Glaucoma is one of the most frequent and severe postoperative complications of penetrating keratoplasty (corneal transplant), as demonstrated by the fact that up to one third of corneal graft failures are caused by a rise in intraocular pressure (IOP).
The ensuing endothelial decompensation finally leads to permanent corneal graft opacification. Endothelium is an important layer on the back of cornea.
There is general agreement that, unless the IOP is preoperatively well under control, a penetrating keratoplasty should be avoided.
Meanwhile, the problem of IOP elevation after penetrating keratoplasty (PKP) has been intensively investigated. Various factors have been identified that are associated with a higher incidence of postoperative IOP rise and graft failure.
These factors include donor age, recipient age, the extent of preoperative astigmatism, the extent of graft-host interface scarring, and the type of donor tissue used for the graft. It is still unclear whether any of these factors alone or in combination, can be used to predict the risk of postoperative IOP rise after penetrating keratoplasty.
Meanwhile, many surgeons still believe that they can prevent IOP-induced complications by performing deep anterior lamellar keratoplasty (DALK) or Descemet stripping automated endothelial keratoplasty (DSAEK) instead of penetrating keratoplasty. This is not justified, because these techniques are far more difficult and time-consuming than penetrating keratoplasty.
What are the Risk Factors for Glaucoma after Corneal Transplant?
From a database of 1122 penetrating keratoplasties performed at Moorfields Eye Hospital in London (1992) a total of 153 eyes (14%) were identified as being complicated by glaucoma within a time period of four years after surgery.
The risk for its development depends on the primary indications for keratoplasty: Keratoconus, some corneal dystrophies and uncomplicated implantations of intraocular lenses have a relatively low incidence of IOP elevation.
However, the risk of glaucoma greatly increases in cases of combined cataract or lens implantation with anterior vitrectomy or “anterior segment revision”. Anterior chamber dysgenesis syndromes appear to have the highest incidence of this complication.
In addition, penetrating keratoplasty performed as a secondary procedure after failure of previous penetrating keratoplasty or endothelial keratoplasty is associated with an even higher incidence of postoperative IOP rise.
IOP rise after penetrating keratoplasty is more common in eyes with astigmatism of more than 5 diopters (D) than in eyes with less than 5 D astigmatism. This shows that the degree of preoperative astigmatism has a greater impact on the risk of developing glaucoma than the extent of donor-recipient interface scarring.
In addition, astigmatism is known to be one of the risk factors for postoperative IOP elevation after cataract surgery.
IOP elevation may develop between one month and five years after penetrating keratoplasty. The mean interval between penetrating keratoplasty and the onset of glaucoma was 4.3 months. It is worth noting that, despite the high incidence of IOP elevation after penetrating keratoplasty, only about 25% of these eyes are symptomatic.
The incidence of IOP elevation after penetrating keratoplasty seems to vary greatly among different studies. The incidence of postoperative IOP elevation in a series of 1340 eyes by Mouton et al. was approximately 5%, whereas the incidence of glaucoma after penetrating keratoplasty reported in a series of 636 patients by Hernández et al. was approximately 18%.
What Causes Glaucoma after Corneal Transplant?
1. Acute Postoperative Elevation of IOP
Immediately after surgery, a temporary rise of IOP can be caused by blood or viscoelastic material that was not completely removed at the end of the operation and obstructs the chamber angle.
In most cases, this spike can be easily treated with topical anti-glaucomatous therapy or it can often be completely avoided by a prophylactic use of carbonic anhydrase inhibitors.
Partial or complete closure of the corneoscleral angle is certainly one of the main reasons for secondary glaucoma. It can develop either during the early or late postoperative phase because of changes in the width of the anterior chamber angle by tight suturing of a relatively small graft.
Improvements in the technique of penetrating keratoplasty – like a peripheral iridectomy or the use of a slightly oversized corneal button – have reduced the rate of postoperative complications.
2. Chronic Secondary Glaucoma
Several mechanisms may be involved in the development of glaucoma:
- Worsening of pre-existing primary open-angle glaucoma.
- Changes of the angle of the anterior chamber, e.g. progressive peripheral anterior synechiae (PAS) formation after previous surgery, inflammation or injuries.
