Glaucoma and corneal surgery

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CHAPTER 40 Glaucoma and corneal surgery

Introduction

The relationship between corneal transplantation and glaucoma is complex. Corneal transplantation may induce glaucoma and the surgical treatment of glaucoma can lead to corneal or graft failure. The successful management of both entities requires close monitoring and coordinated care.

Eduard Zirm is credited with performing the first successful human corneal transplant in 19051. Since then, most corneal transplants have been penetrating keratoplasties (PKPs), replacing all layers of a recipient’s cornea even if the pathology was limited to a single layer. With the advent of endothelial keratoplasty, the ‘big bubble’ technique, and femtosecond laser assisted keratoplasty, the selective replacement of layers of the cornea has become increasingly popular2.

From 2005 to 2008, the Eye Bank Association of America reported an increase in the number of endothelial transplants from 1429 to 17 4683. During this same period, the number of PKPs declined from 45 821 to 32 524. While the number of corneas distributed for lamellar transplantation increased almost 20% from 2005 to 2008, only 1072 lamellar surgeries were performed in 20083. The significance of the shift away from PKP to endothelial and lamellar keratoplasties, and its effect on post-keratoplasty glaucoma, has not been well studied; but, may result in lower rates of post-keratoplasty glaucoma.

Keratoprosthesis have also gained greater acceptance. Of these devices, the Boston Keratoprosthesis is the most popular with nearly 5000 having been implanted during the past decade4. Outside the United States, the osteo-odonto-keratoprosthesis has gained popularity as a surgical option for those with severe ocular surface diseases. Even in patients who have not had a history of glaucoma, implantation of these devices can induce glaucoma. Management difficulties are made worse because the implanted devices prevent accurate IOP measurements.

Irvine and Kaufman reported increased intraocular pressure (IOP) after PKP in 19695. Angle closure, a common cause of post-PKP glaucoma, is difficult to control medically and frequently requires surgical intervention. Trabeculectomy and glaucoma drainage devices (GDDs) have become the mainstays of post-PKP glaucoma management.

Just as corneal transplantation is a risk factor for the development of glaucoma, glaucoma is associated with an increased risk of corneal failure and the subsequent need for corneal transplantation6,7. The mechanisms for corneal failure secondary to glaucoma are not clear. Glaucoma surgery, particularly the placement of GDDs, may contribute to corneal failure through peripheral corneal–tube touch, the close proximity of tube tips to the corneal endothelium, and induced anterior chamber turbulence. In patients for whom vision is already compromised by glaucoma, worsening vision may indicate sub-clinical corneal decompensation.

Epidemiology

The incidence of glaucoma after penetrating keratoplasty is linked to the clinical indication for the transplant. Glaucoma occurs in approximately 1–6% of eyes that undergo surgery for keratoconus810, in 3–16% of patients with corneal dystrophies and Fuchs’ endothelial dystrophy8,10,11, and in 17–44% of eyes with pseudophakic or aphakic bullous keratopathy8,9,1113. Eyes with repeated corneal grafts have higher rates of both graft failure and glaucoma.

Pre-existing glaucoma is often more difficult to control after PKP14. Other factors that contribute to the development of glaucoma after PKP are a history of ocular trauma, pre-existing peripheral anterior synechiae, and combined PKP and cataract surgery9,10,13,15.

Since endothelial keratoplasty (EK) is a relatively new procedure, the incidence of glaucoma after EK has not yet been well established. Early reports suggest that glaucoma is diagnosed or glaucoma medications are started in 0–18% of EK patients1618. In the first year after DSEK, Vajaranant et al. reported starting glaucoma medications in 18% of patients without pre-existing glaucoma and increasing glaucoma therapy in 33% of patients with a history of glaucoma18. While only 0.3% patients without pre-existing glaucoma went on to require glaucoma surgery, 7 of 85 (8%) patients with a history of glaucoma required additional glaucoma surgery after EK. In this study, median IOP peaked 3 months after EK, which led the authors to speculate that many of the patients were steroid responders. Although no long-term data were presented, Lee et al. reported elevations of IOP to greater than 30 mmHg in 13% of patients in the first 6 months after EK16. Most IOP elevations occurred during the first week after surgery.

