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

hemorrhage is new vessels in the corneoscleral wound (79). Intraocular lens implantation may also be complicated by late or recurrent hemorrhage, which has been reported with anterior chamber, iris fixation, and posterior chamber implants (80, 81 and 82). Posterior chamber implants usually have sulcus fixation, and the mechanism in all cases is presumably erosion into the adjacent tissue. Postoperative bleeding from any source may lead to IOP elevation by the mechanisms discussed in Chapter 24, including ghost cell glaucoma from a vitreous hemorrhage (83).

Pigment Dispersion

Variable amounts of pigment granules, primarily from the iris pigment epithelium, are dispersed into the anterior chamber with all cataract operations. Excessive pigment dispersion can lead to transiently elevated IOP in aphakic or pseudophakic eyes, with the latter occasionally leading to a chronic form of glaucoma.

Pseudophakic pigmentary glaucoma is most often associated with posterior chamber lenses (84, 85). Pigment dispersion is produced by rubbing of the iris pigment epithelium against the optic and loops of the intraocular lens. This leads to the dispersion of pigment granules, which cause obstruction of the trabecular meshwork—a process similar to phakic pig mentary glaucoma. Acute pigmentary glaucoma has been reported with one-piece lenses in which one of the haptics has dislocated into the sulcus. Pigment granules on the central corneal endothelium (i.e., Krukenberg spindle) are occasionally noted. Pigment granules may be visualized circulating in the aqueous humor in the anterior chamber, especially after pupillary dilatation. The most useful diagnostic finding is iris transillumination defects at the site of contact with the lens implant. Gonioscopy typically reveals heavy pigmentation of the trabecular meshwork.

Unilateral IOP elevation and bilateral pigmentary dispersion syndrome have been reported after implantation of phakic refractive intraocular lenses (86). Acquired pigmentary glaucoma should be considered for patients with phakic intraocular lenses. These patients should be monitored for this condition.

Vitreous Filling the Anterior Chamber

Grant (87) described a mechanism of acute open-angle glaucoma in which vitreous humor fills the anterior chamber after cataract surgery; this could be cured in some cases by mydriasis to minimize pupillary block, but other eyes required miosis to draw the vitreous from the angle. Simmons (88) observed that many cases resolve spontaneously in several months. When surgical intervention is required, an iridotomy may be curative, but other eyes will require an anterior vitrectomy (89). Pupillary Block

In Aphakia

This is a relatively rare complication of intracapsular cataract extraction (90). It is more likely to occur weeks after a transient flat anterior chamber secondary to a wound leak. The condition may also be more common after surgery for congenital cataracts. A combination of sector and peripheral iridectomies may minimize this complication (91). Modern approaches to congenital cataract surgery render these measures unnecessary, although a peripheral iridectomy is still advisable.

The pathogenesis of pupillary block in aphakia can be caused by adherence between the iris and anterior vitreous face, which increases the resistance of aqueous humor flow into the anterior chamber through the pupil or iridectomy. In these cases, the aqueous humor accumulates behind the iris, causing a forward shift of the iris and narrowing of the anterior chamber angle (Fig. 26.7). The mechanism may be dependent on an intact anterior hyaloid, because fluorescein studies have shown that aqueous will flow preferentially through spontaneous openings in the vitreous face (92). This condition may be distinguished from the much less common malignant glaucoma in aphakia by the deeper central anterior chamber and forward bowing of the peripheral iris in the eyes with aphakic pupillary block glaucoma (93) (Fig. 26.8).

In Pseudophakia

Pupillary block glaucoma in pseudophakia was once seen most often with anterior chamber and irissupported lenses, although there are numerous reports of this complication occurring with posterior chamber lenses (94, 95). It usually appears early after surgery but may rarely be delayed months or

years.

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Many cases are asymptomatic and are discovered on routine postoperative examination. Some may even have a normal IOP, although peripheral anterior synechiae and chronic pressure elevation usually follow if the peripheral anterior chamber depth is not promptly restored. With anterior chamber lenses, the iris bulges forward on either side of the lens (Fig. 26.9), whereas the mechanism with posterior chamber lenses appears to be excessive inflammation with posterior synechiae to the intraocular lens or the anterior lens capsule (96).

