Surgical Management of Neovascular Glaucoma
It is more difficult to achieve an optimal outcome in neovascular glaucoma than in primary open-angle or other more common types of glaucoma. First, the lack of trabecular outflow tends to make a low intraocular pressure (IOP) difficult to achieve (some functional trabecular outflow remains in most eyes having undergone glaucoma surgery and likely improves final IOP control). Second, the rate of complications—bleeding and surgical failure—is higher in eyes with neovascular glaucoma (NVG) than primary open-angle glaucoma (POAG). Last, posterior segment ischemia often limits visual outcome. On the plus side, however, these eyes often do not have a primary glaucomatous optic neuropathy and often do well with an IOP in the high teens or low 20s.
The best glaucoma surgical outcome is achieved when the eye is quiet and neovascularization is regressed. Active anterior segment neovascularization can lead to blocked outflow surgery through hyphema or progressive synechiae. Eyes with active ischemia are more likely to scar or heal poorly. Active inflammation can lead to hypotony, scarring, or fibrin, complicating surgical outcomes.
When possible, it is best to delay surgery until neovascularization, ischaemia, and inflammation are controlled. Typically, this means maximizing medical therapy and following the patient carefully to appropriately time surgical intervention.
Antivascular Endothelial Growth Factor Therapy
Traditionally, ischemia and neovascularization have been treated with panretinal photocoagulation (PRP). However, not only does PRP take days to weeks to produce results, it often cannot be adequately performed in eyes with NVG due to vitreous hemorrhage, corneal edema, poor papillary dilation, or dense cataract.
Recently, anti-vascular endothelial growth factor (VEGF) therapy has revolutionized initial treatment of NVG. Anti-VEGF therapy may reduce surgical complications by inducing rapid regression of neovascularization and control of ischemia, and unlike PRP, it is not dependent on clarity of the eye’s optical media. Additionally, anti-VEGF therapy may reduce scarring and improve the success rate of outflow surgery. It is important to note, however, that because anti-VEGF agents have a limited duration of action, they do not replace PRP. PRP should be performed (or a second anti-VEGF injection given) within 4 to 6 weeks of the initial anti-VEGF injection.
Practically speaking, when an eye presents with uncontrolled NVG, I typically initiate maximum topical therapy and sometimes oral acetazolamide. I ensure that an intravitreal injection of an anti-VEGF drug is given the same day or as soon as possible. I will follow closely and choose to do surgery later if the IOP remains too high. Not uncommonly, especially if the angle is still open on presentation, IOP will respond to medical therapy and surgery may not be needed. If glaucoma surgery cannot be delayed due to pain or extremely elevated IOP, I will inject anti-VEGF therapy intraoperatively.
Bevacizumab and ranibizumab are the 2 agents currently available that are useful in treating neovascular glaucoma. Although neither one is FDA-approved for treating NVG, Lucentis is approved for intraocular injection (for exudative age-related macular degeneration). However, cost considerations and insurance coverage issues dictate that bevacizumab is more commonly given for NVG.
The most effective route of administration for treatment of NVG is intravitreal injection. The typical dose of bevacizumab is 1.25 mg/0.05 mL (25 mg/mL). The vitreous gel acts like a depot and probably allows sustained release of the anti-VEGF agent over 4 weeks or more. Intracameral injection is an option to cause regression of anterior segment neovascularization but likely has a shorter duration of action and may not be as beneficial to posterior segment disease.
Glaucoma Drainage Device Versus Trabeculectomy Versus Cyclophotocoagulation
Three main surgical approaches can be used to lower IOP in medically uncontrolled NVG: glaucoma drainage device (GDD), trabeculectomy with antifibrotics, and cyclophotocoagulation (CPC). When choosing a surgical approach, the following questions should be considered:
- Is there active ischemia and neovascularization?
- Is there active inflammation?
- Are other surgical interventions going to be performed concomitantly or in the future?
- What is the visual potential of the eye?
- What is the target pressure?
- What is the general health of the patient?
Glaucoma Drainage Device
In many cases, GDDs provide the most robust, predictable outcome for treating NVG. They tend to maintain function relatively well through subsequent surgery and through active inflammation, ischemia, and neovascularization. I tend to use a GDD to treat NVG whenever there is any degree of useful vision or if there is any inflammation.
Implanting a GDD in an eye with NVG takes no modification of technique other than that the tube tip probably should not touch the iris, where it can cause hyphema if rubeosis is present. If anterior segment neovascularization is present and hyphema forms, this can lead to tube occlusion (see Chapter 12).
The choice of device is based on surgeon preference. One caveat is that an ischemic eye may be more prone to hypotony due to aqueous hyposecretion, and a Baerveldt 350 -mm2 implant probably should be used only in people who are expected to rapidly generate thick capsules. Person-ally, I tend to prefer the Baerveldt 250 mm2 or Ahmed FP7 in most NVG eyes.
In eyes that also need vitrectomy for nonclearing vitreous haemorrhage, tractional retinal detachments, or other posterior segment problems, I prefer to place the GDD through the pars plana in conjunction with my vitreoretinal colleague. Not only does this technique save the patient from 2 separate trips to the operating room, but placement of the tube through the pars plana eliminates the chance that the tube will contact rubeotic vessels and cause hyphema.
Trabeculectomy With Mitomycin C
In acute NVG, trabeculectomy tends to work poorly due to intense scarring, marked anterior chamber hemorrhage, and fibrin formation. However, in quiet eyes with chronic or regressed NVG, trabeculectomy with mitomycin C (MMC) is the procedure preferred by some. The advantages are the ability to achieve a lower IOP off medication (at least in the short term) and lack of an implanted foreign body.
Trabeculectomy is not the best choice if subsequent vitreoretinal surgery is likely because of the potential to induce scarring and failure of the filtering bleb.
CPC is, in my opinion, underutilized for the treatment of NVG. The transscleral approach is quick, effective, and has almost no bleeding risk. The drawbacks are that it is inflammatory, difficult to titrate, and irreversible. I consider transscleral CPC an excellent choice for eyes with poor visual potential, patients with advanced dementia or other health issues that make incisional surgery less safe, and patients on anticoagulation. I avoid performing CPC in patients with active or recurrent inflammation because this procedure can significantly worsen inflammation.
Ischemic eyes are more likely to develop hypotony, so initial treatment should be limited to 270 degrees (or perhaps even 180). When performing transscleral CPC, I routinely use transillumination to identify the ciliary body and direct my treatment accordingly.
- When rubeosis is present, anti-VEGF therapy should be administered at least 24 to 72 hours prior to surgery, if possible. Otherwise, it may be administered intraoperatively.
- In eyes with rubeosis or otherwise active NVG, GDDs and transscleral cyclophotocoagulation are the most helpful treatment options.
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- Wakabayashi T, Oshima Y, Sakaguchi H, et al. Bevacizumab for iris neovascularization and neovascular glaucoma. Ophthalmology. 2008;115(9):1571-1580.
- Alkawas AA, Shahien EA, Hussein AM. Management of neovascular glaucoma with panretinal photocoagulation, intravitreal bevacizumab, and subsequent trabeculectomy with mitomycin C. J Glaucoma. 2010;19(9):622-626.
- Ramli N, Htoon HM, Ho CL, Aung T, Perera S. Risk factors for hypotony after transscleral diode cyclophotocoagulation. J Glaucoma. 2011;21(3):169-173.