eMedicine Specialties > Ophthalmology > Intraocular Pressure
Glaucoma and Penetrating Keratoplasty: Treatment
Updated: Feb 26, 2009
Treatment
Medical Therapy
Medical management (eg, topical drops, systemic pills) continues to be the first line of treatment in cases of PKPG. Currently available antiglaucoma medications include beta-adrenergic blocking agents (eg, timolol, betaxolol), adrenergic agents (eg, epinephrine, dipivefrin), alpha2-adrenergic agonists (eg, brimonidine, apraclonidine hydrochloride), miotics (eg, pilocarpine, echothiophate iodide, carbachol), prostaglandin analogues (eg, latanoprost), topical carbonic anhydrase inhibitors (eg, dorzolamide, brinzolamide), and systemic carbonic anhydrase inhibitors (eg, acetazolamide, methazolamide, dichlorphenamide).
Beta-adrenergic blocking agents have been the cornerstone of glaucoma treatment for the last 2 decades. They act by decreasing the aqueous production, and they have no effect on the outflow pathways. Lass and Pavan-Langston demonstrated the efficacy of timolol in the treatment of PKPG, even in the presence of chronic angle closure.12 The adverse effects of beta-blockers include, but are not limited to, superficial punctate keratopathy, corneal anesthesia, and damage to the ocular surface by decreasing the aqueous layer production rate and by impairing the quantity and quality of the mucous layer of the tear film, resulting in a dry eye state. All of these may have an adverse effect on the graft epithelium that might compromise graft function.
Adrenergic agents can help in lowering the IOP but should be used with caution in aphakic and pseudophakic patients because they can produce cystoid macular edema. Brimonidine tartrate 0.2%, a relatively selective alpha2-adrenergic agonist, is better tolerated than apraclonidine hydrochloride and has been shown to be a safe drug in the long-term control of the IOP. Apraclonidine 0.5% is a potent anterior segment vasoconstrictor and is useful both to prevent anterior chamber bleeding during the operation and to control the pressure spike resulting from such a bleed.
Miotics should be used with caution in this patient population. They can be useful in patients with open angles but may have very little effect in the presence of significant angle closure caused by peripheral anterior synechiae. Miotics can induce uveitis by breakdown of the blood-aqueous barrier, and they can initiate graft rejection. In aphakic patients, miotics can increase the risk of a retinal detachment.
Topical carbonic anhydrase inhibitors (eg, dorzolamide, brinzolamide) have similar ocular hypotensive efficacy as betaxolol 0.5% and are not associated with clinically significant electrolyte disturbances or systemic adverse effects seen with systemic carbonic anhydrase inhibitors. However, they should be used with caution in patients with PKPG, especially in those with a past history of graft rejection and/or with limited endothelial cell counts13 ; they can contribute to an irreversible corneal decompensation, especially in patients with compromised endothelial function. Systemic carbonic anhydrase inhibitors are useful in the treatment of pressure spikes in the immediate postoperative period. Their long-term use is limited because 30-50% of patients experience adverse effects, such as paresthesias, tinnitus, nausea, gastrointestinal disturbances, fatigue, depression, anorexia, and weight loss.
Prostaglandin analogues, such as latanoprost, appear to decrease IOP by increasing the uveoscleral outflow and can be used with beta-blockers and carbonic anhydrase inhibitors. Latanoprost should be used with caution in patients with a history of herpes simplex keratitis because it has been reported to induce recurrent herpetic infection in humans.14 In patients with aphakia and pseudophakia, latanoprost has been reported to cause cystoid macular edema, and, in patients with a past history of uveitis, it should be used with caution.15
The benefits of pressure reduction with topical glaucoma medications should be weighed against the potential adverse effects. Apart from the specific adverse effects listed above, benzalkonium chloride (BAC), the preservative used in most topical glaucoma medications, can cause severe surface toxicity. These effects include cell wall damage and destruction of the corneal epithelial microvilli, leading to increased permeability of the corneal epithelium.16 The acidic pH of some of the topical drops (eg, Cosopt, 5.8; dorzolamide, 5.6), apart from causing burning sensation, also may be toxic to the corneal epithelium.
