40

Glaucoma in the Pseudophakic and Aphakic Eye

Ian Conner, MD, PhD; Joel S. Schuman, MD, FACS; and David L. Epstein, MD, MMM

A revolution has occurred in cataract surgery in the past 30 years, with the transition from intracapsular to extracapsular surgery (including phacoemulsification) via smaller and smaller incisions. In hindsight, many of the seemingly unique aspects of aphakic glaucoma clearly relate to the larger wounds and the removal of the capsule, zonule, and anterior hyaloid as occurred in intracapsular cataract surgery. Although intracapsular cataract surgery is rarely performed today, there are still many patients with aphakic glaucoma where some of the former issues still have relevance.

The major issue in pseudophakic and aphakic eyes is the less certain prognosis for filtration surgery because of previous conjunctival manipulation. Even prior clear corneal cataract surgery may increase the risk of filtration failure. The use of antimetabolites has improved the surgical prognosis for such eyes and is discussed in Chapter 60. If the conjunctiva is mobile, then filtration surgery with anti-metabolites can and should be performed as in phakic eyes. Sometimes, if there is scarring of the conjunctiva only at the limbus, the scleral flap dissection can be used to carry the surgical site anterior to the limbus underneath this external scarring, or a fornix-based conjunctival flap technique can be used. Subconjunctival fibrosis from previous cataract surgery is not simply a technical barrier to an adequate surgical procedure but also suggests the likelihood of exuberant post-filtration wound healing with a higher risk of bleb failure (“the conjunctiva always remembers”). In cases in which the conjunctiva is severely scarred, one may consider instead using a glaucoma drainage device, which may be placed more posteriorly away from the scar tissue. In the past, trabeculectomy was occasionally performed in the inferior quadrants in cases of significant superior scarring. This is rarely performed today due to concern for serious postoperative complications, including endophthalmitis.¹ With careful technique, tube shunt surgery can be used successfully in inferior quadrant locations. In addition, cyclodestructive procedures (see Chapter 57) are often reasonable surgical options in these challenging cases (Table 40-1).

THE POSTOPERATIVE EYE THAT IS APHAKIC

A large wound was employed with intracapsular surgery. Wound closure was frequently inadequate in these patients, with significant potential for wound leaks to occur that could allow the vitreous to displace anteriorly, potentially initiating pupillary block or malignant-type glaucoma conditions (see Chapter 30). There were many descriptive terms used to explain a postoperative flat anterior chamber, but many were precipitated by transient wound leaks. In addition, alpha-chymotrypsin was instilled into the eye to disrupt the zonular fibers and allow intracapsular delivery of the crystalline lens, but the liberated zonular fragments^2–4 could then obstruct the trabecular meshwork (TM) and produce a temporary but substantial postoperative glaucoma with intraocular pressure (IOP) in the 50s or higher.⁵ In retrospect, it is amazing how late we came to understand the mechanism of this postoperative glaucoma, especially given the potential for acute vascular events (eg, acute ischemic optic neuropathy or retinal vein occlusion). In the intracapsular surgery era, it was common practice to delay postoperative IOP measurement for several days because of concerns about infection. Now we suspect that the corneal edema and postoperative pain that many patients experienced was likely due to high IOP.

When anterior chamber lens implant techniques were added to intracapsular surgery, the acute postoperative IOP spikes were exaggerated by the use of viscoelastic material placed into the anterior chamber. Viscoelastic was not removed as it is now because of the risk of vitreous loss in these aphakic eyes. As we now know, thorough irrigation of viscoelastic from the anterior chamber reduces the incidence and severity of postoperative acute IOP elevation.6

Intracapsular cataract surgery is now rarely if ever performed. The following description is included for those rare occasions, but also for general orientation, historical importance, and context.

Open-Angle Glaucoma Due to Immediate Postoperative Reaction After Intracapsular Cataract Extraction

In the immediate postoperative period after cataract extraction, the IOP should be measured routinely. It is not uncommon to see substantial IOP elevation.⁵ The cornea may be deceptively clear or show only trace edema, despite high IOP. The anterior chamber maintains normal aphakic depth throughout, and the angle remains open.

Although IOP will return to normal usually in several days, these higher levels of pressure should be treated to prevent acute damage. Instances of optic atrophy have been observed from this temporary glaucoma. Aqueous suppressants are effective in lowering IOP in this condition,⁵ but osmotic therapy may also be required. This glaucoma has sometimes been blamed on postoperative iritis, but with little evidence. When alpha-chymotrypsin was introduced as an aid to intracapsular extraction, the incidence of acute, transient, postoperative secondary open-angle glaucoma increased. In a large series of cases, Kirsch⁷ found the incidence of transient postoperative glaucoma to be much higher in eyes in which the enzyme was used than in eyes without the enzyme.

