Definitive diagnosis depends on gonioscopic verification of angle closure. Gonioscopy should be possible in almost all cases of APAC, although clearing of corneal edema with topical IOP-lowering therapy, topical glycerin, or paracentesis may be necessary to allow visualization of the angle. Dynamic gonioscopy, with indentation of the central cornea, may help the clinician determine whether the iris–trabecular meshwork blockage is reversible (appositional closure) or irreversible (synechial closure), and it may also be therapeutic in breaking the attack of acute angle closure. Gonioscopy of the fellow eye in a patient with APAC usually reveals a narrow, occludable angle. The presence of a deep angle in the fellow eye should prompt the clinician to search for secondary causes of elevated IOP, such as a posterior segment mass, zonular insufficiency, anterior segment neovascularization, or the iridocorneal endothelial syndrome, among others. When performing gonioscopy, the clinician should note the effect of the examination light on the angle recess; the slit-lamp beam can cause pupillary constriction, thus artificially opening the inherently narrow angle recess (see Fig 2-9).
During an acute attack, the IOP may be high enough to cause glaucomatous optic nerve damage, ischemic optic neuropathy, and/or retinal vascular occlusion. PAS can form rapidly, and IOP-induced ischemia may produce sector atrophy of the iris, releasing pigment. This causes pigmentary dusting of the iris surface and corneal endothelium. Iris ischemia, specifically of the iris sphincter muscle, may cause the pupil to become permanently fixed and dilated. Glaukomflecken, characteristic small anterior subcapsular lens opacities, may also develop as a result of necrosis. These findings are helpful in the detection of previous episodes of APAC.
The definitive treatment for APAC associated with pupillary block is usually LPI (discussed in Chapter 13). Once an iridotomy has been performed, the pupillary block is relieved and the pressure gradient between the posterior and anterior chambers is normalized, which in most cases allows the iris to fall away from the trabecular meshwork. As a result, the anterior chamber deepens, and the angle opens. However, corneal edema at presentation may interfere with the creation of a patent LPI, and medications or procedures may be needed to break the attack and clear the cornea until iridotomy can be performed.
If the APAC is mild, it may be broken by cholinergic agents (pilocarpine 1%–2%), which induce miosis that pulls the peripheral iris away from the trabecular meshwork. However, these agents may worsen some types of angle closure without pupillary block and exacerbate pupillary block in some eyes. Stronger miotics are ideally avoided, as they may increase the vascular congestion of the iris or rotate the lens–iris interface more anteriorly, increasing the pupillary block. Moreover, when the IOP is markedly elevated (eg, >40–50 mm Hg), the pupillary sphincter may be ischemic and unresponsive to miotic agents alone. Consequently, in most cases, the patient is treated with other topical agents, including β-adrenergic antagonists, α2-adrenergic agonists, and/or prostaglandin analogues; and with topical, oral, or intravenous carbonic anhydrase inhibitors. If needed, hyperosmotic agents may be administered orally or intravenously. Nonselective adrenergic agonists or medications with significant α1-adrenergic activity (apraclonidine) would ideally be avoided to prevent further pupillary dilation and iris ischemia.
Globe compression over the central cornea, dynamic gonioscopy, and careful paracentesis with a 30-gauge needle or sharp blade are all techniques to acutely lower the IOP in order to clear the corneal edema. Care must be taken with these maneuvers, as they can easily injure the lens or iris. A peripheral iridotomy or, in certain circumstances, lens extraction should be performed once the attack is broken and the cornea is of adequate clarity. Following resolution of the acute attack, it is important to reevaluate the angle by gonioscopy to assess the degree of residual synechial angle closure and to confirm the reopening of at least part of the angle. Laser peripheral iridoplasty may also help relieve acute attacks. In rare cases, a surgical iridectomy is required; these procedures are discussed in Chapter 13. Lensectomy is also a viable treatment option, although LPI may be more easily accomplished in the acute setting, especially if the eye is inflamed.
Improved IOP does not necessarily mean that the angle has opened. Because of ciliary body ischemia and reduced aqueous production, the IOP may remain low for weeks following acute angle closure. Thus, IOP may be a poor indicator of angle function or anatomy. A second gonioscopy or serial gonioscopy is therefore essential for follow-up of the patient to be certain that the angle has adequately opened.
In most cases of APAC, the fellow eye shares the anatomic predisposition for increased pupillary block and is at high risk of developing the same condition, especially if the inciting mechanism included a systemic sympathomimetic agent such as a nasal decongestant or an anticholinergic agent. In addition, the pain and emotional upset resulting from the involvement of the first eye may increase sympathetic flow to the fellow eye, resulting in pupillary dilation. It is recommended that a peripheral iridotomy be performed in the fellow eye if a similar angle configuration is present.
Lam DS, Leung DY, Tham CC, et al. Randomized trial of early phacoemulsification versus peripheral iridotomy to prevent intraocular pressure rise after acute primary angle closure. Ophthalmology. 2008;115(7):1134–1140.
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.