reducing the number of patients who develop these diseases and in reducing the risk of blindness. Traditionally, the ACGs are divided into 2 main categories: primary and secondary angle closure.

Each category is subdivided by the symptomatology, etiology, and duration of each of the diseases. In primary angle closure, there is no identifiable underlying pathology; there is only an

anatomical predisposition to pupillary block. In secondary angle closure, an identifiable pathologic cause, such as an intumescent lens, iris neovascularization, chronic inflammation, corneal endothelial migration, or epithelial ingrowth, initiates the angle closure.

Lowe RF. A history of primary angle-closure glaucoma. Surv Ophthalmol. 1995;40(2):163–170.

Yip JL, Foster PJ. Ethnic differences in primary angle-closure glaucoma. Curr Opin Ophthalmol. 2006;17(2):175–180.

Pathogenesis and Pathophysiology of Angle Closure

The hallmark of angle closure is the apposition or adhesion of the peripheral iris to the trabecular meshwork. The portion of the anterior chamber angle affected by such apposition is “closed,” and drainage of aqueous humor through the angle is reduced as a result. Such closure may be transient and intermittent (appositional) or permanent (synechial). The intraocular pressure (IOP) becomes elevated as a result of the reduced aqueous outflow through the trabecular meshwork. Apposition of the iris to the trabecular meshwork is abnormal and requires further assessment.

Conceptually, the mechanism of angle closure falls into 2 categories (Table 5-1):

mechanisms that push the iris forward from behind

mechanisms that pull the iris forward into contact with the trabecular meshwork

In addition to these traditional descriptions of angle closure, more recent work has suggested that the dynamic changes in iris volume and water content normally occurring in the human eye are dysfunctional in patients with ACG and may play an important role in the pathogenesis of angle closure. Indeed, there is mounting evidence that dynamic features of the eye rather than its static anatomy contribute to ACG.

Table 5-1

Pupillary Block

Pupillary block is the most frequent cause of angle closure and is the underlying cause of most cases of primary angle closure. The flow of aqueous from the posterior chamber through the pupil is impeded at the level of the lens–iris interface, and this obstruction creates a pressure gradient between the posterior and anterior chambers, causing the peripheral iris to bow forward against the trabecular meshwork (Fig 5-1). Pupillary block is maximal when the pupil is in the mid-dilated position. In most cases of PACG, pupillary block results from anatomical factors at the lens–iris interface. Though rare, absolute pupillary block occurs when there is no movement of aqueous through the pupil as a

result of 360° of posterior synechiae (secluded pupil). These posterior synechiae can form between the iris and the crystalline lens, an intraocular lens, capsular remnants, and/or the vitreous face. Pupillary block occurs when there is restricted movement of aqueous through the pupil because of iris contact with the lens, intraocular lens, capsular remnants, anterior hyaloid, or vitreous space– occupying substance (air, silicone oil). Pupillary block may be broken by an unobstructed peripheral iridectomy.

Figure 5-1 1, The pupil is constricted and the angle is open. 2, The pupil is in the mid-dilated position. Pupillary block is maximal in this position and as a result the iris is bowed anteriorly and the angle narrows. 3, The pupil is more completely dilated and the pupillary block is diminished, with a return to a flatter iris configuration. If full-blown angle closure occurs, the iris may stay in the mid-dilated position until the angle-closure attack is broken. (Redrawn with permission from Quigley HA, Friedman

DS, Congdon NG. Possible mechanisms of primary angle-closure and malignant glaucoma. J Glaucoma. 2003;12:171. © 2003 Lippincott Williams & Wilkins, Inc. Illustration by Cyndie C. H. Wooley.)

Angle Closure Without Pupillary Block

Angle closure may occur without pupillary block. Iridotrabecular apposition or synechiae can result from the iris and/or lens being pushed, rotated, or pulled forward for a variety of reasons, as outlined in Table 5-1. Each of these underlying mechanisms can usually be identified by a comprehensive examination, including gonioscopy. Many patients may present with multiple underlying causes for their angle closure.

Lens-Induced Angle-Closure Glaucoma

Intumescent or dislocated lenses (complete zonular dehiscence) may increase pupillary block and cause angle closure. Angle closure from an unusually large or intumescent lens is often referred to as phacomorphic glaucoma. With lens subluxation (partial zonular dehiscence), as in Marfan syndrome, exfoliation syndrome, or homocystinuria, pupillary block from the lens or vitreous may occur. Lens block describes an underlying mechanism of primary angle closure, in which the lens’s increased anterior-posterior excursion is due to weakened or lax zonular fibers. This zonular laxity allows the lens to move forward, increasing the relative resistance to aqueous flow through the pupil, which aggravates the pupillary block, inciting angle closure. The prone position may aggravate the tendency of the lens to move forward.

Iris-Induced Angle Closure

Iris-induced angle closure occurs when the peripheral iris, either directly or indirectly, is the cause of