In patients who are allergic to the preservatives, preservative-free drugs, such as an Ocudose form of timolol maleate, should be used. Also, pilocarpine powder can be reconstituted with balanced salt solution locally by the pharmacy without any preservative.
The greatest elevations in IOP due to corticosteroids are seen in patients with glaucoma. Dexamethasone causes a serious rise in IOP more commonly than prednisolone or hydrocortisone. On withdrawal of the drug, the IOP tends to return to normal.In cases of steroid-responsive glaucoma, tapering the dose of steroid drops (prednisolone acetate 1%) to the minimum required or replacing stronger steroid drops (eg, prednisolone acetate) either with steroids with less tendency to increase the IOP (eg, topical fluorometholone, loteprednol etabonate 0.5% or 0.2%, rimexolone 1%) or with cyclosporin A 0.5% topical drops (in combination with topical glaucoma medications) may help in controlling the pressure.
There appears to be a correlation between the length of corticosteroid treatment and the time for the corticosteroid effect to regress. However, the IOP usually returns to normal within 2-4 weeks after discontinuation of corticosteroid therapy.
Loteprednol etabonate has less propensity to cause significant increases in IOP17 and is effective in the treatment of giant papillary conjunctivitis, seasonal allergic conjunctivitis, as well as postoperative inflammation.18,19,20 Loteprednol etabonate undergoes hydrolysis in the cornea and aqueous humor to become an inactive derivative21 and, thus, may not have a marked effect in increasing IOP.
The following table documents the disadvantages of using some of the topical glaucoma medications in patients with PKPG.
Possible Disadvantages of the Various Glaucoma Medications in Patients With PKPG
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Table
| Glaucoma Medications | Potential Problems in Patients With PKPG |
| Beta-blockers | Superficial punctate keratitis, corneal anesthesia, dry eyes, subconjunctival fibrosis |
| Alpha-adrenergic drugs | Superficial punctate keratitis, dry eyes, allergic reactions |
| Miotics | Inflammation, graft rejection, retinal detachment, subconjunctival fibrosis |
| Topical carbonic anhydrase inhibitors | Induce permanent graft failure in eyes with borderline endothelial counts |
| Prostaglandin analogues | Uveitis, cystoid macular edema in aphakia and pseudophakia, and recurrent herpes simplex infection in patients with previous history of herpes |
| Adrenergic agents | Epithelial toxicity and cystoid macular edema in aphakia and pseudophakia |
| Glaucoma Medications | Potential Problems in Patients With PKPG |
| Beta-blockers | Superficial punctate keratitis, corneal anesthesia, dry eyes, subconjunctival fibrosis |
| Alpha-adrenergic drugs | Superficial punctate keratitis, dry eyes, allergic reactions |
| Miotics | Inflammation, graft rejection, retinal detachment, subconjunctival fibrosis |
| Topical carbonic anhydrase inhibitors | Induce permanent graft failure in eyes with borderline endothelial counts |
| Prostaglandin analogues | Uveitis, cystoid macular edema in aphakia and pseudophakia, and recurrent herpes simplex infection in patients with previous history of herpes |
| Adrenergic agents | Epithelial toxicity and cystoid macular edema in aphakia and pseudophakia |
Surgical Therapy
Surgical treatment may be in the form of argon laser trabeculoplasty; glaucoma-filtering procedures, such as trabeculectomy and GDDs; or various cyclodestructive procedures.
Argon laser trabeculoplasty
Argon laser trabeculoplasty (ALT) can result in a 10-40% reduction in the IOP in primary open-angle glaucoma in the short term. The efficacy of ALT depends on the clinical characteristics of the patients and the type of glaucoma treated. The IOP-lowering effect tends to diminish between 1.5-4 years postoperatively with only a 40-50% success rate at 5 years.22 The effects of ALT following keratoplasty are variable and may be tried as a short-term measure in patients with open angles and clear grafts with moderately elevated IOP (ie, 20-25 mm Hg) on glaucoma medications.
