Penetrating Keratoplasty and Glaucoma (PKPG)

Penetrating Keratoplasty and Glaucoma (PKPG)

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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.

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.

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]

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] A 10-year retrospective cohort study of 1657 eyes identified the strongest risk factors to be preoperative glaucoma (or IOP >20 mm Hg), aphakic postoperative lens status, and intraocular lens (IOL) removal/exchange associated with keratoplasty. [9]

In addition, the indication for grafting should be considered. In particular, bullous keratopathy, trauma, herpes simplex infection, and corneal ulceration or perforation are associated with higher risk for PKPG than are keratoconus, stromal dystrophies, and Fuchs dystrophy.. [10, 11, 12, 13]

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

Postoperative inflammation

Viscoelastic substances

Wound leak with angle closure


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

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, repeated corneal transplantation, and peripheral anterior synechiae (including prior history of uveitis). The usual factors that contribute to postoperative glaucoma, such as preexisting glaucoma, postoperative inflammation, use of viscoelastic substances, iatrogenic injury to the angle, and steroid-induced glaucoma, [2] should be considered. Zimmerman et al demonstrated on eye bank human eye models that the depth of sutures during PKP can disrupt outflow channels of the trabecular meshwork via weakening of the iridocorneal angle support, particularly in aphakic eyes. [14]

Rumelt et al reports the incidence of various etiologies of PKPG as closed angle (59%), corticosteroid induced (21%), open angle (11%), angle recession (3%), aqueous misdirection (3%), and unknown cause (3%). [15]

Dada et al reported ultrasound biomicroscopy (UBM) findings in 31 eyes with postkeratoplasty glaucoma. [16] 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. [17] 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. [17] 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. Therefore, donor corneal size should be kept at least 0.5 mm or larger. [18]

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 are discussed in other sections.

Relevant anatomy is discussed in other sections.

Contraindications are discussed in other sections.

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Glaucoma Medications

Potential Problems in Patients With PKPG


Superficial punctate keratitis, corneal anesthesia, dry eyes, subconjunctival fibrosis

Alpha-adrenergic drugs

Superficial punctate keratitis, dry eyes, allergic reactions


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

Kristin Schmid Biggerstaff, MD Assistant Professor, Department of Ophthalmology, Baylor College of Medicine; Staff Physician, Michael E DeBakey Veterans Affairs Medical Center

Kristin Schmid Biggerstaff, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, American Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Weijie Violet Lin Baylor College of Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Louis E Probst, MD, MD Medical Director, TLC Laser Eye Centers

Louis E Probst, MD, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, International Society of Refractive Surgery

Disclosure: Nothing to disclose.

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, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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, American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Ramesh S Ayyala, MD, FRCOphth, FRCS Chief, Section of Ophthalmology, Director of Glaucoma Services, Charity Hospital of New Orleans; Assistant Professor, Department of Ophthalmology, Tulane University School of Medicine

Ramesh S Ayyala, MD, FRCOphth, FRCS is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association

Disclosure: Nothing to disclose.

Edney de Resende Moura Filho, MD Chief of the Glaucoma Department, Pacini Hospital, Brazil

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, Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Rajesh Shetty, MD Glaucoma and Cataract Surgeon, Florida Eye Specialists, Jacksonville, Florida

Rajesh Shetty, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Received honoraria from Alcon for speaking and teaching; Received honoraria from Zeiss for speaking and teaching; Received honoraria from Allergan for speaking and teaching.

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, American Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Penetrating Keratoplasty and Glaucoma (PKPG)

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