Figure 26.7 Pupillary block in aphakia. An adherence between the iris and anterior vitreous face blocks the flow of aqueous into the anterior chamber at the pupil (P) and iridectomy site (I). The posterior accumulation of aqueous (A) causes forward bowing of the peripheral iris with closure of the anterior

chamber angle.

With modern cataract techniques and intraocular lens implantation in the posterior chamber, the incidence of pupillary block glaucoma in pseudophakia is sufficiently low that a peripheral iridectomy is no longer a routine part of cataract surgery. However, when excessive postoperative inflammation is anticipated or when combined with a filtering procedure, an iridectomy is still advisable in most cases.

Figure 26.8 Slitlamp view of an eye with pupillary block in a patient with aphakia shows the hyaloid face (H) well back from the cornea (C) centrally but peripheral anterior bowing of the (I) with closure of anterior chamber angle.

Figure 26.9 Slitlamp view of pupillary block in a pseudophakic eye shows forward bulging of the iris (I) peripheral to the margin of the anterior chamber intraocular lens (IOL).

Peripheral Anterior Synechiae or Trabecular Damage

In most cases of chronic glaucoma in aphakia or pseudophakia, peripheral anterior synechiae are present, presumably because of a flat anterior chamber or the presence of inflammation or debris in the early postoperative period. Flat anterior chambers after cataract surgery may be caused by a wound leak with subsequent hypotony and choroidal detachments. To avoid the complication of peripheral anterior synechiae and chronic glaucoma, a flat anterior chamber should be corrected promptly. In one series of

203 uncomplicated cataract extractions, 47% had some degree of peripheral anterior synechiae, and all of those with associated glaucoma had peripheral anterior synechiae present in more than one quarter of the filtering angle (49).

In other cases of glaucoma in aphakia or pseudophakia, the angle may be open in all quadrants and appear essentially normal. The mechanism of aqueous outflow obstruction in cases of chronic openangle glaucoma (COAG) in aphakia or pseudophakia is uncertain, but it most likely is related to alterations in the trabecular meshwork due to the surgery and possibly a preexisting reduction in outflow facility. In many of these patients, COAG may have been present but undiagnosed preoperatively. Distortion of the Anterior Chamber Angle

Kirsch and colleagues (97) described the gonioscopic appearance of an internal white ridge resembling an inverted snowbank along the inner margins of the corneoscleral incision after routine cataract extraction. For approximately the first 2 weeks, the ridge typically obscures visualization of the trabecular

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meshwork and then gradually recedes over the next few months. There is some controversy regarding the pathogenesis of the internal ridge. Campbell and Grant (98) provided evidence that distortion of the anterior chamber angle is induced by tight corneoscleral sutures, whereas Kirsch and colleagues suggested that edema of the deep corneal stroma is the mechanism (97). Whatever the initiating factors may be, the ridge is known to be associated with the formation of peripheral anterior synechiae, vitreous adhesions, and hyphema. In some cases, it is likely that the white ridge contributes to the early, transient pressure elevation after cataract surgery. In one study of 95 cataract extractions, early IOP rise occurred in 23% of the eyes with limbal incisions but in none with corneal incisions, suggesting that distortion produced by the corneoscleral wound temporarily affects the adjacent trabecular meshwork and aqueous outflow (99).