Thirty-six to 76% of patients undergoing keratoprosthesis surgery were treated preoperatively for glaucoma19,20. The onset or progression of glaucoma as determined by finger tension, visual field progression, or optic nerve head cupping has been reported in 6–28% of cases after keratoprosthesis surgery19,21.

Diagnosis

The diagnosis of glaucoma after PKP can be made challenging immediately postoperatively, by the presence of large epithelial defects, stromal edema, or irregular astigmatism, all of which can complicate applanation tonometry. Early postoperatively, the Tonopen (Reichert, Depew, New York) or the pneumotonometer may more accurately measure IOP. With high regular astigmatism, IOP is best obtained by averaging two Goldmann applanation measurements taken with the prisms 90° apart22. In some cases, digital palpation may be the best way to obtain an estimate of the IOP.

Difficulty visualizing the optic nerve handicaps diagnosis and monitoring of glaucomatous optic neuropathy. Opaque or edematous corneas may make accurate assessments of the optic nerve head impossible. In post-PKP glaucoma, graft edema, a poor ocular surface, and/or astigmatism may compromise the stereoscopic view, distort photos, or invalidate advanced imaging of the optic nerve.

The replacement of the cornea and ocular surface with a keratoprosthesis makes standard methods of IOP measurement inaccurate. Measurements taken at the limbus, on the sclera, or through conjunctivalized cornea are influenced, for example, by corneal sutures and the proximity of the keratoprosthesis back plate. Finger tension may be the best way to approximate IOP and serial measurements, using the same approach on the same part of the eye, may offer some insight into IOP trends. Compared to PKP, a keratoprosthesis provides an astigmatically neutral and clear visual axis through which to view the optic nerve. The view is similar to that obtained through an undilated pupil. Photographs and advanced imaging of the optic nerve are possible through a Boston keratoprosthesis.

Etiology

The development of glaucoma in eyes with a history of corneal surgery is usually attributed to changes in angle anatomy. Peripheral anterior synechiae (PAS) are present in up to 87% of patients after PKP10,15. In our experience, PAS caused by corneal transplantation leads to progressive angle closure which is often difficult to manage without surgical intervention. The slowly progressive and recurrent nature of the angle closure prevents goniosynechialysis from being effective: synechiae tend to re-form. Figure 40.1 demonstrates a patient with areas of synechial angle closure.

Distorted angle anatomy, anterior and posterior to the trabecular meshwork, has been implicated in the development of open angle glaucoma after PKP23. Anterior to the angle, tight and long sutures may compress the trabecular meshwork24. Posterior to the angle, loss of the support normally provided by the ciliary body–lens system allows for collapse of the trabecular meshwork.

Donor tissue diameter may also contribute to the development of glaucoma post-keratoplasty. Using an oversized graft may decrease the incidence of glaucoma after PKP in the early postoperative period. This effect may persist in the long term, but there is limited supporting data2326. In contrast, an undersized graft may decrease angle width and increase the risk for development of PAS with subsequent angle closure.

Immediately post-PKP, elevated IOP may be caused by iritis, hemorrhage, ciliary block glaucoma, and retained viscoelastic. In eyes inflamed preoperatively, the risk of pupillary block due to iritis or hemorrhage may be reduced by an iridotomy. Postoperative steroid response (in 20–32% of patients depending on the definition of steroid induced glaucoma) may elevate IOP in susceptible patients27,28.