The tendency for cataract surgeons to use a large number of interrupted sutures in closing the wound resulted in an increased number of cases of markedly elevated IOP in the immediate postoperative period. IOP usually returned to normal within a few days. These considerable elevations of IOP were less common in the earlier era when suturing was less common. Perhaps a small wound leak behaved as a safety valve, whereas numerous tight sutures prevented this inadvertent accessory aqueous outflow.

Clinical and experimental investigations by D. G. Campbell (personal communication, 1977) have shown that, in patients who had intracapsular cataract extraction with alpha-chymotrypsin and multiple sutures, the IOP was usually at its maximum on the day of the operation and gradually declined thereafter. Based on cadaveric studies, Campbell et al postulated that aqueous outflow was significantly obstructed when numerous limbal sutures were tightly tied.⁸ This pathologic obstruction was shown to be related to compression of limbal tissues and gross distortion of the aqueous outflow system by the sutures. The distortion of the tissues and the obstruction to outflow were readily reversible by loosening the sutures. These effects were subsequently confirmed by others.^6,9

In patients, the postoperative glaucoma that may be attributable to this mechanism generally subsided in a few days, presumably because of spontaneous suture loosening with resolution of postoperative edema.

Another factor that can cause impairment of outflow facility and a postoperative elevation of IOP is the use of ophthalmic viscoelastics during cataract surgery.⁶ Experimentally, a severe obstruction to outflow in enucleated human eyes occurs, additive to the effects of limbal suture compression.⁶ Clinically, severe postoperative glaucoma has been observed, sometimes persisting for several days.

These acute postoperative IOP elevations can be dangerous and difficult to treat, especially in patients with preexisting glaucoma and optic nerve damage.

THE POSTOPERATIVE PSEUDOPHAKIC EYE

With a historical background concerning intracapsular cataract surgery, one should not be surprised to learn that postoperative open-angle glaucoma also occurs after modern extracapsular cataract surgery, including phacoemulsification (Table 40-2). In extracapsular surgery, such severe IOP elevation is much less common, likely owing to several factors: omission of alpha-chymotrypsin, the smaller size wound, and the more efficient removal of ophthalmic viscoelastic material with irrigating/aspirating devices. However, substantial residual cortical material can impair outflow facility (lens-particle glaucoma) acutely (see Chapter 48). It is for this reason that IOP also must be carefully monitored after yttrium-aluminum-garnet capsulotomy, especially in patients with known glaucoma and/or decreased outflow facility.

The mechanism for open-angle glaucoma after extracapsular surgery most likely involves retained viscoelastic in the eye despite intraoperative irrigation, crystalline lens fragments that may have entered the outflow pathway intraoperatively, and wound compression and inflammation. Postoperative hyphema, although uncommon in phacoemulsification, can also contribute to the IOP elevation as the red blood cells are cleared through the trabecular outflow pathway11 and can temporarily obstruct it.

Especially in patients with susceptible optic nerves, the postoperative IOP must be carefully monitored with judicious use of preventative glaucoma therapy. In patients with such susceptible nerves and borderline IOP control, consideration should be given to performing a combined cataract extraction/filtration procedure (see Chapter 62) not only to establish better long-term IOP control but also to blunt this potentially damaging early postoperative IOP spike.

The choice of added glaucoma therapy depends on the patient’s existing regimen. Beta-blockers and/or alpha-agonists are commonly given at the end of surgery (if there is no contraindication), and some clinicians routinely employ a single administration of (often intravenous) carbonic anhydrase inhibitors. Except for the very small risk of blood dyscrasia in patients without a known systemic contraindication, such one-time use of carbonic anhydrase therapy is usually well tolerated. Miotics should be used sparingly because of the possible postoperative inflammatory reaction, and epinephrine-like compounds, used in the past, may cause cystoid macular edema as well as unwanted vascular effects in the acute postoperative eye.

It is important to measure the IOP no later than the next day, especially in patients at an increased risk.