The recommended setting is blue green or all green argon laser with a 50-µm spot size, 0.1 seconds, 50 spots in 180°, and power 400-1000 W. The end point is to visualize blanching or bubble formation. The laser is applied at the junction of the pigmented and nonpigmented trabecular meshwork.
Possible complications include pressure spikes and iritis, both of which can trigger graft rejection.
Trabeculectomy
Conventional trabeculectomy without antimetabolites (5-fluorouracil [5-FU]) and alkylating agents (mitomycin-C) in patients with PKPG has a high failure rate23 secondary to limbal conjunctival scarring from previous surgery, extensive peripheral synechiae, aphakia, and extremely shallow anterior chambers.
The introduction of 5-FU and mitomycin-C has increased the success rate of trabeculectomies, especially in patients with complicated glaucoma. These agents appear to increase the success rate by inhibiting the fibroblast proliferation and by enhancing the formation of filtering blebs. Five milligrams of 5-FU in 0.1 cc is given as a subconjunctival injection in the immediate postoperative period for 10-14 days. Apart from the inconvenience of daily injections, 5-FU injections are associated with a high rate of corneal epithelial toxicity, corneal ulceration, corneal perforation, and stem cell failure, which could prove to be disastrous to the graft.24 Because of corneal toxicity, 5-FU should be used with caution in patients with PKPG.
Intraoperative local application of mitomycin-C (0.2-0.4 mg applied for 1-4 min) has significantly improved the success rate of filtering surgery for glaucoma.25 Apart from the convenience of a single application at the time of surgery, mitomycin-C trabeculectomy has no demonstrable toxicity on the corneal epithelium. However, mitomycin-C trabeculectomy may result in thin cystic bleb formation and an increased risk of bleb-related infection.26 The reported success rate in IOP control with mitomycin-C trabeculectomy in patients with PKPG is 67-91% and that of graft failure is 12-18%.27,28 The bleb failure rate is higher when trabeculectomy is combined with additional surgical procedures, such as cataract surgery and vitrectomy.29
Trabeculectomy with mitomycin-C can be attempted in patients with no or limited superior limbal conjunctival scarring, absence of extensive peripheral anterior synechiae, aphakia, and extremely shallow anterior chambers. Avoid this procedure in patients who use contact lenses because it can predispose them to bleb infection. Avoid shallow or flat anterior chambers in the postoperative period because this could compromise the graft endothelium. Avoid combining trabeculectomy with other intraocular procedures because it compromises the success rate of the trabeculectomy. Avoid 5-FU in patients with a sick epithelium and persistent epithelial defects. Watch for Dellen formation that can trigger thinning of the adjacent graft cornea, leaking blebs, and bleb-related infections.
Glaucoma drainage devices
GDDs create an alternate aqueous pathway by channeling aqueous from the anterior chamber through a long tube to an equatorial plate that promotes bleb formation. In 1987, Kirkness first reported the use of GDDs in PKPG.30 Even though GDDs appear to control glaucoma in a high percentage of patients in all published series (71-96%, with an average of 84.8%), it appears to be associated with a high incidence of graft failure in the range of 10-51% (with an average of 36.2%).31,32,15,30,33 The etiology of graft failure probably is multifactorial. The presence of underlying chronic inflammation, extensive peripheral synechiae, and multiple previous surgeries may compromise the graft. The introduction of a GDD into the anterior chamber also may be associated with increased inflammation and may further compromise the graft.
Ritterband and the Cornea Glaucoma Implant Study (COGIS) group reported on 83 eyes treated with combined penetrating keratoplasty and implantation of a GDD, with tube placement in the pars plana.34 Their graft survival rates are among the best reported for this combination of surgeries, with clear grafts in 93% of the treated eyes at 6 months, 87% at 1 year, and 59% at 2 years. However, no grafts remained clear in the small group of patients at 5-year follow-up.
