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

Figure 12.8 The Spaeth gonioscopic classification of the anterior chamber angle, based on three variables (26). A: Angular width of the angle recess. B: Configuration of the peripheral iris. C: Apparent insertion of the iris root.

Newer Techniques

Several newer forms of technology are being applied to evaluation of the anterior segment of the eye to more accurately quantify the anterior chamber depth and related dimensions. The use of high-frequency ultrasonography, referred to as ultrasound biomicroscopy, allows definition of the relationships of the iris, posterior chamber, lens, zonules, and ciliary body (see Chapter 3). This technique has potential value in understanding the mechanisms of glaucoma and in aiding the diagnosis of pupillary block glaucoma, especially when the media is not clear (56). It may also be of value in identifying eyes with potentially occludable anterior chamber angles. It has been suggested that anterior chamber depth measurement and the biometric calculation of the ratio of lens thickness to axial length can be used as a prognostic indicator of pupillary block glaucoma (57, 58). Ultrasound biomicroscopy has also been used to image the dynamic changes in anterior ocular structures during provocative testing in a dark room (59, 60).

Another technique that appears to be useful for assessing the relationship of the anterior chamber angle structures is optical coherence tomography (61) (see Chapter 3). Like ultrasound biomicroscopy, this technique is noninvasive and can provide a reasonable image of the anterior chamber angle. The main advantage is that it does not require the patient to have a probe with or without a gel or bath present on the eye; one drawback at present is that it does not appear to image structures posterior to the iris (e.g.,

ciliary body area) as well as ultrasound biomicroscopy does.

Specialized photographic techniques are also being used to better understand the anterior segment structures in angleclosure glaucomas. With one of these techniques, Scheimpflug video imaging, the iridocorneal angle can be quantitatively assessed and observed longitudinally (61).

When to Perform a Prophylactic Peripheral Iridotomy

Having decided that a patient has suspiciously narrow anterior chamber angles, the physician is faced with a difficult decision. If it could be predicted that the patient would eventually have an attack of angle-closure glaucoma, the appropriate course in most cases would be prophylactic peripheral iridotomies. The results of one study suggest that optic nerve damage occurs in the early period after IOP increases, supporting the value of detecting potentially occludable angles and performing prophylactic surgery before an attack (62).

If the angle is deemed occludable (i.e., 180 degrees or more of appositional angle closure), prophylactic peripheral iridotomy is warranted (see Chapter 35). The fellow eye should also be examined, and if deemed occludable, our recommendation is to proceed with iridotomy on both eyes at the same sitting. Provocative Tests

Historically, some surgeons used tests to provoke pupillary block glaucoma when attempting to identify patients for whom treatment should be recommended. These tests included the prone test, the darkroom test, the prone darkroom test, and pharmacologic dilation of the pupil. The fourth edition of this textbook provides additional details on these tests.

Most ophthalmologists question the clinical value of any provocative test for angle-closure glaucoma because the falsepositive and false-negative rates of such tests are high. In one study of 129 persons with suspected angle-closure glaucoma who underwent gonioscopy, refraction, anterior chamber pachymetry, ultrasound biomicroscopy, and an angle-closure provocative test, it was concluded that none of the test factors studied showed a high sensitivity or positive predictive accuracy in detecting eyes that later developed angle closure (63). Careful gonioscopic examination put into the context of available historical and clinical information has largely replaced the use of provocative tests to make management decisions about the development of angle-closure glaucoma (64).

Precipitating Factors

In an eye that is anatomically predisposed to develop angle closure, several factors may precipitate an attack.

Factors That Produce Mydriasis Dim Illumination

A common history for the development of pupillary block glaucoma is the onset of an acute attack when the patient is in a dark room, such as a theater or restaurant. The incidence of angle closure is reported to increase in winter and autumn (65, 66). In one study, however, there was a direct association with hours of sunshine and an inverse association with degree of cloudiness, which the investigators thought might be related to the contrast between day and evening levels of illumination (65).

Emotional Stress

Occasionally, an acute angle-closure attack follows severe emotional stress. This may be related to the mydriasis of increased sympathetic tone, although the exact mechanism is not understood.

