Ординатура / Офтальмология / Английские материалы / Shields Textbook of Glaucoma, 6th edition_Allingham, Damji, Freedman_2010

caused by the conventional techniques of penetrating keratoplasty, causing an early postoperative IOP rise and subsequent chronic glaucoma due to peripheral anterior synechiae (178, 179). (Modified techniques that may help to avoid this complication are discussed under “Management.”)

Late Postoperative Period

Gradual flattening of the anterior chamber several months after aphakic keratoplasty has been described (180). This phenomenon appears to be related to an intact anterior vitreous face, and prophylactic vitrectomy has been suggested to avoid this complication. IOP elevation may also occur in association with graft rejection, which may require long-term steroid and antiglaucoma therapy (181). The pigment dispersion syndrome may also be seen with pseudophakic eyes that have undergone corneal transplantation; in these patients, the syndrome has the unique feature of an inferior linear pigmented endothelial line, and it should not be confused with an allograft reaction (182). Another late-developing glaucoma occurs after keratoplasty for congenitally opaque corneas (183). It is not associated with peripheral anterior synechiae, and the mechanism is unknown. Other forms of late-onset glaucoma may result from peripheral anterior synechiae, the long-term use of steroids, or epithelial ingrowth (144, 175, 184).

Management Preventive Measures

On the basis of a mathematical model, 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 (179, 185). Reports conflict regarding whether an oversized corneal donor graft improves outflow and reduces postkeratoplasty 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 (186, 187). 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 (188, 189, 190 and 191). Oversized grafts, however, are contraindicated in treating keratoconus because they cause a significant increase in myopia (192). Another technique to prevent postkeratoplasty angle-closure glaucoma is the placement of sutures near the pupillary portion of a flaccid iris to create a taut iris (193). In addition, glaucoma after keratoplasty can be minimized by using meticulous wound closure and extensive postoperative steroids (194) (with caution for steroidresponsive patients).

Treatment of Glaucoma

Medical Therapy. Medical therapy should be tried first, unless a specific, treatable condition, such as pupillary block, is apparent. However, attempts to alter the early postoperative pressure rise are frequently unsuccessful. Carbonic anhydrase inhibitors were not found to be significantly efficacious in this situation (195), although they may be useful in treating the chronic glaucoma. Reported results with timolol have been conflicting (195), although the drug does appear to have some value, especially in controlling chronic glaucoma after keratoplasty (175). Miotics may occasionally be of value.

Surgical Therapy. Surgical therapy is indicated when the optic nerve head or the graft is threatened by a persistently elevated IOP. No glaucoma operation has been found to be entirely suitable for controlling IOP and preserving graft clarity. One investigation found a 30% incidence of graft failure after any intraocular procedure (196). When penetrating keratoplasty was performed after trabeculectomy in one series, the 5-year probability of successfully maintaining IOP control and a clear graft was only 27%, which increased to 50% in another series of combined trabeculectomy and penetrating keratoplasty (197). Implantation of a Molteno drainage device achieved IOP control of 21 mm Hg or less with one or more procedures in a series of 17 eyes, although seven had allograft rejections (198). In another series, involving 26 eyes with glaucoma drainage devices, final IOP was less than 18 mm Hg in 96% of the eyes but graft failure occurred in 42% (199). Cyclocryotherapy was once the most commonly used surgical procedure for glaucoma after penetrating keratoplasty (200), although the high incidence of serious complications limits its usefulness. Transscleral cyclophotocoagulation has largely replaced

cyclocryotherapy as the cyclodestructive procedure of choice. However, in one series of 39 patients, 77% had a final IOP between 7 and 21 mm Hg, but 44% of those with clear grafts before cyclophotocoagulation had graft decompensation (201).

Descemet-Stripping Endothelial Keratoplasty

Glaucoma after Descemet-stripping endothelial keratoplasty has been reported to occur in 0% to 15% of cases by two mechanisms: pupillary block related to the air bubble in the

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immediate postoperative period and obstruction of the trabecular meshwork resulting from long-term steroid use (202). Management involves use of IOP-lowering medication and release of air from a paracentesis as deemed appropriate.