The timing of GDD surgery is another factor that can contribute to graft failure. In the series published by Beebe et al and Rapuano et al, a trend exists toward a higher incidence of graft failure when GDD surgery was performed after PKP.32,31 GDD surgery–related complications, including inflammation, shallow anterior chamber with iris graft endothelial touch, and tube-endothelial touch, could possibly contribute to graft failure. Meticulous surgery should avoid the complications of flat anterior chamber and tube-endothelial touch. The use of high-dose steroids for 3-6 months in the postoperative phase may help in controlling and suppressing inflammation.
The choice of the GDD in the treatment of patients with PKPG depends upon the case and the surgeon. Four main GDDs are available; the Ahmed implant15 and the Krupin implant offer resistance to the outflow in the form of a sheet valve and a slit valve, respectively, and the Molteno implant and the Baerveldt implant35 have no resistance to the outflow and, thus, may lead to hypotony. However, this problem can be overcome with the use of the ripcord technique.
The advantages of the valved implants, especially that of the Ahmed glaucoma valve, appear to be that of easy insertion following 1-quadrant dissection and a low incidence of hypotony in the immediate postoperative phase. However, the Ahmed valve is associated with a high incidence of the hypertensive phase (as much as 80%), 1-3 months after the operation, which may require needling with 5-FU injections.15 On the other hand, GDDs with a larger surface area, such as the double-plate Molteno and Baerveldt implants,35 appear to exhibit a lesser incidence of the hypertensive phase and may achieve slightly lower IOP. The overall success rate as well as the other complications, including corneal decompensation, appear to be similar to all GDDs.31,36,33,15
Complications of GDD surgery include graft rejection and failure, conjunctival erosion, prolonged hypotony, tube-endothelial touch, tube obstruction, tube failure, retinal detachment, tube plate extrusion, epithelial down growth, and infection. Whereas a graft can usually be repeated, if the optic nerve is damaged from end-stage glaucoma, useful vision cannot be restored.
Cyclodestructive procedures
Cyclodestructive procedures aim to control the IOP by decreasing aqueous humor production by destroying part of the ciliary body. Cyclocryotherapy,37 transscleral cyclophotocoagulation with Nd:YAG,38 and semiconductor diode laser39 are the various cyclodestructive procedures that can be performed on patients with intractable PKPG. The reported success rates and the complications following any of these procedures appear to be similar.37,38,39 The individual surgeon must decide which 1 of the 3 to use, depending on the availability of the instruments and the lasers. The overall success rate in controlling the IOP is 60-80%.
The major complications from any of these procedures are the risk of graft rejection and the loss of vision.
The authors prefer the semiconductor diode laser to the procedures for the following reasons. The diode laser, with a wavelength of 810 nm, has a lower scleral transmission than the Nd:YAG laser (1064 nm) but greater absorption by melanin. Also, because semiconductor diode lasers have solid-state construction, they have the advantages of portability, durability, and smaller size compared with Nd:YAG lasers.
Recommendations are outlined below.
Cyclocryotherapy: The glaucoma cryoprobe is placed for 1 minute, 3 mm behind the corneoscleral limbus. Six burns are made with equidistant spots involving the inferior 180° of the globe at a temperature of -60°C to -80°C. The superior half of the globe is almost never treated. The treatment is repeated in exactly the same fashion when indicated. Avoid doing 360° cyclodestruction to decrease the risk of hypotony.
YAG cyclophotocoagulation: The use of Nd:YAG (Microruptor 11, LASAG, Thun, Switzerland) in a maximally defocused position is recommended. Approximately 15 evenly spaced burns are placed 1-1.5 mm from the limbus for 180°. The recommended mean energy level is 4.1-9.3 joules. Postoperative pain medication and topical steroids are indicated. Low energy settings are preferred in patients previously treated with cyclocryotherapy or filtering procedure to avoid hypotony. Repeated applications may be necessary before adequate control is achieved.
Diode laser cyclophotocoagulation: The recommended power settings with the diode laser are 1750-3000 mW, with a 2-second exposure time. An initial power setting of 1750 mW is increased or decreased by 250-mW increments until it is 250 mW below that producing an audible popping sound.