Glaucoma after Congenital Cataract Surgery

Children tend to have a higher incidence of glaucoma after cataract extraction than adults do. In the United Kingdom, the overall annual incidence of postoperative glaucoma was approximately 5% and the median time to development of glaucoma was 1.3 years (range, 0.4 months to 6.7 years) (100). Younger age at detection of cataract was independently associated with the development of glaucoma. In other studies, the reported prevalence of glaucoma after congenital cataract surgery ranged from 6.1% to 24% (101, 102 and 103). Although most of the reported cases have involved an open-angle mechanism, a pupillary block mechanism is not uncommon in children with aphakic or pseudophakia. This may be another situation in which an iridectomy is indicated as a part of the cataract surgery. The use of a vitrectomy instrument to aspirate the cataract, with wide excision of the posterior capsule, may reduce the incidence of postoperative glaucoma in children (101). However, even with automated lensectomy and vitrectomy in children, some studies reveal glaucoma rates of 12.5% to 24% (102, 103). One study found an increased risk for glaucoma in eyes that underwent postoperative secondary membranectomy for visual axis occlusion, especially when secondary membranectomy was performed within 1 year of primary surgery (104).

Influence of a-Chymotrypsin

Glaucoma via this mechanism is rarely seen today but was common in the era of intracapsular surgery. In 1958, Barraquer (105) demonstrated the value of the enzymatic zonulolysis with a-chymotrypsin in facilitating intracapsular cataract extraction, and the enzyme was commonly used for that purpose. In 1964, Kirsch (106) reported a transient pressure rise in 75% of the eyes in which 2 to 4 mL of a 1:5000 dilution of the enzyme was used, compared with a 24% incidence of high pressures in a group without enzyme. The complication was somewhat more common in patients with preexisting COAG (107). Nd:YAG Laser Posterior Capsulotomy

Another cause of IOP elevation after extracapsular cataract extraction or phacoemulsification is the use of Nd:YAG laser to perform a discission in the posterior lens capsule when that structure becomes significantly opacified after the initial surgery. In numerous studies, the procedure was associated with

significant pressure elevation. The pressure rise may be detected in the first few hours, and the IOP usually returns to its baseline level within 1 week; in some eyes, however, the IOP elevation may last for several weeks, and several large series have revealed persistent or late-onset pressure elevations in 0.8% to 6% of the cases (108, 109). Cases have been reported in which the laser-induced pressure elevation caused progressive glaucomatous visual field loss or transient loss of light perception, requiring emergency paracentesis (110, 111). Other causes of visual loss after Nd:YAG capsulotomy include cystoid macular edema and retinal detachment (112). Risk factors for significant IOP elevations after Nd:YAG capsulotomy differ among studies, but they include preexisting glaucoma or a preoperative IOP greater than 20 mm Hg, large capsulotomies, a sulcus rather than capsular fixed posterior chamber lens, the absence of a posterior chamber lens, myopia, vitreoretinal disease, vitreous prolapse into the anterior chamber, and the total amount of laser energy used (113, 114 and 115).

The mechanism of IOP elevation after Nd:YAG capsulotomy is not fully understood, although tonographic studies have shown that it is related to reduced aqueous outflow (115, 116). Most cases have an open-angle mechanism, and the obstruction of the trabecular meshwork may be with fibrin and inflammatory cells due to a breakdown in the blood-aqueous barrier or debris from the capsule or cortical remnants (117). Other reported mechanisms of IOP elevation include pupillary block due to forward movement of the vitreous and herniated vitreous occluding a preexisting glaucoma surgical fistula (118, 119). Pretreatment with topical apraclonidine, timolol, brimonidine, or topical carbonic anhydrase inhibitors is done to minimize the early postoperative rise in IOP (120).

Management

Preoperative Considerations

In preparing for a cataract operation, certain considerations may help to minimize the risk of postoperative complications related to glaucoma, particularly in eyes with preexisting glaucoma. Pressure Reduction

Many surgeons elect to reduce the vitreous volume and IOP by applying external pressure to the globe before surgery to maintain a deep anterior chamber and to minimize the potential complications of vitreous loss and expulsive hemorrhage. The external force may be accomplished by digital pressure, a rubber ball with an elastic band around the head, or a pneumatic rubber balloon (i.e., a Honan IOP reducer). Each technique has the potential risk of optic atrophy or arterial occlusion from the excessive or prolonged application of pressure, and the Honan device may be the safest in this regard by allowing monitoring of the pressure in the balloon. Although the IOP does not correlate directly or linearly with the pressure in the Honan balloon, studies suggest that it is safe in normotensive eyes, especially when the instrument is set at 30 mm Hg for 5 minutes (121). However, the induced IOP rise is a

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function of the initial ocular tension, and marked pressure elevations may occur in eyes with initial levels above 30 mm Hg, indicating the need for extreme caution in these cases. Use of these approaches may be unnecessary if topical or subconjunctival anesthesia is used.