Drugs

Use of mydriatic agents may precipitate an angle-closure attack in an anatomically predisposed eye. Use of anticholinergics (e.g., atropine, cyclopentolate, tropicamide) increases the risk for angle closure when administered topically (67). In one study, use of cyclopentolate, 0.5%, precipitated attacks in 9 (43%) of 21 high-risk eyes, and use of tropicamide, 0.5%, did the same in 19 (33%) of 58 eyes (68). However, in a population-based screening study of 4870 participants whose eyes were dilated with tropicamide, 1%, and phenylephrine, 2.5%, after penlight examination of the anterior chamber depth, none had an acute angle-closure attack (69). In another population-based study of 6760 persons, tropicamide, 0.5%, and phenylephrine, 5%, were

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used for diagnostic mydriasis (70). No persons were excluded on the basis of narrow angles, and only two participants (0.03%) experienced an attack of acute angle-closure glaucoma. Systemic atropine and other mydriatics can also create a hazard, especially when large doses are used in conjunction with spinal or general anesthesia during surgery (71). It has been suggested that highrisk eyes should be protected with topical pilocarpine before, during, and after surgery (72). However, miosis can also precipitate angle-closure attacks, and an alternative approach to managing the high-risk eye is close observation during the postoperative period or prophylactic peripheral iridotomy, depending on the degree of risk.

Other systemic drugs with weaker anticholinergic properties (e.g., antihistaminic, antiparkinsonian, antipsychotic, and gastrointestinal spasmolytic drugs) also present a risk proportional to their pupillary effect (68, 73, 74). The tricyclic antidepressants have the greatest anticholinergic properties of the various psychoactive drugs, and use of imipramine was believed to trigger pupillary block glaucoma in four reported cases (74). Botulinum toxin, used in the treatment of strabismus and blepharospasm, inhibits acetylcholine release with subsequent mydriasis, and it has been reported to cause acute angleclosure glaucoma (75).

Adrenergic agents (e.g., topical epinephrine) may precipitate an angle-closure attack in the predisposed eye. Phenylephrine can also precipitate an attack, although it was found to be safer than cyclopentolate or tropicamide for dilating highrisk eyes (71). Systemic drugs with adrenergic properties (e.g., vasoconstrictors, central nervous system stimulants, appetite depressants, bronchodilators, and hallucinogenic agents) may present a risk in the predisposed eye (67).

Factors That Produce Miosis

Miotic therapy may occasionally lead to an acute attack of pupillary block glaucoma. This has also been observed after the miosis induced by reading or bright lights. Possible mechanisms include an increase in the relative pupillary block due to a wider zone of contact between iris and lens and relaxation of the lens zonules, allowing a forward shift of the iris-lens diaphragm. With strong miotics, such as the cholinesterase inhibitors (e.g., di-isopropyl fluorophosphate, echothiophate iodide), the mechanism of angle closure may be the miosis or congestion of the uveal tract. Chandler (5) favored the former theory, because he observed that an acute increase in IOP after the use of a miotic did not occur in an eye with a peripheral iridectomy.

Symptoms of Angle-Closure Attack

Angle-closure glaucoma, in marked contrast to chronic openangle glaucoma, is characterized by profound symptoms, although the severity of these symptoms varies considerably in different forms of the disorder.

Acute Angle-Closure Glaucoma

Acute angle-closure glaucoma is characterized by pain, redness, and blurred vision. The pain is typically a severe, deep ache that follows the trigeminal distribution and may be associated with nausea, vomiting, bradycardia, and profuse sweating. The marked conjunctival hyperemia usually consists of a ciliary flush and peripheral conjunctival congestion. The blurred vision, which is typically marked, may be caused by stretching of the corneal lamellae initially and later edema of the cornea, as well as a direct effect of the IOP on the optic nerve head. Rarely, the corneal decompensation may persist, requiring penetrating keratoplasty (76).

Subacute Angle-Closure Glaucoma

Subacute angle-closure glaucoma, a form of pupillary block glaucoma, may have no recognizable symptoms. In other cases, the patient may notice a dull ache behind the eye or slight blurring of vision. A symptom that is especially typical of the subacute attack is colored halos around lights. This is thought to result from corneal epithelial edema, which causes it to act as a diffraction grating, producing a blue-green central and yellowred peripheral halo. These symptoms, which more often occur at night after the patient has been in a dark room, often spontaneously clear by the next morning, presumably because of the miosis of sleep.

Chronic Angle-Closure Glaucoma

Another form of pupillary block glaucoma, chronic angleclosure glaucoma, is typically asymptomatic

until advanced visual field loss develops, although the patient may give a history suggestive of one or more episodes of subacute or acute angle-closure glaucoma.

Clinical Findings during an Acute Attack

The patient who presents during an acute angle-closure attack will typically have marked IOP elevation in the range of 40 mm Hg to greater than 60 mm Hg, with a profound reduction in central visual acuity. In the emergency room, digital palpation of the affected eye through a closed eyelid can be a helpful screening test, especially if a tonometer is not easily available. Digital palpation can reveal a very firm (i.e., rockhard consistency) eye compared with the fellow eye, which feels much softer. The following additional findings help to confirm the diagnosis.

