the iris and vitreous face from moving forward. Laser iridotomies, often multiple, are required to relieve the block.

Pupillary block may also occur following posterior capsulotomy when vitreous obstructs the pupil. A condition referred to as capsular block may also be seen, whereby retained viscoelastic or fluid in the capsular bag pushes a posterior chamber IOL anteriorly, which may narrow the angle.

Secondary Angle Closure Without Pupillary Block

A number of disorders can lead to secondary angle closure without pupillary block, and several are discussed in this section. This form of secondary angle closure may occur through 1 of 2 mechanisms:

contraction of an inflammatory, hemorrhagic, or vascular membrane, band, or exudate in the angle, leading to PAS

forward displacement of the lens–iris interface, often accompanied by swelling and anterior rotation of the ciliary body

Neovascular Glaucoma

This common, severe type of secondary ACG is caused by a variety of disorders characterized by retinal or ocular ischemia or ocular inflammation (Table 5-3). The most common causes are diabetic retinopathy, central retinal vein occlusion, and ocular ischemic syndrome. The disease is characterized by fine arborizing blood vessels on the surface of the iris, pupil margin, and trabecular meshwork, which are accompanied by a fibrous membrane. The contraction of the fibrovascular membrane results in the formation of PAS, leading to the development of secondary ACG. In some cases, a fibrous membrane may be evident without active angle neovascularization. Moreover, angle vessels may be present without vessels on the iris surface.

Table 5-3

Neovascularization of the anterior segment usually presents in a classic pattern, which starts with fine vascular tufts at the pupillary margin (Fig 5-10). As these vessels grow, they extend radially over the iris. The neovascularization crosses the ciliary body and scleral spur as fine single vessels that then branch as they reach and involve the trabecular meshwork (see Chapter 3, Fig 3-6). Often the trabecular meshwork takes on a reddish coloration. With contraction of the fibrovascular membrane, PAS develop and coalesce, gradually closing the angle (Fig 5-11). Because the fibrovascular membrane typically does not grow over healthy corneal endothelium, the PAS end at the Schwalbe line, distinguishing this condition from other secondary ACGs that result from an abnormal corneal

endothelium, such as ICE syndrome, which is discussed in the following section (Figs 5-12, 5-13).

Figure 5-10 The initial presentation of iris neovascularization is usually small vascular tufts (arrows) at the pupillary margin.

(Courtesy of Steven T. Simmons, MD.)

Figure 5-11 Iris neovascularization. With progressive angle involvement, PAS develop with contraction of the fibrovascular membrane, resulting in secondary neovascular glaucoma.

Figure 5-12 With end-stage neovascular glaucoma, total angle closure occurs, obscuring the iris neovascularization. The PAS end at the Schwalbe line because the fibrovascular membrane does not grow over healthy corneal endothelium.

(Courtesy of Steven T. Simmons, MD.)

Figure 5-13 With growth, iris neovascularization extends from the pupillary margin radially toward the anterior chamber

angle. (Courtesy of Steven T. Simmons, MD.)

Clinically, patients often present with an acute or subacute glaucoma associated with reduced vision, pain, conjunctival hyperemia, microcystic corneal edema, and high IOP. While performing gonioscopy in patients suspected of having neovascularization, the clinician may find it helpful to use a bright slit-lamp beam of light and high magnification in order to best visualize these fine vessels.

In rare instances, anterior segment neovascularization may occur without demonstrable retinal ischemia, as in Fuchs heterochromic iridocyclitis and other types of uveitis, exfoliation syndrome, or isolated iris melanomas. When an ocular cause cannot be found, carotid artery occlusive disease should be considered. In establishing a correct diagnosis, the clinician should distinguish dilated iris vessels associated with inflammation from newly formed abnormal blood vessels.

Because the prognosis for neovascular glaucoma is poor, prevention and early diagnosis are desirable. Gonioscopy is vitally important to the early diagnosis because angle neovascularization can occur without iris neovascularization. In central retinal vein occlusion (CRVO), approximately 10% of patients develop angle neovascularization alone. The most common cause of iris neovascularization is ischemic retinopathy, and panretinal photocoagulation should be performed whenever possible. The treatment of choice when the ocular media are clear is panretinal photocoagulation. When cloudy media prevent laser therapy, panretinal cryotherapy should be considered as an alternative to vitrectomy to clear the media with endophotocoagulation or subsequent panretinal photocoagulation. Frequently, marked involution of the neovascularization occurs. The resulting decrease in neovascularization after panretinal photocoagulation may reduce or normalize the IOP, depending on the degree of synechial closure that has occurred. Even in the