Selection of Intraocular Lens

Intraocular lens implantation in the posterior chamber in association with extracapsular cataract extraction and phacoemulsification, although not devoid of potential glaucoma-related complications, is generally associated with a slight reduction in postoperative IOP and is well tolerated even in eyes with advanced preexisting glaucoma where IOP is satisfactorily controlled. Anterior chamber lenses, however, are more problematic, and preoperative glaucoma or anterior chamber angle abnormalities are relative contraindications to their use. In one study of 18 normotensive eyes with angle-supported lenses, synechiae developed around the haptics in 12 cases (94), which can lead to aqueous outflow obstruction, especially in eyes with preexisting glaucoma. In another study, anterior chamber lens implantation in eyes with preoperative peripheral anterior synechiae was associated with corneal endothelial cell loss, fibrous endothelial metaplasia, and angle cicatrization (122).

Intraoperative Considerations

Attention to gentle handling of tissues, hemostasis, and minimal intraocular manipulation may reduce

the risk of postoperative IOP rise associated with hemorrhage or excessive inflammation or pigment dispersion. One study found that the technique of wound closure (specifically, a sutureless sclerocorneal tunnel incision) and the surgeon's experience were more important than prophylactic medications in preventing IOP elevation after phacoemulsification (123). Judicious use of intraocular agents such as viscoelastic substances and thorough irrigation to remove the material at the end of the case, especially in eyes with preexisting glaucoma, may help to minimize the risk of postoperative glaucoma complications.

The miotic agents, acetylcholine and carbachol, are often injected into the eye during cataract surgery to constrict the pupil, especially after implantation of a posterior chamber intraocular lens. Use of acetylcholine, compared with balanced salt solution, was associated with lower IOPs at 3 and 6 hours postoperatively but was not statistically significantly different at 24 hours (124). Use of the combination of preoperative acetazolamide and intraoperative acetylcholine was more effective than either drug alone in controlling postoperative IOP elevation (125). Carbachol was associated with lower postoperative pressures, compared with acetylcholine or balanced salt solution, at 24 hours, 2 days, and 3 days postoperatively (126). The intracameral use of carbachol therefore may be helpful in avoiding early IOP rises, especially in eyes with preexisting glaucoma.

Early Postoperative Period

The IOP can rise a few hours after routine cataract extraction but generally returns to normal within 1 to 3 days. A modest pressure rise (e.g., <30 mm Hg) in a nonglaucomatous eye with a deep anterior chamber is usually of no consequence and requires no antiglaucoma therapy. However, high pressures may cause pain and occasional disruption of the corneoscleral wound. Eyes with preexisting glaucoma and advanced glaucomatous optic atrophy may have further nerve damage with even short episodes of pressure elevation. Anterior ischemic optic neuropathy has occurred during these periods of elevated pressure in eyes with vulnerable optic nerve head circulation (127). If there is pain or a threat to the optic nerve head, cornea, or cataract incision, temporary medical measures should be used.

Several drugs have been evaluated for their efficacy in controlling the early IOP rise in eyes with open anterior chamber angles. Although the results from various studies are somewhat conflicting, a randomized trial showed that topical brinzolamide, brimonidine, 0.2%, timolol, 0.5%, intracameral acetylcholine, and acetazolamide, 250 mg, administered immediately after cataract surgery were more effective than use of no ocular hypotensive medication at reducing the IOP at 6 hours and 20 to 24 hours after surgery (128). Another randomized trial comparing various antiglaucoma drops found that use of a combination of timolol, 0.5%, and dorzolamide, 2%, produced the greatest IOP reduction in the first 24 hours after phacoemulsification cataract surgery (129). Steroids were ineffective in one study (130), but they may help control the pressure when inflammation is excessive. Indomethacin and aspirin have also reduced the postoperative pressure rise (131), presumably by inhibiting prostaglandin synthesis. When uveitis and glaucoma are associated with retained lens fragments in the vitreous, pars plana vitrectomy is reported to yield good results (71).