GLAUCOMA ASSOCIATED WITH KERATOPROSTHESIS

A keratoprosthesis, such as the Boston keratoprosthesis or the osteo-odonto-keratoprosthesis, can be used to provide an optically clear pathway in cases of severe corneal opacification and vascularization— for example, after chemical burns or with autoimmune disorders, such as Stevens-Johnson syndrome. Preexisting glaucoma appears to be a significant risk factor for elevated IOP and visual loss postoperatively (203, 204), and as a result, implantation of a glaucoma drainage device at the time of the keratoprosthesis surgery has been suggested (Fig. 26.11). Close monitoring of patients for development or exacerbation of glaucoma is warranted in the postoperative period, and if medical management does not sufficiently control the IOP, transscleral diode laser cyclophotocoagulation may be a useful adjunctive measure (205). Measuring IOP in these patients remains problematic.

GLAUCOMAS ASSOCIATED WITH VITREOUS AND RETINAL PROCEDURES Glaucomas after Pars Plana Vitrectomy

Incidence

IOP elevation is the most common major complication after pars plana vitreous surgery. The reported incidence of postoperative glaucoma ranges from 20% to 26% (206, 207 and 208). In one prospective study of 222 cases, an IOP rise of 5 to 22 mm Hg during the first 48 hours occurred in 61% of eyes, and an increase of 30 mm Hg occurred in 35% (209).

Figure 26.11 Slitlamp photographs of patients with keratoprostheses. Glaucoma is a challenging accompaniment in many patients with these devices. A: Type I keratoprosthesis used in a patient with intact conjunctiva and adequate tear function. This patient required placement of a glaucoma drainage device for uncontrolled glaucoma. Note the silicone tube in the pupillary space. B: Type II keratoprosthesis used for patients with inadequate tear function or conjunctiva. The keratoprosthesis extends through the closed eyelid. (Courtesy of Natalie Afshari, MD.)

Clinical Findings and Glaucoma Mechanisms

Many of the factors that lead to IOP elevation after pars plana vitrectomy and the management of these conditions are considered in other chapters. These various mechanisms are reviewed here according to the time frame in which they occur after vitreous surgery.

First Day

Air or long-acting gases such as sulfur hexafluoride and perfluorocarbons (perfluoropropane and perfluoroethane) are occasionally injected into the vitreous cavity to tamponade the retina. The expansion of these gases during the early postoperative period can lead to significant IOP elevation (206, 207 and 208). Perfluorocarbons are capable of greater expansion and longevity than sulfur hexafluoride (210). In one study of 10 patients receiving 0.3 mL of perfluoropropane, all eyes had an immediate increase in IOP, which was sufficient in four eyes to collapse the central retinal artery (211). However, the pressure fell to baseline level in 30 to 60 minutes and did not rise again for the subsequent 5 days.

Monitoring IOP in the early postoperative period is important when using any long-acting gas, and attention must be given to the tonometer used. Pneumatic tonometry underestimated IOP in gas-filled human autopsy eyes, whereas Perkins applanation tonometry gave the most accurate readings when using a mercury manometer as a reference standard (212). In a clinical study of 84 gas-filled eyes, the Tono-Pen gave pressure readings similar to those obtained by Goldmann applanation tonometry, but pneumatic tonometry again underestimated the IOP (212).

Occasionally, it is necessary to remove a portion of the gas to relieve extremely high IOPs (206). Patients with a gas-filled eye should be cautioned regarding air travel, although expansion of a 0.6-mL bubble during ascent is usually compensated for by accelerated aqueous outflow without a significant IOP rise (213, 214). On descent, the eye may become hypotonus, and drugs that reduce aqueous production should be avoided, because they may prolong the hypotony, leading to uveal effusion (214). P.379

Figure 26.12 Pupillary block by silicone oil. A: IOP is elevated by minute silicone oil bubbles in the anterior chamber angle, seen here to the left of the corneal reflex and on either side of the line of iris illumination. B: Gonioscopic view of the superior quadrant, where an accumulated bank of silicone bubbles has created an “ inverse pseudohypopyon.”

Another class of agents, heavier-than-water perfluorocarbon liquids, can be used to hydrokinetically manipulate the retina, to remove dislocated intraocular lenses and lens fragments, and as short-term tamponade. One of these, perfluoroperhydrophenanthrene (Vitreon), was associated with chronically elevated IOP in 11% of cases (215). The mechanism of the associated glaucoma appears to be angle closure (216).