EK involves injecting air into the anterior chamber and keeping the patient supine to assist in graft attachment. Typically this involves an anterior chamber air fill of 10–60 minutes followed by an exchange of approximately half of the air for balanced salt solution. This can lead to complications: immediately postoperatively, patients in whom air bubbles extend beyond the inferior pupillary border in the supine position may experience pupillary block. In Tillett’s original description of posterior lamellar keratoplasty, the cornea was clear on the first postoperative day, but the iris was pushed forward against the graft creating anterior synechiae and angle closure with elevated IOP29. A second mechanism for IOP elevations occurring within one week of EK has been postulated by Lee and co-authors: air displaced behind the iris leads to iridocorneal adhesions and elevated IOP16.

Postoperatively, steroid response appears to be a common cause of post-EK IOP elevation18. Fuchs’ endothelial dystrophy, which typically carries a lower risk of glaucoma after PKP, was the most common indication for surgery in the study presented by Vajaranant et al. The median IOP peaked at 3 months postoperatively. Topical steroids were commonly used four times daily for the first 4 months then slowly tapered18. Using a more rapid steroids taper, Lee et al. reported only one patient with IOP elevation after 6 months follow-up16.

Medical treatment of glaucoma after PKP

In patients with a history of corneal surgery, topical medications should be used cautiously with awareness of certain risks and benefits. Most topical medications contain preservatives which can be detrimental to the ocular surface: many glaucoma medications contain benzalkonium chloride. If preservatives in topical medications are harmful to the cornea, alternate products such as brimonidine and travoprost should be considered as they have been formulated with Purite® and Sofzia® preservatives, respectively. Timolol and pilocarpine are available in preservative-free forms.

While prostaglandin analogs are effective in lowering IOP, increased risks of intraocular inflammation and cystoid macular edema have been associated with their use. Increased intraocular inflammation can compromise long-term graft survival. As latanoprost has been associated with recurrent herpetic keratitis, prostaglandin agonists should be used with caution in patients with a history of herpetic eye disease30. We use prostaglandin agonists in patients with post-keratoplasty glaucoma, if the alternative is surgery for IOP control. Many of the reported side effects of prostaglandin analoge have been based upon case reports and no controlled or prospective studies have demonstrated any deleterious effects of prostaglandin analoge on graft survival.

Miotics are usually ineffective and not recommended in the early postoperative period; pilocarpine breaks down the blood–aqueous barrier and increases intraocular inflammation. The risk of shallowing of the anterior chamber with the potential for PAS limits the use of miotics after keratoplasty.

Carbonic anhydrase inhibitors (CAIs) can be used topically or systemically. Although the carbonic anhydrase enzyme is expressed by the corneal endothelium and is associated with endothelial pump function, the effect of CAIs on the graft is likely to be clinically significant only if the graft is near failure. We treat glaucoma in the presence of a graft as we do in patients who have not had a history of corneal surgery.

Preoperative assessment

When assessing a patient with glaucoma after PKP, consider both the degree of pre-existing glaucomatous damage and the target IOP. Prior surgeries have a significant impact on the type and location of the planned surgical intervention. The superior temporal quadrant is preferred for GDDs and trabeculectomies should only be performed superiorly (inferior trabeculectomies carry an increased risk of endophthalmitis). The superotemporal quadrant is more easily accessible, has good eyelid coverage, and avoids the oblique muscles. Previous retinal surgeries or superior incisions for cataract surgery may affect the mobility of the superior conjunctiva and require use of a different site. If the superotemporal quadrant is not available for GDD placement, our preference is to then use the inferonasal quadrant.

Areas of PAS versus open angle should be mapped preoperatively to aid in surgical decision making with regard to tube and sclerostomy placement. If significant corneal scarring prevents good anterior segment visualization, preoperative ultrasound biomicroscopy (UBM) or anterior segment optical coherence tomography (AS-OCT) may be helpful. Since vitreous can block tube and trabeculectomy filtration, the anterior chamber and pupillary plane should be assessed for the presence of vitreous. The lens status and points of fixation in cases of scleral-fixated IOLs are important considerations.

