Ординатура / Офтальмология / Английские материалы / Atlas of Glaucoma, Second Edition_Choplin, Lundy_2007

Figure 11.50 Peripheral iridoplasty in lens-induced angle closure, UBM. Following peripheral iridoplasty in the patient shown in Figure 11.48, the angle widened.

Figure 11.51 Lens intumescence. Occasionally, the lens may become intumescent and cause crowding of the anterior segment.

Figure 11.52 Lens subluxation. Alterations in lens position can result in angle-closure glaucoma in a number of ways. Perhaps the most common and underdiagnosed cause of lens subluxation is exfoliation syndrome. In this disorder, zonular laxity permits the lens to move slightly anteriorly, increasing relative pupillary block and leading to angle closure. Eventually zonular dehiscence from the ciliary body may occur, and lead to lens dislocation. In this figure, dehisced zonules can be seen resting on the equatorial lens capsule.

Figure 11.53 Lens dislocation in exfoliation syndrome. In this patient, nearly complete superior zonular dehiscence has allowed the lens to move inferiorly.

Figure 11.54 Marfan’s syndrome. Lens subluxation and dislocation are a common feature of Marfan’s syndrome. The most common direction for lens movement is superotemporal. In homocystinuria, the subluxed lens tends to move inferonasally.

Figure 11.55 Microspherophakia. In microspherophakia, the smaller lens can dislocate into the anterior chamber, where it can become trapped.

BLOCK RELATED TO PRESSURE POSTERIOR TO THE LENS

Figure 11.56 Traumatic lens dislocation. Long-standing anterior dislocation can lead to progressive cataract formation.

Figure 11.57 Malignant glaucoma, UBM. Malignant glaucoma (ciliary block glaucoma; aqueous misdirection) is a poorly understood clinical entity characterized by angle closure, normal posterior segment anatomy, and patent iridotomy. Most, but not all, cases occur postoperatively. In malignant glaucoma, the lens and iris are forced anteriorly by posterior pressure. In this eye, the anterior lens capsule (LC) is nearly against the corneal endothelium (C).

Figure 11.58 Pseudophakic malignant glaucoma. Following uneventful cataract surgery in this patient with undiagnosed angle-closure glaucoma, the anterior chamber shallowed and the pressure rose. Multiple iridotomies failed to restore normal anatomic relationships. (Reprinted from Tello C, Chi T, Shepps G, Liebmann J, Ritch R. Ultrasound biomicroscopy in pseudophakic malignant glaucoma. Ophthalmology 1993; 100: 1330–4 (Figure 1b).)

Figure 11.59 Pseudophakic malignant glaucoma, UBM. Ultrasound biomicroscopy prior to treatment. The central anterior chamber is shallow. (Reprinted from Tello C, Chi T, Shepps G, Liebmann J, Ritch R. Ultrasound biomicroscopy in pseudophakic malignant glaucoma. Ophthalmology 1993; 100: 1330–4 (Figure 2d).)

Figure 11.60 Pseudophakic malignant glaucoma, UBM. In the temporal angle, peripheral iridocorneal apposition is present (black arrows). The haptic is visible beneath the iris (white arrow).

Figure 11.61 Pseudophakic malignant glaucoma, UBM. Immediately following Nd:YAG laser capsulotomy/anterior hyaloidectomy, the anterior chamber is deeper and the haptic has moved posteriorly (arrow).

Figure 11.62 Phakic malignant glaucoma,UBM. In this phakic patient with a clinical diagnosis of a malignant glaucoma the angle has closed because of anterior rotation at the ciliary body due to annular ciliary body detachment (asterisk), rather than aqueous misdirection. This distinction is clinically important in as much as the treatment involves vigorous topical and occasional systemic steroids, intensive cycloplegia and possible drainage of the supraciliary fluid. It does not typically respond to Nd:YAG laser surgery. Rarely, suprachoroidal effusion may be caused by topiramate.

Figure 11.63 Scleritis and angle closure, UBM. In a similar fashion, anterior rotation of the ciliary body may occur following pan retinal photocoagulation, scleral buckling procedures, central retinal vein occlusion, contraction of retrolental tissue, such as in retinopathy of prematurity, or inflammation of adjoining tissues, such as this patient with anterior scleritis with secondary ciliary body edema. Note the overlying thickened conjunctiva.

Figure 11.64 Intravitreal gas and angle closure, UBM. Intravitreal expansile gas (arrows) may cause progressive angle closure following vitreoretinal surgery. In this particular case, the ciliary body, iris, and lens have been forced anteriorly, closing the angle.

Figure 11.65 Choroidal hemorrhage. Choroidal hemorrhage can result in forward movement of the lens–iris diaphragm and elevated intraocular pressure. Although intraoperative choroidal hemorrhage is relatively rare during glaucoma surgery, delayed choroidal hemorrhage in hypotonus eyes is not. The typical presenting complaint is the abrupt onset of pain, often associated with the Valsalva maneuver, in an eye with known hypotony and choroidal effusion.

Figure 11.66 Uveitis and glaucoma. Intraocular inflammation can cause angle closure by a variety of mechanisms. In this patient acute angle closure has developed because of a pupil secluded by posterior synechiae. The iris is adherent at the pupillary border, and has assumed a bombé configuration elsewhere.

Figure 11.67 Posterior synechiae due to uveitis. Early posterior synechia formation often presages the development of increased pupillary block. Frequent dilatation may prevent complete pupillary block.

Figure 11.68 Keratic precipitates. When peripheral anterior synechiae are present without pupillary block, other evidence of prior intraocular inflammation should be sought. In this patient with multiple synechiae but an otherwise wide-open angle, old keratic precipitates provide evidence of prior anterior uveitis.

