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

glaucoma and delayed suprachoroidal hemorrhage (discussed later in this chapter). Malignant Glaucoma in Pseudophakia

Malignant glaucoma may be associated with an intraocular lens implant in the anterior chamber, presumably by the same mechanism as malignant glaucoma in aphakia (12). It has also been observed in eyes with posterior chamber implants, with or without an associated glaucoma filtering procedure (Fig. 26.1) (13). Malignant glaucoma has also occurred after implantation of an intraocular lens in the posterior chamber of a phakic eye (i.e., malignant glaucoma induced by a phakic intraocular lens in the posterior chamber of a patient with myopia) (14).

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Figure 26.1 Ciliary block after cataract extraction and posterior chamber lens implantation. A: The central chamber is shallow; the peripheral chamber is flat. The intraocular lens is pushed forward, and the haptic posterior to the iris is indenting the iris surface. B: After disruption of the posterior capsule and anterior hyaloid face with Nd:YAG laser, the chamber immediately deepens; the intraocular lens is no longer pressed against the iris. (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.) Miotic-Induced Malignant Glaucoma

The onset of classic malignant glaucoma may correspond to the institution of miotic therapy, suggesting a causal relationship (15). Although the precise mechanism behind this relationship is unknown, the action of miotics may produce malignant glaucoma through contraction of the ciliary body or associated forward shift of the lens with shallowing of the anterior chamber. Similar clinical pictures have been described in unoperated eyes receiving miotic therapy and in an eye treated with miotics after a filtering procedure for open-angle glaucoma (16, 17).

Malignant Glaucoma Associated with Bleb Needling

A case of malignant glaucoma after needling of a trabeculectomy bleb has been reported (18). It is possible that bleb needling results in a shallowing of the anterior chamber that predisposes to malignant glaucoma.

Malignant Glaucoma Associated with Inflammation and Infection

Inflammation and trauma are also precipitating factors of malignant glaucoma (6). A form of malignant glaucoma is associated with endophthalmitis caused by fungal keratomycosis and the atypical bacterium Nocardia asteroides (19).

Malignant Glaucoma Associated with Other Ocular Disorders

Retinal detachment surgery caused the malignant glaucoma syndrome in a patient who developed choroidal detachments after a buckling procedure (20). However, the anterior chamber shallowing in this situation may be secondary to an anterior uveal effusion with forward rotation of the lens or iris diaphragm, producing a secondary angle-closure glaucoma that resembles malignant glaucoma. Several cases of malignant glaucoma-like syndrome have been reported after pars plana vitrectomy (21, 22), and one case reported after diode laser cyclophotocoagulation (23). The condition has also been noted in

children with retinopathy of prematurity and in a patient with corneal hydrops in keratoconus (24, 25). Spontaneous Malignant Glaucoma

Malignant glaucoma may rarely develop spontaneously in an eye without previous surgery, miotic therapy, or other apparent cause (26).

Theories of Mechanism

There is a lack of general agreement regarding the sequence of events responsible for the development of malignant glaucoma, although the following are the more popular theories.

Posterior Pooling of Aqueous

Shaffer (27) hypothesized that an accumulation of aqueous behind a posterior vitreous detachment causes the forward displacement of the iris-lens or iris-vitreous diaphragm. The concept was subsequently expanded to include the pooling of aqueous in vitreous pockets. This theory is supported by an ultrasonographic study of eyes with malignant glaucoma in aphakia demonstrating echo-free zones in the vitreous from which aqueous was reportedly aspirated (28). The mechanisms leading to the posterior diversion of aqueous are uncertain, although strong evidence supports the following possibilities.

Ciliolenticular (Ciliovitreal) Block

In cases of malignant glaucoma, the tips of the ciliary processes rotate forward and press against the lens equator in the phakic eye or against the anterior hyaloid in aphakia, which may create the obstruction to forward flow of aqueous (4, 29) (Figs. 26.2 and 26.3, respectively). Studies involving ultrasonographic P.367

biomicroscopy have confirmed the anterior rotation of the ciliary processes (30, 31); two studies also showed a shallow collection of supraciliary fluid (31, 32). This concept led to the proposed term ciliary block glaucoma as a substitute for malignant glaucoma (4).