DIFFERENTIAL DIAGNOSIS OF ACUTE POSTOPERATIVE GLAUCOMA IN THE PSEUDOPHAKIC EYE

The key question is whether the mechanism of the postoperative glaucoma involves an open or closed angle. This can usually be determined from the slit-lamp examination, evaluating the anterior chamber depth and configuration of the iris. The clinician should not hesitate to gently perform gonioscopy and examine the angle. It is fundamental to know whether one is dealing with angle closure or an open-angle process. In fact, one of the great lessons learned from the previous era of intracapsular cataract surgery and anterior chamber intraocular lenses was how common it was for the clinician to miss a treatable form of angle closure (due to pupillary block) on the basis of the slit-lamp examination alone.¹² Not uncommonly, such unsuspected pupillary block had a delayed onset. Unanticipated pupillary block has also been reported with use of posterior chamber intraocular lenses.¹³

If one is dealing with an open-angle postoperative glaucoma in the pseudophakic eye, then medical glaucoma therapy is used as above. The most common mechanism relates to retained viscoelastic material if the IOP is severely elevated and sustained. Such a viscoelastic-induced secondary open-angle glaucoma is usually self-limited over 4 to 5 days.^14,15 Newer, more cohesive viscoelastics can lead to longer term spikes in IOP related to inadequate intraoperative removal of these materials. Rarely, it may be necessary to take the patient back to the operating room and repeat irrigation of the anterior chamber. Anterior chamber washout can also be employed for a postoperative hyphema judged to be responsible for the IOP elevation. Of course, if a combined cataract/filtering surgery was performed, then suture lysis could be performed in the face of high postoperative IOP. However, in an additional 4 or 5 days, the temporary added obstruction to outflow from the viscoelastic material will have spontaneously cleared (by the normal action of the TM), so one should be cautious not to produce overfiltration with injudicious early suture lysis.

Often, the paracentesis performed at the time of surgery can be gently manipulated at the slit lamp to temporarily lower the IOP, although one should avoid substantially shallowing the anterior chamber, as this could produce other complications such as peripheral anterior synechiae (PAS). In the best-case scenario, a glob of cohesive viscoelastic material will exit the anterior chamber through the paracentesis with this maneuver. Otherwise, postoperative manipulation of the paracentesis site is commonly effective only in lowering the IOP for a few hours, so if the ocular hypertension recurs, then other choices for IOP lowering should be employed.

If the angle is closed, then the most likely diagnosis in the postoperative period is pupillary block. This has been discussed in Chapters 23 and 24, but the typical findings are a normal axial depth but shallow peripheral depth with a ballooning forward, or convex appearance, of the iris. Residual cortical material that has fluffed up behind the iris or capsular fragments may produce postoperative pupillary block. Inflammatory adhesions postoperatively may do likewise. The treatment is to either break the block by either dilating the pupil or placing a laser iridotomy.

It is no longer routine to place a surgical iridectomy at the time of cataract surgery. All patients who have an anterior chamber intraocular lens require a patent iridectomy or iridotomy.

Postoperative angle-closure glaucoma that persists despite a patent laser iridotomy is by definition not secondary to pupillary block, and must be further investigated to determine the cause and subsequent course of treatment. In brief, the differential diagnosis must first rule out choroidal hemorrhage or effusion, but should then be treated as malignant glaucoma until proven otherwise. A careful slit-lamp examination along with a skilled B-scan should be sufficient to determine the nature of the postoperative angle closure without pupillary block.

Primary Open-Angle Glaucoma and the Pseudophakic Eye

In the past, some clinicians felt that (intracapsular) cataract surgery could improve long-term IOP control.^16,17 There was considerable controversy, and interestingly there have been swings of opinion.

The following is what we judge to represent current clinical information about the effect of extracapsular cataract surgery alone on the course of open-angle glaucoma, but this is being continuously evaluated. In the immediate postoperative period,^18,19 there can be instances of acute worsening of the open-angle glaucoma (see Table 40-2) from a few days to weeks that should lead to consideration of combined cataract and fistulizing surgery being performed. Beginning several months after cataract surgery (when routine corticosteroids have been stopped), there is the strong clinical impression of a beneficial effect on IOP control in some patients.^20,21 Because this effect of cataract surgery on IOP is unpredictable, cataract surgery alone should not generally be employed as a strategy for patients with borderline IOP control. Classically, this has been thought to be secondary to transient hyposecretion of aqueous humor, but this mechanism has not been adequately confirmed. Another hypothesis involves a stress response as part of usual postoperative inflammation that may clear debris from the outflow pathway, as has been proposed to occur following the “inflammation” that accompanies laser trabeculoplasty.^22,23 In fact, such an occurrence might explain the generally poorer response of pseudophakic and aphakic eyes to laser trabeculoplasty in that they have already participated in such a TM inflammatory response.