Uveitis, glaucoma, and hyphema may be managed by using mydriatic agents to minimize iris movement against the lens in mild cases. In more severe cases, steroids should be used for the iritis, and a carbonic anhydrase inhibitor or topical ß-blocker or a 2-agonist for the glaucoma. Argon laser photocoagulation

may be effective in controlling the hemorrhage in the rare cases in which the bleeding site is visible (132). Recurrent hyphema and glaucoma is usually an indication to remove the lens implant, although this is often difficult and can lead to serious intraoperative complications. When glaucoma and hyphema are associated with vitreous hemorrhage, pars plana vitrectomy has been recommended (133). Pigment dispersion in pseudophakia can usually be controlled medically and gradually becomes easier to manage in most cases; removal of the lens implant is rarely required.

Pupillary block in aphakia may initially be treated with mydriasis to break the block, although an iridotomy is usually required. To be effective, the iridotomy must be placed over a pocket of aqueous behind the iris, rather than an area in which the vitreous is in broad apposition to the posterior surface of the iris. The laser is particularly useful in these cases, because more than one iridotomy can be made until an aqueous pocket is found as evidenced by a deepening of the peripheral anterior chamber.

Suggested alternative surgical approaches include separating the iris from the vitreous adhesions with laser iridoplasty, an iris repositor, or pars plana vitrectomy.

Pupillary block in pseudophakia may be broken with mydriatic therapy by enlarging the pupil beyond the edges of an anterior chamber lens or by lysing posterior synechiae from

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a posterior chamber lens. Use of one or more of the following agents may also be required as an emergency measure: carbonic anhydrase inhibitor, hyperosmotic agent, ß-blocker, a 2-agonist. The

definitive treatment is an iridotomy, which is best achieved with a laser as soon as possible. The laser may also be used to break the block by dilating the pupil (134). Closed vitrectomy has also been used to relieve pseudophakic pupillary block (135).

Late Postoperative Period

Most patients with chronic glaucoma in aphakia or pseudophakia can and should be managed medically. This is usually done with the use of drugs that reduce aqueous production, such as carbonic anhydrase inhibitors, ß-blockers, and a 2-agonists, although miotic therapy can also be effective. Surgical

intervention is reserved for cases that are uncontrolled on maximum tolerable medical therapy. Laser trabeculoplasty may be effective in cases that do not have extensive peripheral anterior synechiae and is the initial surgical procedure of choice (136). When strict IOP and visual acuity criteria were used to define success in one study, no surgical procedure was highly effective for chronic glaucoma in aphakia or pseudophakia (137). In one series of trabeculectomies in 82 aphakic eyes, fewer than half were successful (138). Other surgeons, however, have had somewhat better results and feel that trabeculectomy with antimetabolite is the procedure of choice if trabeculoplasty fails or is not possible (136). When conjunctival scarring does not allow performance of a trabeculectomy in a superior quadrant, implantation of a glaucoma drainage device is usually indicated. Transscleral cyclophotocoagulation can also be attempted (see Chapter 41), although it should usually be reserved for patients with poor visual potential or in whom incisional surgery is not possible or thought to have a poor chance of success.

When Nd:YAG capsulotomy is required in the late postoperative period, apraclonidine (1.0% or 0.5%), timolol, or acetazolamide given 1 hour before or immediately after the procedure, or both, effectively minimizes the postlaser pressure rise.

Figure 26.10 Epithelial downgrowth. A: Clinical appearance of epithelial downgrowth. Note advancing epithelial line located on the corneal endothelium. B: Gonioscopic image of white, coagulated areas of epithelium on the iris surface after confirmatory surface treatment with argon laser. (Courtesy of E. Hodapp, MD. From Werner MA, Grajewski AL. Glaucoma in aphakia and pseudophakia. In: Tasman W, Jaeger EA, eds. Duane's Clinical Ophthalmology. Vol 3. Philadelphia, PA:Lippincott Williams & Wilkins; 2008:chap 54G.)