Figure 26.2 Concept of ciliolenticular block as the mechanism of malignant glaucoma. Apposition of the ciliary processes to the lens equator (arrows) causes a posterior diversion of aqueous (A), which pools in and behind the vitreous with a forward shift of the lens-iris diaphragm.

Anterior Hyaloid Obstruction

The anterior hyaloid may contribute to ciliolenticular block, and breaks in the hyaloid near the vitreous base possibly allow the posterior diversion of aqueous (5) (Fig. 26.4). The hyaloid breaks, however, have a one-way valve effect, because fluid coming anteriorly closes the vitreous face against the ciliary body, preventing forward flow (5). Some investigators have observed the ciliolenticular contact but noticed that the spaces between the ciliary processes were open, with vitreous visible behind them, suggesting that the obstruction to anterior aqueous flow is the anterior vitreous face, which is compressed forward against the ciliary processes in phakic and aphakic forms of malignant glaucoma

(3).

Figure 26.3 Concept of ciliovitreal block as the mechanism of malignant glaucoma in aphakia. Apposition of ciliary processes against the anterior hyaloid (arrows) leads to posterior diversion of aqueous (A), which causes a forward shift of the vitreous and iris.

In perfusion studies with animal and human eyes, resistance to flow of a fluid through vitreous increases significantly with an elevation of pressure in the eye (33, 34 and 35). The increased resistance might be caused by compression of the vitreous and its displacement against the ciliary body, lens, and iris, thereby reducing the available area of anterior hyaloid through which fluid could flow (34, 35). These clinical and laboratory observations support the concept that an intact anterior hyaloid may be important in preventing the forward movement of aqueous as it travels anteriorly.

Slackness of Lens Zonules

Chandler and Grant (36) postulated that the forward movement of the lens-iris diaphragm in malignant glaucoma might be caused by abnormal slackness or weakness of the zonules of

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the lens as well as pressure from the vitreous. Others have also advocated this theory and suggested that the laxity of the zonules might be the result of severe, prolonged angle closure (7), or ciliary muscle

spasm induced by surgery, miotics, inflammation, trauma, or other unknown factors (6). The concept that the lens subsequently pushes the peripheral iris into the anterior chamber angle led to the proposed term of direct lens block angle closure (6).

Figure 26.4 The anterior hyaloid may contribute to the ciliolenticular block (B), and breaks in the hyaloid near the vitreous base (C) may allow the aqueous (A) to be diverted posteriorly (arrows).

Figure 26.5 Distinctions between pupillary block glaucoma and malignant glaucoma. A: In pupillary block glaucoma, there is moderate depth to the central anterior chamber with forward bowing of the peripheral iris and absence of a patent iridectomy. B: In malignant glaucoma, the entire lens-iris diaphragm is shifted forward with marked shallowing or loss of the central anterior chamber, and a patent peripheral iridectomy may be present.

It seems likely that malignant glaucoma is a multifactorial disorder, in which one or more elements of the aforementioned mechanisms may be involved, depending on the clinical context.

Differential Diagnosis

The diagnosis of malignant glaucoma requires the exclusion of the following conditions (3, 5). Pupillary Block Glaucoma

Pupillary block is the most difficult entity to distinguish from malignant glaucoma but must be ruled out before the latter diagnosis can be made. During slitlamp biomicroscopy, attention should be focused on two questions. First, is the central anterior chamber moderately deep with bowing of the peripheral iris into the chamber angle, as typically noted in pupillary block, or is the entire iris-lens diaphragm shifted forward with marked shallowing or loss of the central anterior chamber, more consistent with malignant glaucoma (Fig. 26.5)? Second, and probably of more diagnostic value, is a patent iridectomy present? If the iridectomy is clearly patent, a pupillary block mechanism is unlikely. However, if patency cannot be

confirmed, the diagnosis of pupillary block cannot be ruled out, and one should proceed with a definitive laser iridotomy.