Complications include a decrease in the Snellen visual acuity (22-56%), graft failure (11-65%), persistent hypotony (5-10%), anterior uveitis, epithelial defects, vision loss, severe pain, phthisis bulbi, hyphema, hypopyon, intractable pain, sympathetic ophthalmia, scleral thinning, and vitreous hemorrhage.
Summary
Uncontrolled IOP after PKP can result in graft failure and vision loss. IOP should be monitored on a regular basis after corneal transplantation. Uncontrolled IOP should be treated aggressively. Any patient with preexisting glaucoma must be carefully evaluated prior to a corneal transplant.
Patients with uncontrolled IOP or patients with borderline IOP control on 2 or more medications may be treated with either mitomycin-C trabeculectomy or GDD surgery prior to or combined with the planned corneal transplant. This is based on the fact that multiple studies have documented preoperative glaucoma to be a high-risk factor for the development of PKPG1,2,3,4,5,6,7,40 and also have documented a higher incidence of graft failure following glaucoma operations following PKP.31 PKPG not responding to medications should be treated surgically. Mitomycin-C trabeculectomy is the safest operation in terms of both IOP control and graft survival. Literature favors a combined mitomycin-C trabeculectomy with corneal graft operation in patients with preexisting glaucoma who need a corneal transplant.31,32,15,28,29,41,33
Additional surgical procedures should be avoided if possible at the time of the trabeculectomy because this is associated with a higher incidence of trabeculectomy failure.29
GDD surgery is the preferred operation over other surgical options in patients with PKPG who have extensive limbal conjunctival scarring, shallow anterior chambers, extensive peripheral anterior synechiae, and failed trabeculectomy. GDD surgery appears to be superior to cyclodestructive procedures in patients who have failed mitomycin-C trabeculectomy or in patients where mitomycin-C trabeculectomy is contraindicated (ie, patients who wear contact lenses). The graft failure rate following GDD surgery and cyclodestructive procedures may be the same, but there appears to be a higher incidence of permanent vision loss and hypotony following cyclodestructive procedures.42 Thus, cyclodestructive measures should be reserved for patients who have failed all other interventions.
Whereas a graft can usually be repeated, if the optic nerve is damaged from end-stage glaucoma, useful vision cannot be restored. Randomized, prospective studies are needed to determine which of the available treatment options should be the treatment of choice in the postkeratoplasty glaucoma population.
Preoperative Details
Preexisting glaucoma is frequently more difficult to treat following keratoplasty in both aphakic and pseudophakic eyes.1 Preexisting glaucoma also is noted to be a risk factor for graft failure.40 Reinhard et al estimated the 3-year graft survival rate in patients with a preoperative history of glaucoma to be 71% in contrast to 89% without such history.40 Some studies suggest a higher incidence of graft failure following glaucoma operation performed after PKP.31 Hence, in this patient population, it is recommended that the glaucoma operation either precede or be combined with PKP.
Intraoperative Details
During PKP, such measures as using an oversized donor button (0.5 mm), deep bites, goniosynechialysis in the presence of peripheral anterior synechiae, iridoplasty (iris-tightening procedure) in cases of a floppy iris, removal of viscoelastic material at the end of the operation, and careful wound closure to prevent postoperative wound leaks are useful in reducing the incidence of postoperative glaucoma.
Postoperative Details
In the postoperative phase, judicious use of steroids controls the inflammation and prevents peripheral anterior synechiae. Cycloplegics (when indicated) keeps the pupil mobile and prevents pupillary block glaucoma.
Follow-up
For excellent patient education resources, visit eMedicine's Glaucoma Center. Also, see eMedicine's patient education articles Glaucoma Overview, Glaucoma FAQs, and Understanding Glaucoma Medications.
Complications
See Surgical therapy.
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 Treatment: Glaucoma and Penetrating Keratoplasty |
| Follow-up: Glaucoma and Penetrating Keratoplasty |
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Further Reading
Keywords
glaucoma and penetrating keratoplasty, penetrating keratoplasty and glaucoma, penetrating keratoplasty, corneal transplant, glaucoma, PKPG, PKP, open angle, closed angle, vision loss, visual deficit