Figure 11.69 Uveitis-related anterior synechiae, UBM. In this patient with sarcoid uveitis, peripheral anterior synechiae have formed in the angle.

Figure 11.70 Anterior chamber fibrin. Severe inflammatory reactions, such as this fibrin mass on the anterior surface of a recently implanted intraocular lens, may result in pupillary block.

Figure 11.72 Central retinal vein occlusion. The most common cause of iris neovascularization is retinal ischemia. Ischemic central retinal vein occlusion (shown here) and proliferative diabetic retinopathy are the two most common offending disorders.

Figure 11.71 Neovascular glaucoma. Neovascularization of the anterior segment causes glaucoma by direct obstruction of the trabecular meshwork by the proliferating neovascular membrane. Neovascular glaucoma, which may be recalcitrant to therapy, is often associated with high intraocular pressures and spontaneous hyphema.

Figure 11.73 Angle neovascularization. As the neovascular membrane proliferates, it slowly covers the angle structures.

Figure 11.74 Ectropion uveae. Contraction of the membrane pulls the iris into the angle, and may cause ectropion uveae, as shown here.

Figure 11.76 Iris–nevus syndrome. Another variant of iridocorneal endothelial syndrome, the iris–nevus syndrome.

Figure 11.75 Iridocorneal endothelial syndrome. Iridocorneal endothelial syndrome is also associated with a proliferating anterior segment membrane. In this disorder, migration of corneal endothelial and associated basement membrane causes obstruction of the trabecular meshwork and iris abnormalities. Essential iris atrophy, shown here, is characterized by corectopia, melting holes, and stretching holes caused by membrane contraction.

Figure 11.77 Hyphema. Anterior segment trauma can cause angle closure because of uveitis or lens subluxation. In this patient with hyphema, pupillary block caused by the obstruction to aqueous flow by the anterior segment clotted blood is part of the differential diagnosis of the elevated intraocular pressure.

Von Graefe first described the condition we now recognize as normalor low-tension glaucoma in the 1850s1–3. Glaucoma as a disease entity associated with elevated intraocular pressure had been recognized for only approximately 50 years. The notion of glaucoma without elevated intraocular pressure was not well received4 and still remains an enigma to this day5. With the development of tonometry in the early 1900s and more widespread use of ophthalmoscopy to examine the optic disc, normal-tension glaucoma became a more widely recognized and accepted entity. Many names were applied to this condition including pseudoglaucoma, amaurosis with excavation, cavernous optic atrophy, paraglaucoma, arteriosclerotic optic atrophy, low-tension glaucoma, and others. The variety of terms applied to this condition underscores our lack of understanding of the pathophysiology of this disease entity or group of entities, which we have come to call normal-tension glaucoma.

DEFINITION

Since little is known of the etiology and pathophysiology of primary open-angle glaucoma, not to mention normal-tension glaucoma, our ability to define this condition or group of conditions has been unsatisfactory. According to the most recent (2003) American Academy of Ophthalmology Preferred Practice Pattern6, primary open-angle glaucoma is defined as ‘a multifactorial optic neuropathy in which there is a characteristic acquired loss of retinal ganglion cells and atrophy of the optic nerve’. Without mention of intraocular pressure, this definition also includes normal-tension glaucoma. We therefore may define normal-tension glaucoma as an optic neuropathy that has certain characteristics that are within the spectrum of disease we recognize as glaucoma. The hallmark of glaucomatous nerve damage is ‘cupping’ (Figure 12.1), though

Figure 12.1 Concentric thinning of the neuroretinal rim.

Optic disc cupping with concentric thinning of the neuroretinal rim in primary open-angle glaucoma. (Note: A striped pattern is projected on the fundus in this image to enhance topographic analysis.)

even this characteristic is highly variable and may take many forms. The level of intraocular pressure may be considered just one of the possible risk factors for this disease process similar to our thinking for primary open-angle glaucoma. As shall be discussed, however, the optic disc and visual field changes in normal-tension glaucoma may contrast with those in primary open-angle glaucoma, though there is conflicting evidence in this regard which is at least in part due to our inability to define appropriate study populations and therefore to accurately discriminate between the various glaucomas. It may also be the case that we are merely describing a disease process with a broad spectrum that would defy discrimination. Historically, different authors have used different benchmarks for the intraocular pressure in defining their study populations, none

by Spaeth and others includes descriptions of clinical entities for which a low intraocular pressure may be characteristic. Nicolela and Drance24 have also presented their impressions that certain disc appearances may be characteristics of specific glaucoma entities, some of which are characterized by low intraocular pressure (Figure 12.2).

The amount of cupping and the topography of the disc rim have been evaluated in normal-tension glaucoma. Caprioli and Spaeth25 concluded that the disc rim in normal-tension glaucoma eyes is thinner than in eyes with primary open-angle glaucoma, especially along the inferior and temporal margins (Figure 12.3), when compared to primary open-angle glaucoma eyes which were matched for visual field loss. This was consistent with the suggestion by Levene14 that there was disproportionate cupping

relative to the extent of visual field loss in normaltension glaucoma. Fazio et al.26, utilizing computerized disc analysis, concluded that the cupping in normal-tension glaucoma is more broadly sloping with less disc volume alteration than in primary open-angle glaucoma.

A common finding in normal-tension glaucoma is focal notching or acquired pits in the neuroretinal rim. Javitt et al.27 found a higher prevalence of acquired pits in normal-tension glaucoma compared to primary open-angle glaucoma eyes with similar degrees of visual field loss. Spaeth15 has referred to this type of disc change as perhaps one of the characteristic types of glaucomatous optic atrophy and suggested that this type of finding be used to develop new ways of classifying glaucoma. Individuals with this pattern of disc change tend to