For patients undergoing a corneal transplant, careful identification of the site(s) of prior glaucoma surgery is critical. An overhanging trabeculectomy bleb may need to be trimmed at the time of the transplant to permit trephination and proper suturing. In patients with GDDs, an anteriorly placed tube may lead to corneal failure and may need to be repositioned to the sulcus or pars plana or trimmed and re-positioned more posteriorly within the anterior chamber.

Surgical decision making

Preoperative decision making must be made in a stepwise fashion by answering the following questions: Is combined or staged corneal and glaucoma surgery indicated? Which glaucoma procedure is most appropriate? In which quadrant should the glaucoma surgery be performed? Into which chamber of the eye should the GDD tube be inserted? Does the pre-existing bleb need to be revised or does a pre-existing tube need to be trimmed or repositioned? Which type of corneal transplant is indicated?

When deciding between combined or staged glaucoma and corneal transplant surgery, retrospective and non-randomized reports have not demonstrated clear differences in graft outcomes31,32. In light of common postoperative complications of glaucoma surgery (such as anterior chamber shallowing or flattening and the development of choroidals), we prefer a staged approach. We aim to control IOP prior to visual rehabilitation with corneal surgery. Should other factors necessitate combined surgery, the pitfalls associated with the type of glaucoma procedure planned need to be considered within the context of graft survival.

What type of glaucoma surgery should be performed? Cyclodestruction was among the first surgeries performed for post-PKP glaucoma33. Drawbacks include resultant inflammation which may lead to a greater incidence of graft failure or rejection and the frequent need for repeat treatment to control IOP adequately. Due to its tendency to produce less inflammation, diode cyclophotocoagulation (CPC) is preferred over older techniques such as cryotherapy or use of the neodymium:yttrium-aluminum-garnet (Nd:YAG) laser. A recent study on the use of trans-scleral diode laser to control post-PKP glaucoma showed a single treatment success rate of 72% after 12 months without ensuing graft failure or phthisis bulbi34.

Trabeculectomy with mitomycin C has been studied for the control of post-PKP glaucoma. Two small studies with 22 and 24 months of follow-up demonstrated IOP control rates of 62% and 50% respectively35,36. Approximately 60% of the grafts remained clear during the study period.

In our opinion, GDDs appear to offer superior IOP control post-PKP. However, the rate of graft survival, while roughly similar to that seen after trabeculectomy, is lower than desired. The outcomes of studies in which GDDs have been performed for post-PKP glaucoma are summarized in Table 40.1. In a few published studies, patients with pars plana tubes demonstrated slightly improved graft survival rates (and similar success rates for IOP control) when compared with those with anterior chamber tubes3740.

In general, we prefer non-valved GDDs in those patient who do not need immediate (within 4–6 weeks) IOP control. In our hands, these implants offer fewer complications and a relatively predictable postoperative course. Should prompt IOP reduction be required, a valved-glaucoma drainage implant can be used. The outcomes of the Ahmed Baerveldt Comparison (ABC) study may influence our GDD preference.

GDDs offer greater flexibility in terms of surgical site compared with trabeculectomies, which are most often superior to minimize the risk of endophthalmitis. GDDs can be implanted in all quadrants of the eye, but the superotemporal and inferonasal locations are preferred. Significant conjunctival scarring from superior extracapsular surgery or trabeculectomy may favor placement of the GDD in the inferonasal quadrant. The presence of a thin superior bleb may also warrant an inferonasal GDD. In most glaucomas after PKP, PAS are present (i.e. chronic angle closure secondary to PKP), and should be considered when choosing a tube entry site.

GDD tubes can be inserted into one of three locations: the anterior chamber, ciliary sulcus, or vitreous cavity. Our decision tree begins with the lens status. Our preference is to place the tube in a location where the tube tip is visible and as far from the corneal endothelium as possible.

