Pathogenesis and Pathophysiology
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 described as “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). These 2 forms of angle closure can be distinguished by means of indentation gonioscopy. The IOP becomes elevated as a result of reduced aqueous humor outflow through the trabecular meshwork.
In addition to these traditional mechanisms of angle closure, more recent work suggests that the dynamic changes in iris volume and water content normally occurring in the human eye are dysfunctional in patients with angle-closure disease and may play an important role in its pathogenesis. In unaffected eyes, iris volume is reduced with pupillary dilation, much like a sponge being squeezed; however, eyes with angle closure demonstrate paradoxical expansion of volume, likely contributing to the crowding and closure of the angle. A variety of factors that cause pupillary dilation—certain drugs, pain, emotional upset, and fright, among others—may precipitate acute angle closure.
In the primary angle-closure spectrum, the major mechanism is pupillary block. In up to one-third of eyes with angle closure, plateau iris is at least a contributing factor to the anatomic abnormality.
Aptel F, Denis P. Optical coherence tomography quantitative analysis of iris volume changes after pharmacologic mydriasis. Ophthalmology. 2010;117(1):3–10.
Quigley HA. The iris is a sponge: a cause of angle closure. Ophthalmology. 2010;117(1):1–2.
Pupillary block is the most frequent cause of angle closure. Although the pathophysiology of the PAC spectrum is complex and not completely understood, pupillary block is the main or a contributing cause in most cases. The flow of aqueous humor 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 1-9). Pupillary block is maximal when the pupil is in the mid-dilated position. In most cases of angle closure, pupillary block results from anatomic factors at the lens–iris interface. Pupillary block may be broken by an unobstructed peripheral iridectomy or iridotomy.
In phakic eyes, the lens (and its alteration with age) plays a critical role in pupillary block. Recent studies have found that a high lens vault (defined as how far the lens protrudes anterior to the plane of the scleral spur) is a major risk factor for angle-closure disease. Iris thickness, area, and volume have also been strongly correlated with narrower angle and risk for angle closure. Smaller anterior chamber dimensions, including anterior chamber depth (ACD), width (ACW), area (ACA), and volume (ACV), are also risk factors.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.