Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001

250 Glaucoma Associated with Ocular Surgery

tored and the patients have not been using topical steroids for a prolonged period of time, then stopping the offending medication will usually result in the IOP returning to baseline.

Generally, patients with preexistent glaucoma may find their condition worsening after ocular surgery. As noted previously, both open-angle and angle-closure glaucomas may be encountered in patients undergoing ocular procedures.

Can Glaucoma Occur Following Laser Procedures?

Yes, there are four laser procedures that will be highlighted here: laser iridotomy, laser photocoagulation, neodymium:yttrium-aluminum-garnet (Nd:YAG) capsulotomy, and laser trabeculoplasty.

A transient increase in IOP may arise following any intraocular procedure. However, since well-tolerated and fast-acting antiglaucoma medications have been introduced, the incidence of pressure elevation following these procedures occurs less often. Consider a series of patients who underwent laser iridotomy described by Lewis and coworkers3; 289 eyes of 179 patients underwent peripheral laser iridotomy. Patients’ diagnoses were narrow occludable angles, open-angle glaucoma, or chronic angle closure. Patients were treated perioperatively with pilocarpine and apraclonidine. No patients developed an increase in IOP of 25 mm Hg or greater. Only 0.7% of eyes with narrow occludable angles, 0.9% of eyes with open-angle glaucoma, and none of the patients with chronic angle-closure glaucoma developed an IOP elevation of more than 10 mm Hg compared to baseline. Thus, to avoid an increase in IOP in the immediate postoperative period, it is prudent to pretreat with an antiglaucoma medication such as apraclonidine, brimonidine tartrate, dorzolamide, brinzolamide, or pilocarpine. However, if a patient is chronically using an agent, the efficacy may be reduced in the perioperative period. Such reduced efficacy has been noted in patients who were chronically treated with apraclonidine and received this same drug following laser therapy.4

Malignant glaucoma or ciliary block glaucoma has been reported following laser iridotomy. This process may be worsened by the use of miotics postoperatively. It has been postulated that some of these eyes may have begun the process of aqueous misdirection prior to the completion of the laser procedure.5 Bilateral malignant glaucoma has been described in a 50-year-old patient who underwent bilateral laser iridotomies. The patient failed to respond to miotics but did respond to atropine and cyclopentolate. It was postulated that systemic hydrochlorothiazide therapy may have contributed to this presentation.6 Nevertheless, malignant glaucoma should be suspected if the anterior chamber shallows and the pressure elevates following laser iridotomy.

Another secondary glaucoma that may occur in association with laser iridotomy procedures is pupillary block glaucoma. In uveitic patients, it is common for laser iridotomies to close if there is a significant degree of inflammation. When one completes a laser iridotomy using the argon laser, posterior synechiae can form. Thus, in the presence of a once-patent laser iridotomy now closed, pupillary block can occur. This phenomenon is more likely to occur if pilocarpine is used postoperatively, considering the tendency of this medication to increase inflammation.

Secondary angle closure can occur following panretinal photocoagulation. Intense treatment of the retina can result in choroidal edema and detachment. Subsequently there may be rotation of the ciliary body anteriorly and narrowing of the anterior chamber angle. A patient who may have previously evidenced a narrow angle prior to the laser therapy may perilously slip into angle closure with an associated sustained increase in IOP.

Treatment and Management

How Are the Complications of Malignant Glaucoma and

Pupillary Block, Which May Occur Following Laser

Iridotomy, Managed?

Malignant or ciliary block glaucoma following laser iridotomy is initially treated with cycloplegic and mydriatic agents, agents that relax the ciliary body enabling its rotation posteriorly, and aqueous suppressants, which reduce the production of aqueous that may become loculated posterior to the vitreous. Essentially the cycloplegic agent paralyzes the circular ciliary muscle fibers and epinephrine tightens the zonules between the ciliary muscle and the lens. Using vitreous dehydrators such as isosorbide 45% at 1.5 cc/kg body weight or intravenous mannitol may assist in eliminating the continued accumulation of fluid in or behind the posterior hyaloid face as well as reduce the pressure of the vitreous body on the anterior segment. Topical antiinflammatory agents should be added to control the inflammation. Peripheral iridoplasty may also be helpful.

