurements. The visual field done 3 months prior revealed both eyes to be essentially normal. The posterior capsule was not intact as he had history of central Nd:YAG capsulotomy for posterior capsule opacification OD.


Owing to irritation from the medications and the patient’s desire to reduce the number of medications, selective laser trabeculoplasty (SLT) was performed with 2 sessions of 180 degrees treatment at 11 and 12 months after last Nd:YAG procedure. The SLT reduced the IOP from a baseline of 20–23 mm Hg OD preoperatively to a new baseline of 17–18 mm Hg postoperatively.


After SLT, a trial off of latanoprost resulted in IOP elevation to 23 mm Hg, and the medicine was reinstituted. The IOP reduced to 16 mm Hg OU with visual acuity (VA) of 20/40 pinhole to 20/25+2 OD, 20/15 OS while taking brimonidine 0.2%/timolol maleate 0.5% 1 drop (gtt) BID OD, latanoprost 1 gtt qHS OD, and cyclosporine ophthalmic solution 0.05% 1 gtt BID OU. Sixteen months after SLT, the cup-to-disc ratio was 0.7 OD and 0.5 OS. The visual field revealed no specific glaucomatous defect OU. A trial discontinuation of brimonidine/timolol was performed 18 months after laser, and the IOP has remained in the 18–22 mm Hg range on latanoprost monotherapy. The patient was not interested in further surgery or medications and the patient was observed on latanoprost monotherapy.


Cases 2 and 3


A 59-year-old white female patient with a history of Nd:YAG laser vitreolysis floater disruption OU performed at an outside institution presented with complaints of intermittent visual blurring 8 months following the procedure. The amount of laser energy used was not known. Uncorrected visual acuity was 20/40 OU with improvement on pinhole to 20/30. IOP measured 48 OD and 46 OS by Goldmann applanation on no medications. The anterior segment examination showed pseudophakia OU with accommodative intraocular lenses in good position. The patient had a history of posterior capsulotomy OU for posterior capsule opacification. There was no evidence of iris transillumination defects or pseudoexfoliation material or evidence of current pigment dispersion, but the possibility of prior undiagnosed pigmentary dispersion cannot be ruled out entirely. The optic nerves appeared healthy with a cup-to-disc ratio of 0.35 OU. On gonioscopy, the angles were 4+ open to ciliary body band with 3+ pigment OU.


Left eye


After 3 weeks on maximum medications (latanoprost 0.005% qHS OU, brimonidine tartrate 0.2%/timolol maleate 0.5% BID OU, and oral acetazolamide 500 mg BID) with reported good compliance, the IOP OS was 38 mm Hg with VA of 20/40. Trabectome surgery OS was performed. Loteprednol etabonate 0.05% 4 times daily (QID), moxifloxacin QID, and pilocarpine 1% BID were started postoperatively. On postoperative day 1, visual acuity was 20/hand motions left eye. The IOP measured 9 mm Hg OS. A diffuse microhyphema was present OS and pilocarpine was discontinued. At this time, acetazolamide 500 mg dosing was reduced from BID to every morning (qAM). At 1-week follow-up, visual acuity improved to 20/60 OS with an IOP of 14 mm Hg. Acetazolamide and moxifloxacin drops were discontinued at this time point. Two weeks after Trabectome OS, vision further recovered to 20/40 with an IOP of 16 mm Hg OS. At this time, loteprednol etabonate 0.05% QID was tapered to thrice daily (TID), BID, and daily (QD) by weekly intervals.


At the last follow-up, the IOP OS was 21 mm Hg, 24 months after glaucoma surgery. Cup-to-disc ratio was 0.7 and OCT revealed full peripapillary retinal nerve fiber layer. The Humphrey visual fields (SITA standard 24-2) at this time showed no specific glaucoma defect, but indicated a questionable artifact in the peripheral inferior field.


Right eye


At 12 months following Trabectome OS, and 20 months following laser vitreolysis, the patient was noncompliant with her medications (latanoprost, brimonidine tartrate 0.2%/timolol maleate 0.5%) for a period of 2 weeks and her IOP increased to 45 OD with a VA of 20/20-2. She complained of side effects of brimonidine/timolol as well as topical carbonic anhydrase inhibitors. The medical regimen was simplified to latanoprost OD qHS; however, while the patient was being compliant with medications, the IOP increased to 48 mm Hg. The patient elected to have SLT OD (101 spots at 0.6–0.7 mJ, treating 360 degrees) and was prescribed oral acetazolamide 250 mg BID in addition to latanoprost qHS OD. One week after SLT OD, visual acuity was 20/20 and IOP measured 23 mm Hg. At the 2-month interval following SLT, the IOP was 20 mm Hg and acetazolamide was reduced from 250 mg BID to QD. However, when the acetazolamide was discontinued, the IOP rose to 26 mm Hg and the patient desired surgery in order to be able to discontinue the oral carbonic anhydrase inhibitor.


Five months after SLT, the patient underwent Trabectome procedure OD and continued latanoprost qHS OD, acetazolamide 250 mg BID, with the additional postoperative medications: loteprednol etabonate 0.05% QID OD and moxifloxacin QID OD. On postoperative day 1, the patient’s VA was 20/80 and IOP was 9 mm Hg OD. At 1-week-postoperative follow-up, the patient’s VA was 20/25-2 with an IOP of 36 mm Hg OD. A steroid-induced rise in IOP was suspected; therefore, the loteprednol etabonate 0.05% drops were discontinued and replaced with fluorometholone 0.1%, taper from BID for 2 days to QD for 2 days, then discontinued. Two weeks after Trabectome procedure OD, the IOP was 18 mm Hg OD, the acetazolamide was reduced to 250 mg qAM, and the moxifloxacin was discontinued. One month status post Trabectome OD, the IOP was 17 mm Hg, and the acetazolamide dosing was reduced to every other day. Ten weeks after the surgery, IOP was 20 mm Hg, and the acetazolamide was stopped completely. Five months after Trabectome OD, IOP was controlled at 20 mm Hg and latanoprost was discontinued. At follow-up 18 months after Trabectome OD, the IOP was 19 mm Hg, with cup-to-disc ratio of 0.4 and a full OCT peripapillary retinal nerve fiber layer. The Humphrey visual fields (SITA standard 24-2) at this time showed no specific glaucoma defect.

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Jan 7, 2017 | Posted by in OPHTHALMOLOGY | Comments Off on Refractory Open-Angle Glaucoma After Neodymium–Yttrium-Aluminum-Garnet Laser Lysis of Vitreous Floaters
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