GLAUCOMAS ASSOCIATED WITH EPITHELIAL INGROWTH AND OTHER CELLULAR PROLIFERATIONS

A group of rare but potentially devastating conditions may complicate cataract surgery, incisional glaucoma procedures, or any other incisional operation, and some forms of trauma. These conditions have as their common denominator a proliferation of cells into the anterior chamber.

Epithelial Ingrowth Clinical Features

With this condition, also referred to as epithelial downgrowth, an epithelial membrane grows into the eye through a penetrating wound. It extends over the posterior surface of the cornea, causing corneal edema, and grows down across the anterior chamber angle and onto the iris, which may lead to a refractory form of glaucoma. It occurs in 0.09% to 0.12% of eyes after cataract surgery (139, 140, 141 and 142). The incidence appears to be declining with newer cataract techniques, although a case has been reported with a sutureless scleral tunnel incision (142). It may also occur after penetrating trauma, penetrating keratoplasty, and glaucoma surgery (143, 144 and 145).

Early in the disease process, a wound leak may be present. By slitlamp biomicroscopy, the epithelial ingrowth on the cornea is seen as a thin gray translucent or transparent membrane with a scalloped, thickened leading edge (Fig. 26.10A). Specular microscopy may reveal a characteristic pattern of cell borders, which may have some diagnostic value (142). Fluorophotometry has also been reported to have diagnostic value by showing a delayed disappearance of the topically applied fluorescein in the area overlying the membrane (142). The membrane on the iris is more difficult to see, but it typically causes a flattening of the stroma and can be delineated by the characteristic white burns that result from diagnostic application of argon laser photocoagulation (Fig. 26.10B) (146). In one case with a

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penetrating foreign body, the membrane had a gelatinous appearance, which by histology revealed goblet cells and mucinous material (143). Gonioscopy often reveals peripheral anterior synechiae. Cytologic evaluation of an aqueous aspirate has been described as a diagnostic aid (147), although the clinical features are usually sufficient to establish the diagnosis.

Mechanisms of Ingrowth and Glaucoma

A wound leak is generally felt to be the initial factor leading to epithelial ingrowth and is frequently seen at the time of diagnosis (146). Ultrastructural studies show well-developed epithelium, resembling that of the bulbar conjunctiva, growing over posterior cornea, anterior chamber angle, and the iris (148, 149). Mechanisms that have been proposed for the glaucoma associated with epithelial ingrowth include the growth of epithelium over the trabecular meshwork, areas of necrosis in the trabecular meshwork, peripheral anterior synechiae, pupillary block, and desquamated epithelium or mucinous material in the aqueous outflow system (139, 143, 150).

Management

When epithelial ingrowth is present, radical surgical intervention is usually required. Maumenee (146) described a technique of excising the fistula and involved iris and destroying the epithelium on the posterior cornea with cryotherapy. Subsequent modifications have included en bloc excision of the involved chamber angle tissues, excision of all involved tissue followed by keratoplasty, and the use of vitrectomy instruments to remove involved iris and vitreous (151, 152 and 153). In an eye treated with filtering surgery and adjunctive subconjunctival 5-fluorouracil (5-FU), the epithelial membrane grew rapidly to involve the entire posterior cornea when the injections were stopped (154). A case report described intracameral application of 5-FU resulting in complete clearance of the epithelial membrane (155). Implantation of a Molteno drainage device has provided effective palliative treatment for the associated glaucoma in these cases (156), and a double-plate Molteno shunt combined with penetrating keratoplasty provided IOP control and restoration of vision in two cases (157).