Figure 12–1 presents a decision tree that outlines the course of management for malignant glaucoma. Essentially, before one can diagnose ciliary block glaucoma, a patent iridotomy should be present. Otherwise the patient needs to be treated initially for pupillary block glaucoma with the completion of an iridotomy. If there is still a shallow chamber and the IOP is still somewhat elevated, then a choroidal effusion must be ruled out. If there is choroidal effusion, then this patient has angle-closure glaucoma with ciliochoroidal detachment. Cycloplegics and aqueous suppressants should be prescribed and the underlying cause of the ciliochoroidal detachment should be addressed. Argon laser iridoplasty can be tried, or surgical drainage of the choroidal detachment may be required if there is an excessively high IOP or corneal decompensation. However, usually patients will recover with medical therapy over time. If, on the other hand, there is no choroidal effusion, then the eye indeed has developed malignant or ciliary block glaucoma. Medical therapy should be instituted, specifically atropine 1% q.i.d., phenylephrine 10% q.i.d., acetazolamide 250 q.i.d., and a hyperosmotic agent usually b.i.d. This regimen is continued for 4 or 5 days. If this medical regimen is successful then systemic and the mydriatric agents are discontinued.7 If the problem persists then laser or surgical therapy may be necessary as outlined in Figure 12–1. If the patient is aphakic or pseudophakic, then one can proceed directly to laser or surgical therapy.

If one encounters pupillary block in a uveitic patient following an unsuccessful laser iridotomy procedure, then it is important to reestablish a patent iridotomy. The Nd:YAG laser is less likely to close, and thus completing a laser

iridotomy with this laser should be attempted. Intense use of antiinflammatory agents should be considered, and systemic agents may be necessary to overcome the inflammation. Finally, if laser iridotomy is not successful, then a surgical iridectomy should be completed. However, if there is extensive permanent closure of the trabecular meshwork, then a trabeculectomy with adjunctive use of antimetabolites such as mitomycin-C should be performed.

How Are the Complications of Laser Photocoagulation

Managed?

This secondary angle-closure problem should be successfully managed by performing laser iridoplasty to deepen the angle recess, initiating cycloplegics to deepen the anterior chamber, and adding topical and systemic antiinflammatory agents. Antiglaucoma medications, particularly aqueous suppressants can be used as needed. Once the inflammatory insult has subsided, the pressure often decreases.

What Is the Etiology of Pressure Elevation Following

Nd:YAG Capsulotomy and How Is It Managed?

An increase in IOP may occur following posterior capsulotomy. In a series of 897 Nd:YAG laser posterior capsulotomies, newly diagnosed glaucoma was noted in seven patients (0.78%), and five patients (0.56%) evidenced worsening of preexisting glaucoma.8

It is unknown what causes the increase in IOP following Nd:YAG capsulotomy, however, some authors have postulated that small amounts of lens and/or capsular particulates may seriously impair outflow. The Nd:YAG may also cause shock-wave damage to the trabecular meshwork.9 Patients with preexisting glaucoma are more likely to develop an IOP greater than 30 mm Hg within 1 hour following surgery.10

With the advent of -agonists, the incidence of pressure elevation has markedly decreased. Either apraclonidine 0.5 or 1% or brimonidine tartrate 0.2% can be administered prior to or after the laser procedure, thus blunting the increase in pressure. Topical carbonic anhydrase inhibitors have also been used in this setting. Patients who are already taking an -agonist have been shown to demonstrate less of an effect when an additional dose is given either before or after laser therapy. If the IOP is sustained, then the medical regimen will need to be adjusted. The frequency of postoperative follow-up of patients is dictated by the level of IOP following the procedure. In most instances, patients are seen in 1 week and then in 4 to 6 weeks.

Interestingly, malignant glaucoma has also been reported following Nd:YAG posterior capsulotomy. A 50-year-old pseudophakic man underwent posterior capsulotomy. The anterior chamber shallowed and the IOP increased. A laser iridotomy failed to lower the IOP. Eventually the patient responded to medical therapy, specifically, atropine, phenylephrine, mannitol, and acetazolamide. The anterior chamber deepened and the IOP decreased.11

Are There Specific Types of Patients Who Are at Greater Risk for Developing Glaucoma Following Cataract Surgery Besides Those Patients Who Have a History

of Glaucoma?

Yes. Patients with a history of primary open angle glaucoma uveitis, pigmentary dispersion, exfoliation syndromes, a previous history of trauma, or preexisting peripheral anterior synechiae from any cause have a risk of developing an elevation in IOP following cataract surgery2 (Table 12–1).

What Is the Incidence of an Elevation of IOP Following

Cataract Surgery?