In a phakic eye not requiring cataract extraction, we prefer anterior chamber tubes. In an eye with a stable sulcus or in-the-bag posterior chamber intraocular lens (IOL), the tube can be placed into the ciliary sulcus (Fig. 40.2). If pars plana vitrectomy is planned or anterior chamber or sulcus tube insertion are not desirable, pars plana tube insertion is possible. Insertion of the tube into the pars plana requires shaving of the vitreous base to minimize the risk of vitreous incarceration in the tube and tube failure.

During anterior chamber tube placement, areas of PAS should be avoided as progressive PAS may lead to tube-corneal touch. Ideally, anterior chamber tubes are placed within quadrants with a deep anterior chamber. If the tube is to be inserted into the ciliary sulcus, PAS and iridocorneal adhesions may facilitate tube insertion by creating more space between the iris and the IOL.

An anterior chamber GDD tube can be visualized directly, by AS-OCT or by UBM if fluid is not present over the GDD plate. If vitreous occludes the tube tip, vitreolysis with YAG laser might clear it. Iris incarceration at the tube tip can be released with a 30 G needle, argon iridoplasty or YAG laser ablation. Unless a posterior chamber tube is left long and approaches the visual axis, it may be difficult to diagnose tip occlusion as a cause of GDD failure.

In patients with endothelial dysfunction, EK may be preferable over PKP. Concurrent EK and GDD surgery can be complicated by the escape of air around a tube sclerostomy site that has not yet fibrosed or through a tube that has not been ligated. In our experience, if concurrent EK and GDD surgery is performed, the tube should be completely ligated without fenestrations. EK combined with trabeculectomy can be complicated by air leakage through the sclerostomy and into the bleb. As with PKP, postoperative courses complicated by hypotony and hypertensive phases may have consequences for newly transplanted endothelial cells. For these reasons, we prefer glaucoma intervention and maximal IOP control prior to EK. Although it may be difficult to maintain a full air fill after penetrating glaucoma surgery, successful subsequent EK has been reported in eyes with valved and non-valved GDDs (Fig. 40.3)41,42. Case reports have described successful EK in eyes with a functioning trabeculectomy as well as in an eye with two tube shunts41,43.

Pre-existing changes to the anterior segment can be aggravated after placement of a Boston keratoprosthesis. Crowding of the anterior chamber from the device can obstruct the tube. Partly because of our inability to accurately assess IOP after a keratoprosthesis, we prefer pars plana tube insertion with vitrectomy in most eyes planned for a keratoprosthesis.

Trabeculectomy

A bleb that is low, diffuse, and amenable to rigid gas permeable (RGP) contact lens wear is ideal in an eye with a corneal transplant. We use an anti-metabolite (mitomycin C or 5-fluorouracil) to create a broad, diffuse fornix-based bleb. Mitomycin C allows for statistically improved, long-term IOP control. However, the focal and/or ischemic blebs that Mytomycin C’s use tends to produce may be more susceptible to the development of leaks and infection, especially with contact lens use. In reports of trabeculectomy following PKP with greater than 18-month follow-up, success rates for IOP control ranged from 50% to 77%35,36,44,45.

Glaucoma drainage devices

To insert an anterior chamber (AC) tube, we create a sclerostomy as posteriorly as possible so that the tube rests parallel to the iris surface. A posterior limbal insertion allows the patch graft to be placed away from the cornea, thereby minimizing corneal neovascularization, subsequent suture loosening, and/or rejection. We prefer to enter the AC posterior to Schwalbe’s line so that the corneal endothelium is not in contact with silicone tubing at any point along its course past the sclerostomy (created with a sharp 23 G needle). A tube is ideally placed when it rests parallel to and just anterior to the iris, with an anterior bevel.

We cut our tubes long enough to extend into the deepest portion of the anterior chamber, which should minimize damage to the endothelium from turbulence at the tip of the tube. In phakic patients, tubes should not extend past the undilated pupillary border in order to minimize cataract formation from tube-lens contact. Provocative, intraoperative testing with a cotton-tipped applicator pressing forcefully on the globe to mimic hard eye rubbing should not demonstrate tube-cornea contact.

