Background
Glaucoma following penetrating keratoplasty (PKP) is one of the most common causes for irreversible visual loss and the second leading cause for graft failure after rejection. The management of penetrating keratoplasty and glaucoma (PKPG) remains controversial mainly because of the high risk of graft failure associated with the treatment.
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.
Epidemiology
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, 8]
The causes for elevated IOP in the early postoperative period are as follows:
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Postoperative inflammation
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Viscoelastic substances
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Wound leak with angle closure
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Operative technique
- Tight suturing and long bites with compression of the angle
- Larger recipient bed with same size donor button
- Increased peripheral corneal thickness
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Pupillary block glaucoma
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Preexisting peripheral anterior synechiae
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Preexisting glaucoma
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PKP in aphakic eyes secondary to mechanical angle collapse
The causes for elevated IOP in the late postoperative period are as follows:
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PKP in aphakic eyes
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PKP combined with cataract extraction
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Preexisting glaucoma
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Steroid-induced glaucoma
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Graft rejection with glaucoma
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Ghost cell glaucoma
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Misdirected aqueous or ciliary block (malignant) glaucoma
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Epithelial downgrowth
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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 reported ultrasound biomicroscopy (UBM) findings in 31 eyes with postkeratoplasty glaucoma. [9] 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. [10] 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. [10] 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.
Tables
| 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 |