The incidence of IOP elevation is dependent on the technique and complexity of surgery and the type of viscoelastic surgery that is used. When extracapsular cataract surgery was more commonly performed, it was estimated that 55% of patients evidenced a pressure elevation of 25 mm Hg or more.16 The newer techniques of phacoemulsification and smaller incisions have resulted in lower rates of pressure elevation. Clear corneal incisions are associated with a lower risk of pressure elevation.17 These episodes are often transient; however, patients with moderate or severe glaucomatous disease should be treated prophylactically in the first 24 hours following surgery.

What Are Some of the Reasons Associated with an

Increase in IOP Following Cataract Surgery?

There are several ways in which IOP may become elevated following cataract surgery. It is helpful to consider those causes that may be associated with a deep anterior chamber versus a shallow anterior chamber. First, consider a deep anterior chamber. If the incision is made at the corneoscleral limbus, then distortion of the aqueous outflow pathway can contribute to a decrease in out-

Table 12–1. Glaucoma Associated with Cataract Surgery

256 Glaucoma Associated with Ocular Surgery

flow facility.18 Another reason may be that the choice of viscoelastic substance and its incomplete removal from the eye may contribute to an elevation in IOP. Among the currently available substances, such as 1% sodium hyaluronate (Healon), a mixture of 3% sodium hyaluronate (AmVisc), 4% chondroitin sulfate (Viscoat), there is no particular one that causes a pressure elevation more frequently than another. Other causes of elevated IOP following cataract surgery include pigment dispersion, hyphema, and residual lens material and epithelial or fibrous ingrowth. This latter complication is caused by poor wound construction and can be difficult to manage. The diagnosis is made by observing a scalloped border on either the corneal endothelium or the anterior iris surface. One can apply an argon laser burn to the surface and if a fluffy, white lesion occurs, then it is likely epithelium.

If the patient presents with a shallow chamber and elevation of IOP, then the differential is as follows: pupillary block, iridovitreal block, malignant glaucoma or ciliary block glaucoma, and choroidal effusion or hemorrhage. Pupillary block occurs more commonly in the setting of an anterior chamber lens implant and less commonly with posterior chamber lens implants. Iridovitreal block may occur if the anterior hyaloid face is adherent to the posterior iris, thus limiting the egress of fluid from the posterior chamber.19 Malignant glaucoma is characterized by entrapment of aqueous in the vitreous cavity or posterior to the posterior hyaloid face and can also present as a shallow anterior chamber and elevated IOP. Finally, if the patient reports severe pain and decreased vision, then choroidal hemorrhage must be considered. This complication may occur more commonly in patients who are high myopes, in patients with previously inflamed eyes, or in elderly patients who have undergone previous vitreous surgery, in particular. The surgical management of these complications will be discussed in Chapter 11.

How Is Glaucoma Associated with

Cataract Surgery Managed?

For those patients who may simply evidence a transient increase in IOP, one can initiate antiglaucoma medications as needed. Intracameral acetylcholine (Miochol) and carbachol (Miostat) can effectively lower IOP.20 Postoperatively, if a problem persists, adrenergic antagonists, -agonists, and topical carbonic anhydrase inhibitors may be considered as potential agents that can be used. Generally it may take up to 72 hours for the pressure to return to baseline if absolutely no viscoelastic substance was removed from the eye. Latanoprost may be considered if other drugs are not effective. Antiinflammatory drugs should be used, particularly in those instances in which residual lens material is present. If the IOP elevation persists beyond the immediate postoperative period, then the patient should be monitored by undergoing serial visual fields and close observation of the optic nerve. Laser trabeculoplasty may be a consideration for those patients who are not controlled with antiglaucoma medications, once the eye has healed and is quiet.21 The success among pseudophakic patients is approximately 50% following laser trabeculoplasty. If vitreous is present in the anterior chamber, laser trabeculoplasty should not be performed.22

258 Glaucoma Associated with Ocular Surgery

What Are the Causes of the Distorted Anatomic Changes in the Aqueous Outflow Pathway?

Tight incision closure and employing a donor button that is the same size are two causes that have been implicated. Campbell and Grant23 experimentally sutured corneas without making incisions; when sutures were tightly knotted, there was an increase in outflow facility and collapse of the trabecular meshwork. This problem rarely occurs in phakic patients and has been reported to occur in as many as 70% of aphakic eyes.24 Apparently without the countersupport of the natural lens, the trabecular meshwork fails to maintain its normal anatomy. It is unclear if a pseudophakos provides sufficient counterbalance. Finally, same-size donor buttons have been implicated, as well, in distorting the angle, thus leading to an elevation in IOP.25

What Types of Angle-Closure Glaucoma Can Occur?

