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Glaucoma After Penetrating Keratoplasty

Mina Pantcheva, MD; Joel S. Schuman, MD, FACS; Malik Y. Kahook, MD; and David L. Epstein, MD, MMM

A common form of glaucoma that is difficult to manage is one that occurs after penetrating keratoplasty (PKP).^1–3 Most often, the mechanism involves peripheral anterior synechiae (PAS) formation and represents a form of chronic angle-closure glaucoma. However, the chronic use of topical steroids is responsible for some cases of secondary open-angle glaucoma. This latter diagnosis, which is often unrecognized because the time of onset may be late and the steroid dosage low, should always be suspected in these patients. Attempts should be made to reduce or discontinue the topical steroids. Intraocular pressure (IOP) may be substantially lower only a few days after steroids are totally discontinued, thus indicating an extreme sensitivity to these agents. It is important to note that increases in IOP place the corneal transplant at risk for rejection (Figure 38-1). One of the main risk factors for developing glaucoma post-PKP is the indication for surgery. Keratoconus is reported to have 1% incidence of induced glaucoma, whereas the incidence rises to 29% to 44% in patients undergoing surgery for aphakic bullous keratopathy.^2,4

The mechanism of angle-closure glaucoma is not well understood in these patients (Table 38-1). Pupillary block can occur, and for this reason, peripheral iridectomy should be routinely performed at the time of surgery. However, cases are encountered in which surgical iridectomy was performed, but in the postoperative period, the iris and iridectomy were observed to be adherent to the cornea and thus was nonfunctional. A transient wound leak must always be suspected. Some have questioned whether the iris may be more reactive after keratoplasty and whether iris swelling may lead to PAS formation and angle closure, especially if the iris is in contact with an intraocular lens haptic.⁵ Eyes with corneal disease often do demonstrate inflammatory ocular disease and the iris may thus be more “sticky.” Alternatively, one of us (DLE) has questioned whether choroidal detachment may occur intraoperatively from ocular hypotension, which may develop more commonly than suspected, leading to rolling forward of the ciliary body and iris into the angle. A choroidal detachment postoperatively from a transient wound leak would have the same effect. In addition, choroidal detachment may result in forward lens movement similar to that seen after retinal detachment surgery, which may add a pupillary block component to the angle closure. Lens swelling, if it occurs, may also cause pupillary block.

If acute angle-closure glaucoma is observed, laser iridectomy can alleviate the glaucoma. In the case of a choroidal detachment, surgical drainage may be required.

More commonly, acute postoperative glaucoma is not observed in these patients, but several weeks to months after keratoplasty, elevated IOP due to angle-closure glaucoma is first detected. In some of these cases, earlier elevations of IOP may simply have been missed, but in others, hyposecretion, perhaps due to a choroidal detachment, may have masked the angle closure and delayed IOP elevation. It is only later after the choroidal detachment resolves, and aqueous humor production returns to normal, that elevated IOP is observed.

Unfortunately, most of these cases are complicated, and the factors that have led to the chronic angle-closure glaucoma are unclear. With regard to prevention, a peripheral iridectomy should be performed at the time of surgery and the period of ocular hypotony minimized. Sodium hyaluronate can be used to maintain the anterior chamber. However, this agent can cause substantial IOP elevation postoperatively6 and should be removed from the anterior chamber at the conclusion of the operation. The anterior chamber should be well formed at the conclusion of surgery. Tightening the iris by direct suturing at the time of surgery may decrease the occurrence of angle closure.⁷

Experimental tight suturing close to the limbus in enucleated eyes can cause obstruction to outflow through an open-angle mechanism (not involving iris-trabecular apposition).6,8,9 However, if this occurs in living eyes, it most likely is a short-lived phenomenon. Slightly oversized corneal grafts may decrease the occurrence of such a secondary open-angle glaucoma.^10–12 Laser trabeculoplasty may be effective for patients with open-angle glaucoma after PKP.¹³ Secondary pigmentary glaucoma after anterior segment surgery can also occur.¹⁴

In the last several years, many forms of endothelial keratoplasty have been developed. The techniques aim to replace the diseased corneal endothelium with donor corneal endothelium, Descemet’s membrane, with or without a small amount of posterior stroma. Descemet’s stripping automated endothelial keratoplasty (DSAEK) and Descemet’s membrane endothelial keratoplasty (DMEK) have several advantages over conventional PKP. The most impressive is the rapid healing and early visual rehabilitation, but they also require few, if any, corneal sutures. Another major advantage is that the structural integrity of the recipient eye is maintained throughout the surgery. However, it involves injecting air into the anterior chamber, which can lead to pupillary block glaucoma if the air bubble extends beyond the inferior pupillary border when the patient is upright.^15,16 PAS can be formed if pupillary block occurs. PAS may also be formed if air enters the posterior chamber during the procedure and remains behind the iris while the patient remains supine. Lee and colleagues¹⁵ described a patient with pupillary block glaucoma and 6 patients with air in the posterior chamber leading to iridocorneal adhesions and increased IOP. The true incidence of glaucoma after DSAEK is not clearly known. It has been reported to be from 0% to 18%.¹⁷ Recently, Vajaranant and colleagues¹⁸ reported a relatively high incidence of IOP elevation after DSAEK in 35% of patients with no prior glaucoma, 45% of patients with prior glaucoma, and 43% of patients with prior glaucoma with preexisting glaucoma surgery, but no adverse visual outcomes related to IOP elevation in any group. The reported 12-month incidence of IOP elevation ranges from 6.5% to 11.1% after DMEK.^19,20

Patients who have had prior large iridectomy are at increased risk of air passage through the iridectomy into the posterior chamber. Superior iridotomies and iridectomies can be particularly challenging in the setting of unicameral eye, as air escapes from the anterior chamber into the vitreous cavity.

The major long-term clinical glaucoma problem after PKP and DSAEK/DMEK is chronic synechial angle closure. Medical therapy (Table 38-2) of this form of glaucoma is challenging because drugs that facilitate outflow, such as pilocarpine, are limited due to PAS formation. However, a trial of miotics is warranted because, in some cases, the PAS may be bridging over an otherwise functional trabecular meshwork to the cornea. Aqueous suppressants are useful. For surgical therapy, if PAS formation is recent, then, as discussed elsewhere, lysing of synechiae should be contemplated by use of argon laser gonioplasty or surgically.21–23 In long-standing cases with good central acuity, filtration surgery should be attempted initially, but special attention to the problem of flat anterior chamber is required due to the vulnerability of the recently transplanted cornea. Immediate or delayed suprachoroidal hemorrhage as a complication of filtration surgery may be more common in these eyes. Ciliodestructive procedures are effective means of IOP control,^23–28 but there is risk of macular edema in eyes with good acuity and risk of cataract formation in phakic eyes. Such treatment, however, is often the only effective means for pressure control. The use of glaucoma drainage devices (GDDs) can be effective but are accompanied by a high incidence of corneal graft rejection.^29,30

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