Choroidal Detachments

Choroidal separation with serous fluid is common after glaucoma filtering procedures and might be confused with malignant glaucoma because of the shallow or flat anterior chamber. These eyes typically are hypotonus. However, when the anterior chamber is flat, IOP measurements by Goldmann applanation tonometry, pneumotonometry, or a Tono-Pen are often highly inaccurate, tending to overestimate the IOP, and therefore cannot be relied on to distinguish between excessive filtration and malignant glaucoma (37). A more helpful diagnostic finding is the presence of a choroidal detachment, which is easily seen if there is adequate visibility of the posterior segment—or alternatively, the

presence of choroidal fluid observed by ultrasonography.

Most serous choroidal detachments will resolve spontaneously as IOP rises. However, those that are persistent or massive with central touch can be approached surgically by making scleral incisions in the inferior quadrants. If a characteristic

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straw-colored fluid is obtained from the suprachoroidal space, the diagnosis of serous choroidal detachment is confirmed, and the procedure is completed by draining as much suprachoroidal fluid as possible and reforming the anterior chamber with air or saline, or both.

A case series has been reported of patients with occult annular ciliary body detachment giving rise to angle-closure glaucoma that is clinically indistinguishable from malignant glaucoma (38). Ultrasonographic biomicroscopy facilitated the diagnosis and guided subsequent management. Suprachoroidal Hemorrhage

Suprachoroidal hemorrhage may occur hours or days after ocular surgery and create shallowing or loss of the anterior chamber, which is typically associated with pain and elevated IOP. It is often preceded by ocular hypotony. The eye is usually more inflamed than with serous choroidal detachment, and the choroidal elevation is frequently dark reddish-brown. The surgical approach is the same as that for serous choroidal detachments, with drainage of the blood from the suprachoroidal space though the sclerotomies and reformation of the anterior chamber.

Management of Malignant Glaucoma Medical Management

Chandler and Grant (36) reported in 1962 that mydriatic-cycloplegic treatment was effective for malignant glaucoma, and the next year Weiss and colleagues (39) recommended the use of hyperosmotics to combat this condition. Cycloplegics, by virtue of stimulating contraction of the ciliary body, help pull the lens back by tightening the zonules, helping to break the ciliary block, whereas the presumed benefit of a hyperosmotic agent is to reduce the pressure exerted by the vitreous (5, 36, 39). These two measures, along with the use of aqueous suppressants, help reduce the flow of aqueous that perpetuates shallowing of the anterior chamber and resultant malignant glaucoma. A standard medical regimen includes the use of topical atropine two to three times daily, intravenous mannitol, topical ß - blocker or a2-agonist (or both), and oral or topical carbonic anhydrase inhibitors. After the attack is

broken, the patient should be maintained indefinitely on atropine therapy to prevent recurrences. Surgical Management

Medical treatment of malignant glaucoma is effective in approximately one half of cases within 5 days (2, 3). If the condition persists beyond this time, surgical intervention is usually indicated.

Laser Techniques

Argon laser photocoagulation of the ciliary processes that can be visualized through an iridectomy or transscleral diode laser cyclophoto coagulation has been reported to relieve malignant glaucoma, presumably by breaking the ciliolenticular block (40, 41). Nd:YAG laser can also be effective in treating aphakic and pseudophakic malignant glaucoma by disrupting the anterior hyaloid face or the posterior lens capsule and hyaloid face (42).

Figure 26.6 Posterior sclerotomy and air injection in the management of malignant glaucoma. Fluid is drained or aspirated from the vitreous by means of a pars plana incision (a) and the anterior chamber is deepened with air (b).

Slitlamp Needle Revision

When the anterior hyaloid face is accessible in the anterior segment and an Nd:YAG laser is not accessible, performing transcorneal needling to disrupt the anterior vitreous face and reform the anterior chamber may be possible (43).