Severe choroidal and ciliary body hemorrhage, the equivalent of an expulsive hemorrhage in open-eye surgery, can also cause angle-closure glaucoma in the immediate postoperative period (207).

First Week

IOP elevation during this period is most likely caused by hyphema, ghost cells, or hemolytic glaucoma (see Chapter 24); retained lens material with phacolytic glaucoma (see Chapter 18); uveitis (see Chapter 22); or preexisting glaucoma. Another cause of IOP elevation in the early postvitrectomy period is overfill of the anterior chamber (with an open angle) or fibrin pupillary block (217). The latter has been successfully treated with the use of argon laser to make holes in the fibrin pupillary membrane and by the intracameral injection of recombinant tissue plasminogen activator to dissolve the fibrin clot (218,

219).

Two to Four Weeks After Surgery

Between 2 and 4 weeks postoperatively, the cause of newly developed glaucoma is most often neovascular glaucoma (discussed in Chapter 19).

Silicone oil is occasionally used as a retinal tamponade in unusually difficult vitreoretinal procedures. The reported frequencies with which this technique is associated with postoperative IOP elevation vary widely, ranging from 5% to 50% (217), and one series showed no influence of silicone on ocular tension (220). This discrepancy may be related to the numerous variables produced by the intraocular silicone and to the underlying disease of the eye, which may reduce aqueous outflow and inflow, with the resulting IOP representing a balance of the two. Most studies, however, suggest that a high percentage of patients do have a transient postoperative pressure rise, with a small proportion retaining chronic glaucoma.

Mechanisms of IOP elevation that are directly attributable to the silicone include pupillary block and silicone oil in the anterior chamber (Fig. 26.12). Histologic studies have shown obstruction of the trabecular meshwork by minute silicone bubbles, pigmented cells, and silicone-laden macrophages (221). However, these findings are not always associated with glaucoma. In one study, new glaucoma developed in 10% of eyes with emulsified silicone oil in the anterior chamber (222). The absence of glaucoma in other cases may result from the pressure-lowering effect of ciliary-body detachment by cyclitic membranes or total retinal detachments (223, 224). Fibrous tissue has been shown to form around silicone vesicles, the retraction of which may lead to these detachments (224).

An iridectomy may relieve the pupillary-block mechanism and some cases of COAG by allowing the silicone to fall back into the vitreous cavity. Because the silicone oil rises to the top of the eye, the iridectomy should be placed inferiorly, and this should be a standard part of all vitreoretinal procedures that include use of silicone oil. It has been suggested, however, that the iridectomy should be placed peripherally and should be no larger than 2 mm, because a larger, more centrally located inferior iridectomy may allow silicone oil to enter the anterior chamber, creating a form of reverse pupillary block with a deep anterior chamber (225). When the iridectomy does not relieve the chronic IOP elevation, antiglaucoma medications may be adequate, but other patients may require surgical intervention, including removal of the silicone oil, implantation of a glaucoma drainage device, or a cyclodestructive procedure (226).

GLAUCOMAS AFTER SCLERAL BUCKLING PROCEDURES

Scleral buckling procedures are reported to cause a transient shallowing of the anterior chamber with elevation of the IOP in 4% to 7% of cases (227). However, this is frequently asymptomatic and may go undetected unless slitlamp biomicroscopy

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and tonometry are performed in the early postoperative period. Findings of an experimental study with monkeys suggest that occlusion of the vortex veins by an encircling band or sectoral scleral indentation causes congestion and forward rotation of the ciliary body with subsequent shallowing of the anterior segment (228). The same study showed that occlusion of the vortex veins also caused the ciliary processes to produce a protein-rich aqueous, which might further reduce outflow. These changes in the early postoperative period rarely lead to serious sequelae. Many eyes have reduced IOP months after retinal detachment surgery, which is caused by a decrease in aqueous production (229). However, peripheral anterior synechiae may develop with subsequent chronic glaucoma. The physician must be alert for this because reduced scleral rigidity in these patients may give falsely low IOP readings, especially with indentation tonometry (230).