Fibrous Proliferation

Two forms of this condition have been described: fibrous ingrowth and retrocorneal membranes. Fibrous ingrowth is the result of inadequate wound closure after intraocular surgery or penetrating trauma. It has been reported to occur in approximately one third of eyes enucleated after cataract extraction (158). The hallmark of this form of fibrous proliferation is a break in the corneal endothelium and Descemet

membrane, which allows fibroblasts to enter the anterior chamber from subepithelial connective tissue or from corneal or limbal stroma (159, 160 and 161). The fibrous tissue, which is often vascularized, may grow over the corneal endothelium, the anterior chamber angle, and the iris, and into the vitreous cavity. Peripheral anterior synechiae are frequently seen in these cases (161). Clinically, the condition may be difficult to distinguish from epithelial ingrowth, although it is usually less progressive and less destructive. When glaucoma is present, it may be the result of damage from the surgery or trauma or from the direct effect of the fibrous tissue in the anterior chamber angle. Treatment is generally confined to controlling the IOP, preferably with use of medications, although surgery, such as a cyclodestructive procedure, may be necessary.

Retrocorneal membranes may result from various inflammatory or traumatic insults to the cornea. Descemet membrane is typically intact and the fibrous tissue is believed to represent metaplastic endothelial cells (162). Glaucoma is not commonly associated but may result from the initial insult. Melanocyte Proliferation

A proliferation of melanocytes from the iris across the trabecular meshwork and posterior surface of the cornea has also been described as a mechanism of glaucoma after cataract extraction (163). GLAUCOMAS ASSOCIATED WITH CORNEAL PROCEDURES

Penetrating Keratoplasty Incidence

Penetrating keratoplasty, by using modern techniques of tight wound closure, is complicated by a significant incidence of IOP elevation in both the early and late postoperative periods, although reported incidences vary considerably. One study revealed a 31% incidence of early increases in IOP and a 29% incidence of late (>3 months) increases (164); another large survey had a 9% incidence of immediate postoperative glaucoma and an 18% incidence of chronic postkeratoplasty glaucoma (165). Late, chronic glaucoma is more likely to occur in eyes that had early postoperative pressure rise (166). Factors associated with glaucoma after penetrating keratoplasty include recipient age older than 60 years, aphakia, preexisting glaucoma, preoperative diagnosis of adherent leukoma, bullous keratopathy, herpetic keratitis, trauma or keratoconus, associated vitrectomy, and anterior segment reconstruction (164, 165, 166, 167, 168, 169 and 170). In one series, the average maximum pressure in the first week was 24 mm Hg in phakic eyes, 40 mm Hg in aphakic eyes, and 50 mm Hg in eyes that had combined cataract extraction and keratoplasty (171). When keratoplasty was combined with cataract extraction, the incidence of glaucoma was higher with intracapsular extraction than with extracapsular surgery (172). The incidence of postkeratoplasty glaucoma is also increased after repeated penetrating keratoplasty (173). Glaucoma after corneal grafting is dangerous not only from the standpoint of glaucomatous optic atrophy but also from the high incidence of associated graft failures (174).

Clinical Findings and Glaucoma Mechanisms Early Postoperative Period

In some cases, the postoperative glaucoma after penetrating keratoplasty has the same pressure-elevating mechanisms associated with other intraocular procedures, including uveitis,

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hemorrhage, pupillary block, and steroid-induced glaucoma (175). However, additional mechanisms of early postoperative glaucoma are unique to eyes that have undergone penetrating keratoplasty, especially when aphakia is also present. Two such mechanisms have been postulated.

Collapse of the Trabecular Meshwork. Collapse of the trabecular meshwork may result from the loss of anterior support due to the incision in the Descemet membrane, which may be compounded in the aphakic eye by a reduction in posterior support from the loss of zonular tension (176, 177). This hypothesis is supported by the observation that through-and-through suturing in one study was associated with better facility of outflow in autopsy eyes and lower early postoperative IOP, compared with conventional suturing (176, 177). Some surgeons, however, report less postoperative pressure rise with use of superficial sutures, which they believe prevents angle distortion (178).

Compression of the Anterior Chamber Angle. Compression of the anterior chamber angle may be