External Examination

Characteristic findings include conjunctival hyperemia, a cloudy cornea, and an irregular (usually vertically oval), mid-dilated, fixed pupil (Fig. 12.9). The pupillary change is thought to result from paralysis of the sphincter, which apparently is caused by a reduction in circulation induced by the elevated IOP and possibly by degeneration of the ciliary ganglion (77, 78, 79 and 80).

Slitlamp Examination

This step of the evaluation confirms the presence of the corneal edema, which frequently must be cleared by topical application of glycerin before the anterior chamber can be studied. The corneal edema usually clears after the pressure is normalized, although this is not always the case (76). Specular microscopic examination has revealed significant corneal endothelial cell

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loss in these cases, which correlates with the duration of IOP elevation (81), the degree of visual field loss, a large cup-to-disc ratio, and previous intraocular surgery (82).

trabecular meshwork to the left of the view.

The anterior chamber is shallow, but it typically is formed centrally with anterior bowing of the midperipheral iris, often making contact with peripheral cornea. Aqueous flare is often present. Other findings may include pigment dispersion, sector atrophy of the iris, posterior synechiae, and glaukomflecken, which are irregular white opacities in the anterior portion of the lens that correlate to areas of lens epithelial ischemia or necrosis (Fig. 12.10).

Gonioscopy

It is essential to confirm the diagnosis of angle-closure glaucoma by demonstrating a closed anterior chamber angle. If gonioscopy is not possible because of persistent corneal edema, gonioscopy of the fellow eye may provide useful information if it reveals an extremely narrow angle. In a study of 10 eyes with angle-closure glaucoma, the Koeppe lens was found to be more reliable than the Goldmann threemirror or Zeiss fourmirror lenses in determining whether the angle was open or closed, because it caused no artifactual widening of the angle and allowed the best view over a convex iris (83). From a practical perspective, the Goldmann three-mirror lens is more easily available than a Koeppe lens and provides a higher magnification view of the angle.

glaukomflecken of the anterior lens capsule and sector iris atrophy.

Peripheral anterior synechiae may also be present, and documenting the presence and extent of the synechiae is important in establishing the nature of the angle-closure glaucoma and in selecting the appropriate treatment (discussed later). Forbes (84, 85) described compressive gonioscopy in which the degree of synechial closure is determined by indenting the central cornea with a Sussman or Zeiss goniolens. This forces aqueous into the peripheral portion of the anterior chamber, which deepens it and facilitates visualization of the angle (Fig. 12.11).

Fundus Examination

The optic nerve head may be hyperemic and edematous in the early stages of the attack. Monkeys exposed to high IOPs usually developed congestion of the optic nerve head within 12 to 15 hours, which persisted for 4 to 5 days (86). The disc then became pale, and glaucomatous cupping was observed after 9 to 10 days. In a study of human eyes with a history of angle-closure glaucoma, pallor without cupping was seen in eyes after acute

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attacks, but pallor and cupping occurred in chronic cases (87). Central retinal vein occlusion may also occur during acute angleclosure glaucoma (88). Conversely, central retinal vein occlusion may induce a secondary form of angle-closure glaucoma (see Chapter 19). There is also a case report of nonarteritic anterior ischemic optic neuropathy developing bilaterally about 2.5 weeks after the patient had an attack of angle closure in each eye (89).

Figure 12.11 Compressive gonioscopy with a Zeiss four-mirror gonioprism deepens the peripheral anterior chamber by displacing aqueous from the central portion of the chamber (arrows). This facilitates gonioscopic examination of the anterior chamber angle before surgery by helping to distinguish between appositional (A) and synechial (B) closure of the angle (84, 85).

Visual Fields

Visual field changes associated with an acute elevation of IOP most often show nonspecific constriction.

In one study of 25 patients with acute angle-closure glaucoma that had been surgically corrected, the most common field defect was constriction of the upper field (90), whereas another study revealed nerve fiber bundle defects in 7 of 18 acute cases and 9 of 11 chronic cases (87).

Figure 12.12 The strongest evidence in support of the pupillary block mechanism of angle-closure glaucoma is the excellent response to peripheral iridotomy, which circumvents the block (arrow). THEORIES OF MECHANISM

Relative Pupillary Block

The most common mechanism leading to angle-closure glaucoma appears to be increased resistance to aqueous flow from the posterior to the anterior chamber between the iris and lens. This concept was suggested by Curran (4) and Banziger (6) in the early 1920s and was advanced by the teachings of Chandler (5), who observed that an eye with a shallow anterior chamber has a wider zone of contact between the surfaces of the iris and lens. He postulated that the musculature of the iris exerts a backward pressure against the lens that increases the resistance to flow of aqueous into the anterior chamber. This increases the pressure in the posterior chamber, causing the thin peripheral iris to bulge into the anterior chamber angle. On the basis of gonioscopic studies, the angle closure may occur in two stages: iridocorneal contact anterior to the trabecular meshwork, followed by apposition of the iris to the meshwork as the pressure rises (91, 92). Considerable clinical evidence strongly favors the basic concept of pupillary block, the most convincing of which is the excellent response to peripheral iridotomy, which presumably works by circumventing the block (5) (Fig. 12.12).