Figure 26.13 Panretinal photocoagulation with elevated IOP. A: The IOP increased in the first few hours after scatter laser photocoagulation of proliferative diabetic retinopathy. B: The patient had blurred vision 4 days later and was found to have peripheral choroidal detachments, a closed peripheral angle, and an IOP of 35 mm Hg. Use of cycloplegics, topical corticosteroids, timolol maleate, and acetazolamide rapidly reduced the pressure. The choroidal detachments resolved in 10 days. (From Reiss GR, Sipperley JO. Glaucoma associated with retinal disorders and retinal surgery. In: Tasman W, Jaeger EA, eds. Duane's Clinical Ophthalmology. Vol 3. Philadelphia, PA:Lippincott Williams & Wilkins; chap 54E.)

Treatment of angle closure after scleral buckling includes use of atropine to relieve ciliary muscle spasm and use of corticosteroids to reduce the inflammation and prevent synechia formation. Carbonic anhydrase inhibitors, ß-blockers, and a 2-agonists may be used when necessary for temporary pressure

control. When surgical intervention is required, drainage of suprachoroidal fluid is usually the procedure of choice. A peripheral iridectomy is rarely of value in these cases.

Scleral buckling surgery also causes marked intraoperative IOP elevations. One study, using a pars plana infusion cannula attached to an electronic pressure transducer, documented pressures as high as 210 mm Hg during scleral depression and cryopexy, although the long-term consequences of these pressure elevations are unknown (231). Scleral buckling also may reduce ocular blood flow because of decreased ophthalmic perfusion pressure (232).

GLAUCOMAS AFTER RETINAL PHOTOCOAGULATION

An elevated IOP may follow extensive laser photocoagulation of the retina (Fig. 26.13) (233, 234). In many cases, the anterior chamber angle remains open, and the mechanism of pressure elevation in these eyes is unknown. Other patients have a closed angle initially or later in the course of the pressure elevation. The mechanism of angle closure is thought to be swelling of the ciliary body or an outpouring of fluid from the choroid to the vitreous with subsequent forward displacement of the lens-iris diaphragm (233). The condition is temporary, with normal or slightly reduced pressures recorded after 1 month (235), although an analysis of data from the Diabetic Retinopathy Study did not support the belief that panretinal photocoagulation could reduce IOP (236). Pretreatment with apraclonidine reduced the incidence of IOP elevations greater than 6 mm Hg during the first 3 hours after laser surgery, compared with placebo drops (25% vs. 32%, respectively), although the difference was not statistically significant (237). The pressure rise should be managed medically in the same manner described for early pressure rise and shallow anterior chamber after scleral buckling.

KEY POINTS

Malignant or ciliary block glaucoma:

Malignant or ciliary block glaucoma occurs most often as a complication of anterior segment incisional surgery in patients with angle-closure glaucoma or shallow anterior chambers.

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The mechanism appears to be increased aqueous flow resistance into the anterior chamber, producing accumulation of aqueous humor in the posterior segment, which leads to a collapse of the anterior chamber from forward vitreous displacement.

Atropine is the mainstay of medical therapy for malignant glaucoma, although about half of the patients require laser or incisional surgery.

Elevated IOP after cataract extraction:

Causes of increased pressure during the early postoperative period include inflammation, hemorrhage, pigment dispersion, anterior chamber angle distortion, angle closure, vitreous in the anterior chamber, and the use of viscoelastic.

Chronic glaucoma after cataract surgery may result from peripheral anterior synechiae or trabecular meshwork damage. The implantation of an intraocular lens may induce some additional mechanisms of glaucoma associated with pupillary block, inflammation, hemorrhage, or pigment dispersion.

YAG laser capsulotomy can also lead to IOP elevation in association with cataract surgery.

Epithelial ingrowth and other cellular proliferations in the anterior chamber may be the mechanism of glaucoma after incisional procedures involving the anterior segment and some forms of trauma.

Penetrating keratoplasty may be complicated by associated glaucoma, with the common glaucoma mechanism being angle closure.

Newer corneal procedures, such as Descemet-stripping endothelial keratoplasty, can also be associated with glaucoma. Vitreoretinal procedures, including vitrectomy, the intravitreal injection of gas or silicone oil, scleral buckling, and retinal photocoagulation, may also be associated with postoperative IOP elevation.

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