Insertion of a tube into the ciliary sulcus may offer the best compromise for pseudophakic eyes, not undergoing vitrectomy, and without vitreous prolapse into the anterior chamber. Sulcus tubes should be posteriorly beveled and long enough so that the tip of the tube can just be visualized through an undilated pupil. The tract should allow the tube to rest parallel to the anterior surface of the IOL (see Fig. 40.2).

Pars plana tubes should be inserted only after a complete vitrectomy, including shaving of the vitreous base in the quadrant of tube insertion. These tubes should be long enough so the posteriorly beveled tip can be visualized postoperatively when pressure is applied at the tube’s insertion site. To reduce tube mobility, the extraocular portion of the tube should be secured to the sclera with a non-absorbable fixation suture.

Endothelial keratoplasty (EK)

EK can be successfully performed after penetrating glaucoma surgery. If the GDD tube is too anterior or its position will limit the size of the EK graft, tube shortening during the EK or tube repositioning prior to EK is preferred. Figure 40.3 demonstrates an inferonasal tube encroaching on the visual axis. Since the tube was well positioned close to the iris surface, it did not interfere with graft placement. Alternatively, to accommodate an AC tube, a small notch can be placed in the transplanted tissue allowing for a larger size graft (and more endothelial cells) to fit within the anterior chamber46. A well positioned sulcus or pars plana tube is unlikely to affect EK.

Injected through the limbus with a 30-gauge needle, air may escape through the trabeculectomy or GDD tube. The pressure between the subconjunctival space and the anterior chamber must reach equilibrium before a full anterior chamber air fill is possible. Since air bubble pressure against the endothelium is critical to graft-host adherence, a sustained injection of air may be required. As air may reflux from the subconjunctival space into the anterior chamber post-operatively, an inferior iridectomy may be made to reduce the chance of pupillary block. Other measures to prevent the escape of air through the trabeculectomy or tube do not seem necessary.

Should glaucoma surgery be required after EK, our preference is to allow the graft to heal for as long as possible. Several weeks after successful EK, the graft is usually well-attached and is unlikely to dislocate with manipulations typical for either GDD or trabeculectomy surgery. As most patients who have had EK surgery are pseudophakic, we prefer sulcus implantation of a GDD tube to maximize the distance between the tube and the graft. Anterior chamber implantation requires the sclerostomy to be as posterior as possible and parallel to the iris in the deepest part of the anterior chamber so as not to interfere with the transplanted tissue. Patients who have had a complete vitrectomy are ideal candidates for pars plana tube placement.

Postoperative care

Postoperative inflammation should be managed aggressively to minimize both harm to transplanted tissue and the risk of graft rejection. Topical steroids should be used liberally particularly in pseudophakic eyes. While there is not strong evidence for long-term topical steroids, in eyes with glaucoma and corneal transplants we feel they are indicated. Early reports of rejection rates for EK appear to be lower than for PKP. This may be attributable to increased topical steroid use post-EK (as it does not have to be balanced against wound healing as in PKP)47. Newer steroid formulations with lower incidences of steroid-induced ocular hypertension may also benefit those with a history of or who subsequently develop steroid response glaucoma.

Trabeculectomies should be monitored closely. Since anti-metabolites can slow epithelial healing, their use postoperatively should be considered carefully. An epithelial defect that persists beyond 1–2 postoperative weeks can be associated with stromal haze. Persistent epithelial defects should be managed aggressively with ocular surface lubricants, a contact lens (if tolerated), or tarsorraphy. Occasionally amniotic membrane grafts or autologous serum tears may be helpful. For vascularized trabeculectomy blebs and post-PKP corneas, anti-vascular endothelial growth factor (VEGF) compounds have been considered to regress new blood vessels. More studies are needed.

With non-valved GDDs, we prefer to maintain steroids beyond the time at which the tube opens, since tube opening can be very pro-inflammatory. Steroids are then tapered very slowly.

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