CASE PRESENTATION

A 42-year-old African American man with primary open-angle glaucoma was referred by his local glaucoma specialist to the Kellogg Eye Center for uncontrolled IOP in his left eye. The patient had previously undergone two trabeculectomies with mitomycin C in each eye. He was using timolol 0.5% b.i.d., brimonidine 0.2% b.i.d., latanoprost (Xalatan; Pfizer, Inc) q.h.s., plus oral acetazolamide 250 mg b.i.d. His visual acuities were 20/300 OD and 20/20 OS. The IOP was 10 mm Hg OD and 27 mm Hg OS. Goldmann visual field testing of the right eye showed a small superior island of vision, and Humphrey visual field testing (Carl Zeiss Meditec, Inc.) of the left eye showed dense inferior and superior arcuate defects. There was a functioning filtering bleb located superiorly in the right eye, two failed blebs superiorly in the left eye, and mild cataracts bilaterally. Gonioscopy revealed open angles in both eyes, and both optic nerves were almost completely cupped.

We proceeded to place a Baerveldt-350 glaucoma drainage device (Abbott Medical Optics Inc.) with a ripcord, three venting slits, and a scleral patch graft in the superotemporal quadrant of the patient's left eye. The surgery was uncomplicated. On the first postoperative day, the patient's visual acuity was 20/30, and his IOP was 37 mm Hg OS. The anterior segment and fundus examinations of the left eye were notable only for good positioning of the tube in the anterior chamber and a flat bleb over the Baerveldt plate. Because he had not taken his glaucoma medications overnight, in the clinic, the patient was given oral acetazolamide (immediate release) 500 mg as well as timolol 0.5% and dorzolamide 2% eye drops for his left eye. He was instructed to start moxifloxacin q.i.d. and prednisolone acetate 1% q.i.d. in his left eye as well as to restart all of his previous glaucoma eye drops q.i.d. plus oral acetazolamide 250 mg q.i.d.

Seven days after surgery, the patient presented to his local ophthalmologist with a complaint of blurred vision. The IOP in his left eye was 57 mm Hg. The local ophthalmologist performed an anterior chamber tap and sent the patient directly to us. Upon examination, his visual acuity was 20/25 with an IOP of 41 mm Hg OS. The cornea was clear with a deep, quiet anterior chamber and a mild cataract without evidence of pupillary block. The tube was well positioned against the iris, and there was a flat bleb over the Baerveldt plate. The fundus examination was unremarkable without choroidal effusion or hemorrhage.

HOW WOULD YOU PROCEED?

  • Would you treat the patient medically or surgically?
  • If you chose to treat the patient surgically, what procedure would you perform (eg, exchange a Baerveldt device for an Ahmed Glaucoma Valve [New World Medical, Inc.], make additional venting slits to the Baerveldt device, or place a second tube)?
  • Did any aspects of the patient's ocular history affect your treatment choices?

SURGICAL COURSE

We felt that the patient most likely had a rapid steroid-induced IOP spike. Given that he was essentially monocular from end-stage glaucoma, we needed to intervene immediately to reduce his IOP. Medical therapy was already maximal, and opening the Baerveldt tube by releasing the ripcord only 1 week after implantation would risk severe hypotony. We placed an Ahmed Glaucoma Valve-Pediatric (S3; New World Medical, Inc.) in the superonasal quadrant of the patient's left eye that day. The surgery was uncomplicated.

OUTCOME

On the first day after the placement of the pediatric implant, the patient's visual acuity was 20/40, and the IOP measured 20 mm Hg OS. There was a bleb over the Ahmed plate. The patient was restarted on prednisolone acetate 1% q.i.d., moxifloxacin q.i.d., and timolol 0.5% b.i.d. in the left eye. His IOPs remained in the low to mid-20s in the left eye for the next several weeks until we opened the Baerveldt device by releasing the ripcord in the clinic 1 month after the original tube's implantation. Three months after the implantation of the Baerveldt device, the patient's visual acuity was 20/15 OS, and his IOP was 10 mm Hg on brimonidine 0.2% b.i.d., timolol 0.5% b.i.d., and latanoprost q.h.s. He subsequently returned to his local glaucoma specialist for follow-up.

