SIGNS AND SYMPTOMS
Patients with angle closure glaucoma manifest symptoms of ocular and facial pain, unilateral blurring of vision, photopsiae in the form of colored haloes around lights, and occasionally nausea and vomiting. Acuity may be reduced significantly in the involved eye, often to 20/80 or worse.

The hallmark signs of angle closure include significantly elevated intraocular pressure, a closed angle upon gonioscopic evaluation, deep conjunctival and episcleral injection in a circumlimbal fashion, and a fixed, mid-dilated pupil. Upon slit-lamp examination, you may also see an edematous or "steamy" cornea and shallow anterior chamber.

Applanation tonometry may reveal IOP in the range of 30 to 60mm Hg, or even higher in some cases. Gonioscopy, which may prove difficult because of microcystic corneal edema, reveals no visible angle structures without indentation. There may be evidence of previous angle closure episodes in the form of peripheral anterior synechiae (PAS) in the fellow eye.

PATHOPHYSIOLOGY
Angle closure occurs when the peripheral iris physically opposes the trabecular meshwork or corneal endothelium and impedes aqueous outflow. Several mechanisms are possible. The most common etiology of angle closure is pupillary block, whereby the flow of aqueous from the posterior to anterior chamber is inhibited, causing iris bombé. This may be simply due to genetic predisposition and anterior segment anatomy (primary pupil block), or from posterior synechiae, lenticular enlargement or displacement of the lens or IOL (secondary pupil block).

Another mechanism which may induce angle closure involves an abnormal configuration of the iris, the so-called "plateau iris syndrome." Patients with this presentation may boast a deep anterior chamber centrally; however, the iris demonstrates an unusual laxity, coming into close approximation with the angle peripherally. These patients may be prone to "angle crowding" and subsequent closure during physiologic or pharmacologic dilation. Other etiologies of angle closure without pupil block include neovascular membranes inducing PAS, anterior uveal displacement (such as in choroidal detachment) or, rarely, posterior segment inflammation or tumors.

MANAGEMENT
The paramount concern in managing an angle closure attack is to lower IOP quickly. Your choice of primary medication depends upon the pressure at presentation. As most miotics are ineffective at pressures over 40mm Hg due to iris ischemia, immediately treat such patients with a beta-blocker of 0.5% concentration and/or apraclonidine 1%.

Next, perform corneal compression with a gonioprism to aid in lowering the IOP by forcing aqueous into the trabeculum and temporarily opening the angle. It may be necessary to use topical glycerin to clear the cornea if there is significant edema. Perform tonometry every 15 minutes after initiating therapy.

If the patient does not achieve significant reduction in IOP after 45 minutes, administer an oral carbonic anhydrase inhibitor (acetazolamide 2 x 250mg tablets). You may also wish to use a hyperosmotic agent such as three to five ounces of oral glycerin or isosorbide over ice. Once the IOP is below 40mm Hg, instill pilocarpine 2% as well as prednisolone acetate 1% every 15 minutes to abate the attack and reopen the angle. It is safe to discontinue this regimen when the IOP is below 30mm Hg and the angle structures are again visible with gonioscopy. Maintain the patient on the following medications: pilocarpine 2% QID, prednisolone acetate 1% QID, timolol (or equivalent) 0.5% BID, and oral acetazolamide 500mg BID.

When the inflammation has diminished and the AC is quiet, refer the patient for a peripheral iridotomy. This provides a secondary outflow channel for aqueous, and commonly causes a permanent anatomical "deepening" of the anterior chamber.

CLINICAL PEARLS

• The most important consideration in handling an acute angle closure attack is accurate diagnosis and prompt intervention. First distinguish between angle closure glaucoma and other acute open angle conditions such as uveitic glaucoma, glaucomatocyclitic crisis and phacolytic glaucoma. Once you have established angle closure as the cause, you must also differentiate the nature of the attack, whether due to primary pupillary block, plateau iris, or secondary pupillary block. If you are uncertain of the etiology or if an inflammatory glaucoma is present, do not use a miotic, as this will only exacerbate the condition.

Other Reports in This Section

• Primary Open Angle Glaucoma
• Uveitic Glaucoma & Glaucomatocyclitic Crisis
• Pigment Dispersion Syndrome & Pigmentary Glaucoma
• