eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma and Penetrating Keratoplasty

Rajesh Shetty, MD, Assistant Professor of Ophthalmology, College of Medicine, Mayo Clinic; Consultant, Department of Ophthalmology, Mayo Clinic, Jacksonville
Edney de Resende Moura Filho, MD, Fellow, Department of Ophthalmology, Mayo Clinic, Jacksonville; Saiyid A Hasan, MD, Assistant Professor of Ophthalmology, College of Medicine, Mayo Clinic; Senior Associate Consultant, Education Coordinator, Department of Ophthalmology, Mayo Clinic, Jacksonville; Ramesh S Ayyala, MD, FRCS, FRCOphth, Chief, Section of Ophthalmology, Charity Hospital of New Orleans; Director of Glaucoma Services, Assistant Professor, Department of Ophthalmology, Tulane University School of Medicine

Updated: Feb 26, 2009

Introduction

Recent developments in the management of glaucoma, including newer classes of drugs, surgical procedures (eg, trabeculectomy with mitomycin-C), glaucoma drainage devices (GDDs), and cyclodestructive procedures with Nd:YAG and diode lasers, have increased the options available to the clinician in the management of PKPG.

This article addresses the etiology, diagnosis, and treatment of PKPG.

History of the Procedure

In 1969, Irvine and Kaufman reported the high incidence of increased intraocular pressure (IOP) following PKP.¹ They reported a mean maximum pressure of 40 mm Hg in aphakic transplants and 50 mm Hg in combined transplants and cataract extraction in the immediate postoperative period. Since then, numerous authors have reported on the incidence and management of PKPG.

Frequency

The incidence of PKPG varies from 9-31% in the early postoperative period^2,3,4 and from 18-35% in the late postoperative period.^1,2,4,5,6

Etiology

The important risk factors for glaucoma in patients undergoing PKP include aphakic and pseudophakic bullous keratopathy, mesodermal dysgenesis, irido-corneal-endothelial syndrome, preexisting glaucoma, perforated corneal ulcer, adherent leukoma, previous PKP, posttraumatic cases, combined PKP and intracapsular cataract extraction, and performance of vitrectomy during PKP.^{1,2,3,4,5,6,7}

The causes for elevated IOP in the early postoperative period are as follows:

• Postoperative inflammation
• Viscoelastic substances
• Wound leak with angle closure
• Hyphema
• Operative technique
  • Tight suturing and long bites with compression of the angle
  • Larger recipient bed with same size donor button
  • Increased peripheral corneal thickness
• Pupillary block glaucoma
• Malignant glaucoma
• Preexisting peripheral anterior synechiae
• Preexisting glaucoma
• PKP in aphakic eyes secondary to mechanical angle collapse

The causes for elevated IOP in the late postoperative period are as follows:

• PKP in aphakic eyes
• PKP combined with cataract extraction
• Chronic angle-closure glaucoma
• Preexisting glaucoma
• Steroid-induced glaucoma
• Graft rejection with glaucoma
• Ghost cell glaucoma
• Misdirected aqueous or ciliary block (malignant) glaucoma
• Epithelial downgrowth
• Fibrous ingrowth

Pathophysiology

The pathophysiology of PKPG is multifactorial; it may be related to distortion of the angle with collapse of the trabecular meshwork, suturing technique, postoperative inflammation, corticosteroid use, and peripheral anterior synechiae. The usual factors that contribute to postoperative glaucoma, such as preexisting glaucoma, postoperative inflammation, use of viscoelastic substances, and steroid-induced glaucoma,² should be considered.

Dada et al reportedultrasound biomicroscopy (UBM) findings in 31 eyes with postkeratoplasty glaucoma.⁸ The types of synechiae noted on UBM included peripheral anterior synechiae in 30/31 (96.7%) eyes, synechiae at the graft-host junction in 13/31 (41.93%) eyes, both peripheral anterior synechiae and graft-host junction synechiae in 12/31 (38.7%) eyes, central iridocorneal synechiae in 6/31 (19.3%) eyes, and intraocular lens iris synechiae in 3/31 (9.6%) eyes. The authors concluded that secondary angle closure caused by anterior synechiae formation is one of the important causes of PKPG in eyes with opaque grafts. The authors also concluded that UBM serves as a useful tool for anterior segment evaluation in such cases and can help in planning the site for glaucoma filtering surgeries and drainage devices.

Other factors that are peculiar to patients who have undergone keratoplasty exist. Olson and Kaufman, using a mathematical model, proposed that the elevated IOP following keratoplasty in an aphakic patient might be the result of angle distortion secondary to a roll of excess compressed tissue in the angle.⁹  Because of edema and inflammation, trabecular meshwork function is compromised. According to Olson and Kaufman, factors that contribute to angle distortion include tight suturing, long bites (more compressed tissue), larger trephine sizes, smaller recipient corneal diameter, and increased peripheral corneal thickness.⁹ Conversely, less tight wounds, smaller trephine sizes, donor corneas larger than the recipient, thinner recipient corneas, and larger overall corneal diameter tend to alleviate the angle distortion.

Presentation

The diagnosis of PKPG is made based on IOP measurements in the early postoperative period, and, in the late postoperative period, it is based on IOP, optic disc changes, and progressive visual field changes. Patients with extremely high IOPs might present with graft edema and/or failure.

Indications

Indications are discussed in other sections.

Relevant Anatomy

Relevant anatomy is discussed in other sections.

Contraindications

Contraindications are discussed in other sections.

Workup

Diagnostic Procedures

The accurate measurement of IOP in patients with keratoplasty can be difficult. IOP in the early postoperative period, when the corneal surface is irregular, can be measured with the Mackay-Marg electronic applanation tonometer, the Pneumatic applanation tonometer, the Tono-Pen, or the dynamic contour tonometer.

If the graft surface is smooth, the epithelium is intact, and the mires are regular, then Goldmann applanation can be used to measure the IOP. Marked corneal astigmatism causes an elliptical fluorescein pattern. To obtain an accurate reading with the Goldmann applanation tonometer, the clinician should rotate the prism so that the red mark on the prism holder is set at the least curved meridian of the cornea (along the negative axis). Alternately, 2 pressure readings, taken 90 degrees apart, can be averaged.

The accuracy of applanation tonometry is reduced in certain situations, such as corneal edema, scars, bloodstaining, or any condition that thickens or alters the cornea. Corneal epithelial edema and stromal edema predispose to inaccurately low readings, whereas pressure measurements taken over a corneal scar will be falsely high. Thin corneas result in underestimation, and thick corneas result in overestimation. Tonometry performed over a soft contact lens and following scleral buckling procedures gives falsely low values.

The Pneumatic tonometer has a pressure-sensing device that consists of a gas-filled chamber covered by a Silastic diaphragm. The gas in the chamber escapes through an exhaust vent. As the diaphragm touches the cornea, the gas vent is reduced in size and the pressure in the chamber rises. Because this instrument applanates only a small area of the cornea, it has the advantage of measuring the IOP in the presence of corneal scars, in the presence of corneal edema, or when only a small portion of the cornea is visible (large tarsorrhaphy). In addition, in patients with neurotrophic corneas, it is possible to measure the IOP with minimal disturbance of the epithelium.

In cases with complete tarsorrhaphy, an attempt must be made to measure the IOP by digital palpation. Measuring the IOP in the normal eye using one of the standard techniques (eg, Goldmann applanation tonometer) is helpful; then, perform digital palpation on both eyes. IOP should be measured on every visit following PKP.

Optic disc changes should be monitored in all cases of elevated IOP. This can be completed either by serial disc photography (where possible) or by serial optic disc diagrams from the same observer. Visual fields may be difficult to perform in patients with corneal grafts, especially in the early postoperative period. In patients with reasonable vision, Humphrey visual fields or Goldmann visual fields should be performed.

Histologic Findings

Chronic elevations of IOP potentially compromise the graft endothelial function, leading to graft failure. The degree and duration of elevated IOP has been shown to result in significant endothelial cell loss. Following an acute attack of angle-closure glaucoma, endothelial cell loss of 10-33% has been reported,¹⁰ and cell loss of 77% has been reported in eyes with acute angle-closure glaucoma lasting more than 12 days. Morphologic changes in the endothelial cells, such as vacuolization, loosening of cell junctions, blebbing, disruption of the plasma membrane, exkaryocytosis, and loss of whole cells, have been observed in experimentally induced acute glaucoma.¹¹ Corneal sensation is also noted to be decreased in cases of angle-closure glaucoma.

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.

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 PKPG^{1,2,3,4,5,6,7,40} 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.

Outcome and Prognosis

The surgical success rate of the 3 procedures (ie, trabeculectomy with mitomycin-C, GDD surgery, cyclodestructive procedure) in controlling the IOP to less than 21 mm Hg is similar (70-75%).

The prognosis for graft survival is less clear. The lowest incidence of graft failure follows trabeculectomy (10-20%), as compared to GDD surgery (10-50%) and cyclodestructive procedure (20-50%). Therefore, the long-term prognosis for graft survival appears to be 40-60% in patients with PKPG.

Future and Controversies

Eye care professionals should be educated to monitor the IOP in all patients following PKP. Patients with PKPG who are not responding to medications should be treated surgically.

Controversy still exists as to which of the 3 surgical procedures is the best initial treatment option in terms of graft survival. In addition, the timing of the surgery (ie, whether to perform the surgery prior to, combined with, or after the corneal transplant operation) is still not clear.

Some authors recommended placement of the GDD into the posterior chamber combined with vitrectomy or placement into the ciliary sulcus anterior to the lens and posterior to the iris. These authors believe that placing the tube behind the iris diaphragm decreases the risk of graft failure.

Similarly, diode laser cycloablation is believed to result in less inflammation and more precise ciliary process destruction. However, definitive evidence is still lacking in both situations. Randomized, prospective studies are needed to determine which of the available treatment options should be the treatment of choice in the postkeratoplasty glaucoma population.

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Keywords

glaucoma and penetrating keratoplasty, penetrating keratoplasty and glaucoma, penetrating keratoplasty, corneal transplant, glaucoma, PKPG, PKP, open angle, closed angle, vision loss, visual deficit

Contributor Information and Disclosures

Author

Rajesh Shetty, MD, Assistant Professor of Ophthalmology, College of Medicine, Mayo Clinic; Consultant, Department of Ophthalmology, Mayo Clinic, Jacksonville
Rajesh Shetty, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, American Society of Cataract and Refractive Surgery, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Coauthor(s)

Edney de Resende Moura Filho, MD, Fellow, Department of Ophthalmology, Mayo Clinic, Jacksonville
Edney de Resende Moura Filho, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Saiyid A Hasan, MD, Assistant Professor of Ophthalmology, College of Medicine, Mayo Clinic; Senior Associate Consultant, Education Coordinator, Department of Ophthalmology, Mayo Clinic, Jacksonville
Saiyid A Hasan, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and American Society of Cataract and Refractive Surgery
Disclosure: Nothing to disclose.

Ramesh S Ayyala, MD, FRCS, FRCOphth, Chief, Section of Ophthalmology, Charity Hospital of New Orleans; Director of Glaucoma Services, Assistant Professor, Department of Ophthalmology, Tulane University School of Medicine
Ramesh S Ayyala, MD, FRCS, FRCOphth is a member of the following medical societies: American Academy of Ophthalmology and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Bradford Shingleton, MD, Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary
Bradford Shingleton, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Ophthalmology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Louis E Probst, MD, Medical Director of Refractive Surgery, Chicago, Madison, Milwaukee, and Windsor Centers, TLC the Laser Eye Centers
Louis E Probst, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, and International Society of Refractive Surgery
Disclosure: Nothing to disclose.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

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