As occurs following cataract surgery, pupillary block and malignant glaucoma can occur in these cases, too. Even in the absence of pupillary block, the eye can experience closure due to peripheral anterior synechiae formation, which may be due to hypotony, a flaccid iris that becomes adherent, or uveitis.

What Are Some Additional Reasons for Either Elevated

IOP or Glaucoma Occurring Postoperatively?

Steroid-induced glaucoma likely occurs more commonly than suspected, given the necessary frequent use of potent steroids following postpenetrating keratoplasty. The need for long-term use of these drugs contributes to the likelihood of this problem occurring.26 Moreover, as stated earlier, if a patient has preexisting glaucoma, then it is likely that the glaucoma will worsen if one does not take the necessary precautions to avoid IOP elevation.

How Is Elevated IOP or Glaucoma Following Penetrating

Keratoplasty Managed?

There is little one can do to primarily correct the distortion of the trabecular meshwork. However, one can begin antiglaucoma medications early on, primarily aqueous suppressants. Miotics and prostaglandin analogues should be avoided due to the propensity of these agents to enhance inflammation in some eyes. Alpha-agonists may be considered as either a first-line or second-line class of drugs. The question of whether one should use a topical carbonic anhydrase inhibitor is an interesting one given the presence of carbonic anhydrase II in the corneal endothelium. It is probably wise not to use the topical agent in the acute or subacute period, but use the systemic agents instead. Considering that the corneal endothelium has carbonic anhydrase isoenzyme II as an important cellular component, the application of a topical carbonic anhydrase inhibitor may affect the ability of these endothelial cells to function. Generally, one should consider using through-and-through sutures and a oversized donor graft to decrease the chances of distorting the trabecular meshwork.

If there is evidence of pupillary block, then it is important to complete a laser iridotomy, preferably with a Nd:YAG laser. If there is extensive peripheral anterior synechiae formation, laser gonioplasty or iridoplasty can be performed. However, a clear corneal graft is necessary to visualize the angle. These techniques are more successful if they are performed within the first year of surgery.

For patients who evidence malignant glaucoma, treatment begins with medical therapy first, particularly in phakic patients. In pseudophakic and aphakic patients, there is the advantage of being able to proceed directly to the application of the Nd:YAG laser to the anterior hyaloid face and, if necessary, into the vitreous.

The management of steroid-induced glaucoma can be a little tricky in this setting, given the need to continue potent steroids to avoid graft rejection. It is more important to keep the inflammation controlled rather than shift to less potent steroids. There are steroids, however, that claim similar potency to Pred forte 1% (prednisolone acetate 1%) but do not elevate IOP. Vexol 1% (Rimexolone 1%) and Lotemax 0.5% (Loteprednol 0.5%) are examples of such steroid formulations and thus may be tried in this setting. Nevertheless, antiglaucoma medications can be initiated.

If there is significant visual field deterioration, optic nerve change or anticipated changes in either parameter in the presence of a sustained increase in IOP, then surgery may be necessary. If the angle is open and there is no previous history of laser trabeculoplasty, then this procedure can be performed. Van Meter and coworkers27 noted a 80% success of argon laser trabeculoplasty in aphakic and pseudophakic eyes following keratoplasty. Other options include a trabeculectomy with adjunctive use of antifibrotic agents, implantation of a glaucoma filtration device, or laser cycloablation. A summary of the abovediscussed approach to the management of patients postkeratoplasty is highlighted in Figure 12–2.

What Types of Glaucoma Are Noted Following

Retinal Surgery?

Three retinal procedures are considered here: (1) scleral buckling procedures,

(2) pars plana vitrectomy, and (3) intraocular gas or silicone oil (Table 12–3).

What Causes Glaucoma Following Scleral Buckling

Procedures?

When a snug scleral buckle is applied, there is blockage of the vortex veins, which leads to increased transmural pressure in the capillaries of the ciliary processes and marked distention of the ciliary body vasculature. As the ciliary body swells, it rotates anteriorly and pushes the iris root into the angle. This mechanism has been confirmed experimentally.28,29 Pavlin and coworkers30 documented supraciliary effusions and ciliary body thickening in 15 patients 1 week following scleral buckling procedures using ultrasound biomicroscopy. Supraciliary fluid was noted in 80% of patients. The thickness of the ciliary body increased on average 0.15 0.1 mm, and 55% of the patients evidenced anterior bowing of the iris. In three patients, the angle closed in one to three