POST-KERATOPLASTY GLAUCOMA

INTRODUCTION:

A number of mechanisms can cause elevated intra-ocular pressure (IOP) following penetrating keratoplasty (PK). These include both open-angle and closed-angle mechanisms. The eye could be prone to glaucoma prior to surgery (such as iridocorneal endothelial {ICE} syndromes, which led to the PK), have controlled glaucoma which became uncontrolled following surgery, steroid induced or other mechanisms discussed ahead. Glaucoma after corneal grafting is dangerous not only from the standpoint of glaucomatous optic atrophy but also from the high incidence of associated graft failures.

The prevalence of glaucoma following PK ranges from 10-53%. In a prospective series of 137 consecutive eyes with follow-up ranging from 7 to 30 months, 27% developed chronically elevated IOP after PK. Kirkness and Ficker reported a 14% incidence of glaucoma in 1122 post-PK eyes. One study revealed a 31% incidence of early increases in IOP and a 29% incidence of late (>3 months) increases; another large survey had a 9% incidence of immediate postoperative glaucoma and an 18% incidence of chronic post-keratoplasty glaucoma.

A number of risk factors have been described for the development of post-PK glaucoma. These include pre-existing glaucoma, aphakia, uncontrolled inflammation, explantation of intra-ocular lens (IOL), combined vitrectomy or anterior segment reconstruction, higher age (>60 years) and corneal diseases such as ICE syndromes, bullous keratopathy, adherent leukomas, anterior segment trauma, herpetic keratitis, and anterior segment dysgenesis syndromes. The incidence of postkeratoplasty glaucoma is also increased after repeated PK.

MECHANISMS:

In the early post-operative period, IOP elevation can be attributed to inflammation, hyphema, pupillary block or steroid-induced mechanisms. In aphakic patients IOP elevation occurs due to collapse of trabecular meshwork as a result of loss of anterior support due to incision in the Descemet’s membrane as well as reduction in posterior support from loss of zonular tension. Another mechanism postulated is compression of the anterior chamber angle caused by the conventional suturing techniques of PK, causing an early postoperative IOP rise and subsequent chronic glaucoma due to peripheral anterior synechiae. Other mechanisms include retained viscoelastic agents, inflammation and lens induced mechanisms.

Late mechanisms include gradual flattening of the anterior chamber several months following aphakic-PK. This is attributed to an intact anterior vitreous face; hence, prophylactic vitrectomy has been suggested to minimize this complication. The risk of graft rejection requires long-term steroid administration and the attendant side-effect of steroid-induced glaucoma. Progressive synechial angle closure is also responsible for IOP elevation in a significant number of patients. The incidence of glaucoma is proportional to the amount of synechial angle closure. More the degree of closure higher the incidence of surgery required for the control of the glaucoma. Yet another mechanism which could lead to the development of glaucoma is epithelial ingrowth.

MANAGEMENT:

PREVENTIVE MEASURES

Angle compression may be minimized and trabecular support improved by the following factors: a donor graft that is larger than the recipient trephine; looser or shorter suture bites to minimize tissue compression; smaller trephine size; a thinner peripheral host cornea; and a larger host corneal diameter. [Shields Text book of glaucoma]

It is controversial whether an oversized corneal donor graft improves outflow and reduces post-PK glaucoma. A perfusion study with autopsy eyes revealed no improvement in outflow, and the use of 0.5-mm oversized grafts in a clinical series afforded no protection against postoperative glaucoma. However, other clinical studies indicate that the use of oversized grafts is associated with deeper anterior chamber depths, a lower incidence of progressive angle closure, and significantly lower postoperative pressures, compared with use of same-sized grafts.

Other measures to minimize IOP elevation include meticulous wound closure and extensive postoperative steroids to reduce inflammation, but with caution for steroid-responsive patients.

SPECIFIC TREATMENT OF GLAUCOMA

Pharmacological therapy should be tried first, unless a specific, treatable condition, such as pupillary block, is apparent. Carbonic anhydrase inhibitors are usually ineffective in controlling early post-operative rise in IOP. However, they are useful in treating chronic glaucoma. They should be avoided in the presence of corneal decompensation. Timolol and miotics have also been found useful in a number of cases to manage post-PK glaucoma. However, miotics may increase the pupillary block and inflammation. Prostaglandin inhibitors should be avoided where the indication for PK was herpetic keratopathy as the risk for recurrence is increased.

Pupillary block can be overcome by laser iridotomy.

Surgical therapy is indicated if the IOP elevation is unresponsive to medical treatment and the optic nerve or the graft is threatened from the elevated IOP. A 30% incidence of graft failure after any intraocular procedure to reduce IOP has been reported. In a study, performing PK after trabeculectomy had a 5-year probability of successfully maintaining IOP control and a clear graft of 27%; however, combined PK and trabeculectomy improved the rate to 50%.

Trabeculectomy augmented by anti-metabolites has higher chances of success. In a retrospective study of 34 eyes, those eyes that were treated with trabeculectomy with mitomycin C had better control of IOP than eyes that did not receive the antimetabolite (73% vs. 25%, respectively), with graft survival of 69.2% in the mitomycin C group and 37.5% in the group that did not receive mitomycin C. Studies also report combined filtration surgery and PK to be associated with a higher graft survival rate compared with staged surgery.

Glaucoma drainage device implant is often considered superior to glaucoma filtering surgery in post-PK glaucoma. In a series, final IOP of less than 18 mm Hg in 96% of the eyes was achieved; but graft failure occurred in 42% eyes.

Trans-scleral Cyclophotocoagulation was reported to reduce IOP between 7 and 21 mmHg in 77% patients.

DESCEMET-STRIPPING ENDOTHELIAL KERATOPLASTY:

Glaucoma after Descemet-stripping endothelial keratoplasty (DSEK) has been reported to occur in 0% to 15% of cases. Two mechanisms for its causation have been proposed: pupillary block related to the air bubble in the immediate postoperative period and obstruction of the trabecular meshwork resulting from long-term steroid use. Management involves use of IOP-lowering medication and release of air from a paracentesis as deemed appropriate.

CONCLUSION:

Post-PK glaucoma is associated with multiple mechanisms and has the potential to adversely affect graft survival. It is often refractory to management. Ideal management should be individualized.