Posterior Sclerotomy and Air Injection

A pars plana incision with aspiration of liquid vitreous with reformation of the anterior chamber with an air bubble (Fig. 26.6) is felt by some to be the incisional surgical procedure of choice for classic malignant glaucoma (2, 3, 5). It has been suggested that the sclerotomy should be placed 3 mm posterior to the limbus to break the anterior hyaloid, thereby reducing its contribution to the blockade (5). Postoperatively, patients are generally maintained on atropine to avoid recurrence.

Anterior Pars Plana Vitrectomy

Other surgeons prefer a careful removal of the anterior vitreous including the anterior hyaloid with

vitrectomy instruments (44, 45 and 46). Failure to include the anterior hyaloid may result in recurrence of malignant glaucoma. Results with posterior sclerotomy and anterior vitrectomy techniques are favorable, but both have the potential for serious complications. The preferred method of treatment depends on the surgeon's experience and preference.

Lens Extraction

This is favored by some surgeons as the incisional surgical procedure of choice, whereas others use this approach if the posterior sclerotomy and air injection or anterior vitrectomy fails (47). To be effective, lens extraction should be combined with an incision of the anterior hyaloid and possibly with deep incisions into fluid pockets in the vitreous (2, 3).

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Management of the Fellow Eye

When malignant glaucoma has already occurred in one eye, the fellow eye will also probably develop the condition if it undergoes intraocular surgery. For this reason, it is best to do a prophylactic laser iridotomy, if indicated. However, if angleclosure glaucoma is present, every effort should be made to break the attack before surgery and, if the attack cannot be broken, mydriatic-cycloplegic therapy should be used vigorously after iridotomy and continued indefinitely.

GLAUCOMAS IN APHAKIA OR PSEUDOPHAKIA Terminology

The term aphakic or pseudophakic glaucoma is occasionally seen in the literature. It is mentioned in this text only to discourage its use because it implies that a single form of glaucoma is associated with aphakia or pseudophakia. There are many mechanisms by which cataract extraction, with or without intraocular lens implantation, can lead to glaucoma, and it is best to refer to these glaucomas in aphakia or pseudophakia by terms that describe the particular events leading to the IOP elevation.

Incidence

The IOP may be elevated transiently in the early postoperative period or may become chronically elevated at any time after cataract surgery.

Aphakia

In the days before intraocular lens implantation, a rise in IOP during the first several days after cataract extraction was not uncommon, although the frequency of this complication varied according to the surgical technique used for wound closure (48). Chronic glaucoma in aphakia was much less common than the early, transient pressure rise. In one series of 203 uncomplicated cataract extractions, persistent glaucoma occurred in 3% of the eyes (49). However, these chronic cases posed a much greater threat to vision and a much more difficult therapeutic challenge than the eyes with transient pressure elevation did.

Pseudophakia

The advent of extracapsular cataract extraction and posterior chamber intraocular lens implantation was generally associated with a reduced incidence of long-term IOP elevation (50). In one series of 373 eyes undergoing cataract surgery, those receiving intracapsular extraction and anterior chamber (133 eyes) or iris fixation (31 eyes) lenses had a late mean IOP rise of 0.8 mm Hg, whereas those undergoing extracapsular surgery with posterior chamber implants (209 eyes) had a mean IOP fall of 0.6 mm Hg (51). Eyes undergoing phacoemulsification cataract extraction also had IOP lowering of 1.1 to 2.5 mm Hg for at least 6 months postoperatively (52). However, extracapsular and phacoemulsification cataract surgeries are associated with pressure complications in the early and late postoperative periods. In eyes without preexisting glaucoma, more than one half in one series had an IOP of 25 mm Hg or more 2 to 3 hours postoperatively (53), and the IOP exceeded 23 mm Hg on the first postoperative day in 29% of eyes in another study (54). Chronic glaucoma was seen in 4% of eyes after standard extracapsular extraction in one series and in 2.1% of another large series (54, 55). Postoperative glaucoma also occurred in 11.3% of eyes receiving secondary anterior chamber implants (56).