- Malformation of the iris.
The incidence of post-keratoplasty glaucoma depends mainly on the initial anterior chamber findings: with no developmental abnormality of the anterior chamber angle only 0% to 4% of the eyes will develop a glaucoma, whereas this incidence can rise to a number ranging from 20% to 87% in eyes with previous damage of the angle.
3. Secondary Inflammatory Glaucoma
Bacterial corneal ulcerations with impending perforation or post-herpetic scars often may require a penetrating keratoplasty. Minimizing postoperative uveitis is not only important for the prevention of corneal graft rejection, but also for the prevention of secondary glaucoma.
4. Steroid-induced Glaucoma
Topical and sometimes long-term systemic steroids are routinely used for preventing corneal graft rejections. This need for a continuous use of steroids can be responsible for a slow increase of IOP. With some patients, the so called “steroid-responders”, a very high intraocular pressure may develop within quite a short time of treatment.
How do Surgeons Prevent Post-keratoplasty Glaucoma?
Improvements in the surgical technique of penetrating keratoplasty certainly have reduced the rate of postoperative complications.
It is now recommended to use a corneal button slightly larger than the recipient bed. A smaller graft additionally seems to have less influence on the peripheral cornea and the aqueous outflow in the trabecular meshwork. Sutures that try to reestablish a continuity of Descemet’s membrane will also reduce the risk of trabecular meshwork collapse.
Peripheral anterior synechiae formation due to a shallowing of the anterior chamber is one of the reasons for the development of glaucoma. Maintenance of anterior chamber depth during surgery is therefore crucial. “Watertight” suturing and the use of viscoelastic materials such as hyaluronic acid result in a better maintenance of the anterior chamber.
In some cases, even a goniosynechiolysis can be performed successfully with the use of viscoelastics. At the end of surgery, however, these substances have to be removed as completely as possible.
Some authors also recommend a routine peripheral iridectomy to avoid a postoperative pupillary block. Topical steroids and cycloplegics are also applied frequently after surgery to maximally suppress postoperative inflammation.
How is Diagnosis of IOP Elevation Made?
Because of the highly irregular corneal surface in the early postoperative phase, it is sometimes very difficult to precisely measure IOP by applanation tonometry alone. Further information is gained by thorough slit lamp examination of the cornea: epithelial oedema speaks for Descemet’s folds and stromal oedema against an increased IOP.
Certainly every additional (e.g. anti-herpetic) treatment has to take the underlying disease, such as keratoconus or herpetic eye disease, into consideration.
How is Post-Keratoplasty Glaucoma Treated?
Both acute and chronic IOP elevation after penetrating keratoplasty are, at times, very difficult to control. Medical therapy is tried first, because every surgical procedure can further endanger the survival of the graft.
- Medical treatment
Beta-blockers (e.g., Timolol eye drop) are generally accepted as the drugs of first choice. They can also be used in combination with other anti-glaucomatous preparations. Miotics are generally not recommended in eyes with peripheral anterior synechiae formation; in addition, they may enhance postoperative inflammation because of a breakdown of the blood-aqueous barrier which further compromises the corneal graft.
- Laser treatment
Depending on the aetiology and severity of the glaucoma, all available modalities of laser therapy can be useful: laser trabeculoplasty, laser iridotomy and cyclophotocoagulation. Argon-, Nd:YAG- or diode lasers are routinely used in clinical practice.
- Surgical treatment
Filtering procedures with or without adjunctive therapy of antimetabolites have only a low long-term success rate. Some authors report good results using aqueous drainage devices, with success rates of up to 70%.
Eyes requiring a penetrating keratoplasty often carry a long history of previous diseases, recurrent inflammation, trauma and/or multiple surgeries. Frequently, a more complex surgical procedure is necessary that causes a more severe postoperative inflammatory reaction. This, in turn, reduces the success rate of post-keratoplasty glaucoma surgery. One has also to take into consideration the fact that graft failures are described with an incidence of 30% to 50% after additional intraocular surgical procedures, such as filtering operations.
Glaucoma certainly is one of the most threatening complications following penetrating keratoplasty. Taking care of possible risk factors, improving the surgical techniques and closely following the patient can significantly increase the overall success rate.