Historically, it has been felt that in the long term (after a year) the open-angle glaucoma returns to baseline with no residual beneficial effect. In fact, the long-term beneficial effect that was reported by some in the intracapsular era was likely due to continued occult filtration that was probably initiated because of a loosely sutured wound. However, the final word may not have been spoken in this regard, especially in light of numerous more recent publications demonstrating modest sustained IOP lowering after phacoemulsification.²¹ Unfortunately, more work is needed to better understand the mechanism, magnitude, and duration of this effect. Given the common coexistence of cataract and glaucoma, it nonetheless seems clear that cataract extraction at least plays a role in the management of IOP in glaucoma patients.

Patients with open-angle glaucoma who are pseudophakic can be treated with the usual antiglaucoma medications, with the exception that epinephrine-like compounds should be avoided in both the pseudophakic as well as aphakic eye in order to avoid the potentiation of cystoid macular edema. Fortunately, these agents are uncommonly used today. Miotics can play an important role in pseudophakic eyes but require proper attention to the retina because of the slight increase in risk of retinal detachment. Indeed, miotics are usually well tolerated by the pseudophakic patient, and weak concentrations of strong miotics, such as echothiophate iodide (Phospholine Iodide) are often remarkably effective. Both echothiophate and pilocarpine gel also offer the advantage of infrequent dosing and are usually very patient friendly.

Eyes with pseudoexfoliation have a tendency toward earlier cataract formation,²⁴ and the clinician should be alert to possible previously undiagnosed pseudoexfoliation in pseudophakic eyes, especially because pseudoexfoliation eyes also have some tendency for rapid worsening of glaucoma control. In the pseudophakic eye with an absent anterior lens capsule, the light gray amorphous exfoliation material may still be seen on the pupillary border, the posterior surface of the iris, the ciliary processes, the zonules, and the anterior capsular remnants.

When considering cataract surgery in the prephacoemulsification era on a patient with currently well-controlled primary open-angle glaucoma, it was prudent to save some of the superior conjunctiva (eg, in the superonasal quadrant) for possible future filtration surgery and, therefore, to perform the cataract surgery more temporally. With the dominance of phacoemulsification and the clear corneal approach, this is much less of a concern.

Gonioscopy should be routinely performed on all eyes with glaucoma several months after cataract surgery (if not sooner in response to acute problems) to establish a new baseline. An unpleasant surprise is sometimes experienced when one views the presence of new PAS and thus loss of some of the angle circumference for outflow in a situation where the trabecular outflow was already abnormal due to primary open-angle glaucoma. Such PAS formation may result from an undetected transient wound leak, pupillary block, or may be a result of postoperative inflammation. Sometimes, residual lens cortex will fluff up postoperatively and mechanically force the iris into the angle, resulting in synechiae formation. An anteriorly displaced intraocular lens haptic may do the same.25 After a combined cataract/filter operation where there is overfiltration and a transient shallow chamber, there may also be resulting formation of PAS. This is much more common after (combined) cataract surgery than after filtration surgery alone, presumably because of the greater amount of postoperative inflammation that seals the iris to the apposed TM.

If extensive PAS formation is observed, then consideration should be given to laser iridogonioplasty. Recently formed PAS can sometimes be pulled from the angle using this technique. Unfortunately, such PAS are often tightly cemented in the angle and not able to be broken.

Sometimes, PAS formation may seem extensive but the IOP, and especially the response to outflow drugs, such as miotics, is normal. In such cases of normal outflow, one must be certain that one is not dealing with an inadvertent cyclodialysis cleft produced at the time of surgery (although if the IOP is controlled and not hypotonous, glaucoma therapy should just be continued; cyclodialysis was at one time a very useful surgical procedure for glaucoma but was unfortunately unpredictable). More likely, with controlled clear corneal incisions, one must be certain that the low IOP following initiation of miotic therapy is not due to a retinal detachment. However, it is also possible that the angle synechiae are actually bridging the TM to the peripheral cornea at Schwalbe’s line and that there is functional underlying TM. With shallow anterior chambers due to overfiltration (and usually quiet eyes), it is not rare for such bridging synechiae to occur.

Nevertheless, it is a cause for great concern when a patient with open-angle glaucoma, especially one with marginal control, now develops a secondary angle-closure component. Unobserved, transient pupillary block^12,13 in the postoperative period may also have been the cause of occult PAS.

APHAKIC PUPILLARY BLOCK

Aphakic pupillary block is rarely seen now except in previously aphakic eyes undergoing subsequent additional surgery. Chandler and Grant offer a classic description of the clinical findings, which should be treated with a laser iridotomy:

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