DISCUSSION

The implantation of a glaucoma drainage device is most commonly indicated for uncontrolled glaucoma with an IOP refractory to medication, laser, and filtering surgery.1 The Baerveldt and Ahmed implants are the most common drainage devices used today. Several recent studies suggest better IOP control with the Baerveldt versus the Ahmed device.2-4 Although these studies also found more early postoperative complications associated with the Baerveldt device compared with the Ahmed device, we initially chose to implant a Baerveldt device for better long-term IOP control, given the patient's young age and severe disease.

Longer-term IOP control is more likely achieved with the Baerveldt device due to its larger surface area, lower profile, and open-tube design.4 Because it is not a valved device, temporary tubal ligation is needed initially to allow encapsulation of the Baerveldt plate. Generally, encapsulation takes about 1 month; opening the tube earlier may risk hypotony. The management of elevated IOP following the device's implantation during the initial postoperative month before the tube can be opened may be tricky. Venting slits can be placed in the tube to help lower the IOP, but their effect can be highly variable. For our patient, despite the creation of venting slits, his early postoperative IOP was markedly elevated, most likely due to a rapid steroid response. Stopping the prednisolone eye drops or switching to a milder steroid formulation would not have lowered the IOP quickly enough, and reducing the steroid treatment might have resulted in increased encapsulation of the plate. Viable surgical options in this situation included cyclodestructive procedures or the placement of a second glaucoma drainage device.

Cyclodestructive procedures can be associated with numerous side effects such as vision loss, uveitis, hypotony, and phthisis.5,6 This surgical option, therefore, is typically reserved for eyes with end-stage glaucoma and poor baseline vision. Although there are a few reports of successful outcomes after cyclodestructive procedures to reduce IOP in eyes with good visual potential,5,7,8 larger studies with long-term follow-up are lacking. Moreover, it can take weeks for the IOP to stabilize after cyclodestruction. In this case, because we only needed to lower the IOP temporarily until the Baerveldt device could be safely opened, we felt the risks of cyclodestruction outweighed its benefits.

The placement of a second aqueous shunt, specifically an Ahmed Glaucoma Valve-Pediatric, was an appropriate choice in this situation for several reasons. The device features a venturi-based, flow-restrictive valve designed to prevent postoperative hypotony, which allows it to be effective immediately after placement. Several randomized controlled trials have confirmed the immediate reduction of IOP with the Ahmed device.2,3 Because the first glaucoma drainage device was placed superotemporally, a second device needed to fit superonasally, inferonasally, or inferotemporally (Figure). Placing glaucoma drainage devices inferiorly can be a problem due to exposure, so superonasal placement of a second glaucoma drainage device is reasonable if the implant fits easily. The smaller plate area of the pediatric device fits well in the superonasal quadrant. In a few small retrospective studies of sequential glaucoma implants, hypotony and corneal decompensation were the most common complications.9-11 The smaller plate area of the pediatric Ahmed device reduces the risk of postoperative hypotony. The long-term survival of the pediatric Ahmed device is often poor, because the smaller plate is more likely to become encapsulated than the adult-sized Ahmed device. The pediatric model served its primary purpose of lowering the IOP immediately after implantation, however, and keeping the IOP controlled until the Baerveldt device could be opened.

Jennifer S. Weizer, MD, is an associate professor of ophthalmology and visual sciences at the Kellogg Eye Center at the University of Michigan in Ann Arbor. She acknowledged no financial interest in the products or companies mentioned herein. Dr. Weizer may be reached at jweizer@med.umich.edu.

Linda Zhang, MD, is a glaucoma fellow at the Kellogg Eye Center at the University of Michigan in Ann Arbor. She acknowledged no financial interest in the products or companies mentioned herein. Dr. Zhang may be reached at zlinda@med.umich.edu.

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