Anatomic Factors Predisposing to Pupillary Block

Several anatomic aspects of the eye combine to produce a shallow anterior chamber. These include a thicker, more anteriorly placed lens, a smaller diameter and shorter posterior

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curvature of the cornea, and a shorter axial length of the globe (93, 94, 95, 96, 97, 98 and 99). A study of patients of Asian or African ethnic background with chronic angle-closure glaucoma revealed an abnormal anterior lens position without an increase in lens thickness, suggesting an ethnic influence on

these biometric parameters (100). The ratio of the lens thickness to the axial length appears to correlate best with the predisposition to angle closure (58). It has also been shown that the anterior chamber depth is not a static dimension; it can undergo rapid, transient change (101). Alsbirk (22) suggested that a shallow anterior chamber confers a survival advantage for populations living in extremely cold climates (e.g., Northern China, Mongolia, and Alaska). He suggested that the rich vascular plexus of the iris near the cornea might help to raise the temperature of the ocular surface and prevent the cornea from freezing. The narrow palpebral fissure typical of East Asians may offer a similar advantage.

Relatives of patients with pupillary block glaucoma have a more anterior insertion of the iris into the ciliary body, a narrower angular approach to the recess of the anterior chamber angle, and a more anterior peripheral convexity of the iris, compared with average eyes of persons in the general population (26). All of these parameters are variably influenced by hyperopia, increasing age, and genetics.

Another factor predisposing to a pupillary block mechanism may be a forward displacement to the lens due to loose zonules, which is worsened by miotic therapy and relieved with cycloplegia (David G. Campbell, MD, personal communication).

Significance of Pupillary Dilatation

Chandler (5) emphasized that a mid-dilated pupil of 3.5 to 6 mm is the critical degree of dilatation that seems to bring on the acute attack. He thought this might be caused by continued pupillary block combined with sufficient relaxation of peripheral iris to allow its forward displacement into the anterior chamber. Mapstone (102) proposed a mathematical model to explain the influence of a mid-dilated pupil, in which the combined pupil-blocking forces of the dilator and sphincter muscles and the stretching force of the iris were greatest with the iris in the mid-dilated position. Tiedeman (103), using basic physical principles, found that the Mapstone model involved incorrect use of the physical concepts of force and tension. He developed a model that can predict the profile of the iris by using the radii of the pupil and iris root and the anterior displacement of the pupil from the iris root. If the latter measurement were constant, the angle between the peripheral iris and trabecular meshwork would progressively narrow as the pupillary radius increased. However, because of the contour of the lens, the anterior displacement of the pupil decreases as the pupil dilates, resulting in the narrowest angle when the pupil is mid-dilated (103). Biometric photographs of eyes with narrow anterior chamber angles supported the validity of the Tiedeman model (104), whereas ultrasound biomicroscopic quantitative analysis of light-dark changes in eyes with pupillary block lends some support to the Mapstone model (105).

Chronic Angle-Closure Glaucoma

Peripheral anterior synechiae may eventually develop with prolonged or recurrent acute or subacute attacks, leading to chronic angle-closure glaucoma. The peripheral anterior synechiae in patients after acute angle-closure attacks tend to be broad based, are most commonly seen in the superior quadrant, and correlate with the duration of the acute attacks (106). A more insidious form has been recognized in which the angle slowly closes from the periphery toward the Schwalbe line (9, 10, 11 and 12). The synechial closure usually begins superiorly, where the angle is normally narrowest, and progresses inferiorly (10). This condition has been referred to as shortening of the angle or creeping angle closure (11, 12). These cases are frequently cured by peripheral iridotomy in white patients if detected early enough, but may require additional medical therapy or filtering surgery (0% to 8%) (107, 108). In Asian patients, however, filtering surgery may be required in 29% to 63% of eyes (109, 110). Most eyes developing elevated IOP did so in the first 6 months in a study of Asian eyes, indicating the importance of close follow-up for this group (109, 111).

One study evaluated the retrobulbar hemodynamics of patients with well-controlled chronic angleclosure glaucoma using color Doppler imaging. Patients were found to have decreased retrobulbar blood-flow velocities and increased vascular resistance in the central retinal artery and temporal short posterior ciliary artery, compared with ageand sexmatched healthy controls (112). The degree of hemodynamic impairment correlated well with the degree of glaucomatous visual field loss.

Plateau Iris