With any cataract procedure, early and late postoperative IOP elevations can occur by a wide variety of mechanisms.

Mechanism of Intraocular Pressure Elevation

Influence of Viscoelastic Substances

To protect the corneal endothelium and maintain anterior chamber depth during certain stages of cataract extraction and intraocular lens implantation, filling the anterior chamber with a viscous aqueous substitute has become common practice. The viscoelastic substance that has received the most extensive evaluation for this purpose is sodium hyaluronate (Healon). Although some surgeons have found no significant postoperative pressure rises associated with the use of sodium hyaluronate (57), others have documented high pressures in the first few days after surgery (58). Sodium hyaluronate injected into the anterior chamber of rabbit and monkey eyes caused marked pressure rises (59), and perfusion in enucleated human eyes decreased the outflow facility by 65% (60). This was not reversed by vigorous anterior chamber irrigation, but facility was restored to baseline by irrigation with hyaluronidase. The most likely mechanism of IOP elevation is temporary obstruction of the trabecular meshwork by the viscoelastic.

Alternative viscoelastic substances have also been evaluated. Chondroitin sulfate caused minimal pressure elevation when used during lens implantation in various animal eyes or when injected as a 10% concentration into the anterior chamber of rabbit and monkey eyes (59, 61). A formulation of chondroitin sulfate and sodium hyaluronate (Viscoat) was compared with sodium hyaluronate and was less advantageous during cataract surgery in one study and caused IOP rises in the immediate postoperative period in many patients (62). In another study, the duration of IOP elevation was found to be shorter with formulation including chondroitin sulfate (63). A modified sodium hyaluronate viscoelastic (Healon GV), which has a higher molecular weight, viscosity, and sodium hyaluronate concentration than Healon, was associated with a similar postoperative IOP course to that of the latter agent (64). Patients receiving a newer viscoelastic, Healon 5, with special rheologic properties had a lower IOP in the postoperative period, compared with patients receiving Viscoat (65); however, in other studies, postoperative IOP spike did not differ between patients receiving Healon 5 and those receiving other viscoelastics (66, 67). Use of ethylcellulose (1% to 2%) did not cause a significant postoperative pressure rise in animal or human eyes and appeared to provide good protection of the corneal endothelium (60, 68). In comparative trials, hydroxypropyl methylcellulose, 2%, was found to have the same effect on corneal thickness as balanced salt solution with no rise in IOP and the same early, mild IOP elevation as with sodium hyaluronate 1% (69, 70).

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Inflammation and Hemorrhage

Transient postoperative inflammation occurs to some degree after every cataract extraction. When excessive, obstruction of the trabecular meshwork by inflammatory cells and fibrin may lead to IOP elevations. The inflammatory response and associated glaucoma may be particularly prominent when lens fragments are retained in the vitreous after extracapsular cataract extraction (71).

Intraocular lens implants increase the risk of serious postoperative uveitis, especially with anterior chamber lenses and, historically, with iris-supported lenses (72). This may be associated with hyphema and glaucoma, which has been referred to as the uveitis, glaucoma, and hemorrhage (UGH) syndrome (73). Uveitis was particularly common with the iris-supported lenses, apparently because of the movement of the lens against the iris and the subsequent cellular reaction (74, 75). The inflammation and hemorrhage with anterior chamber lenses is thought to be caused by the contact of the rough posterior surface of the lens with the iris. This has been borne out on ultrasonographic biomicroscopy, which can help detect malpositioned haptics (especially with posterior chamber lenses) and be used to plan subsequent surgical intervention (76). The degree to which lensiris contact liberates pigment may be related to the design and quality of the specific lens (73, 77). Posterior chamber lenses are least likely to induce uveitis. Fluorophotometric studies have shown that pseudophakic eyes with a posterior chamber lens and an intact posterior lens capsule have minimal alteration in the blood-aqueous barrier (78).

In addition to hyphema associated with uveitis, bleeding in the aqueous or vitreous compartments may be seen immediately after cataract surgery or as a late or recurring complication. One source of the late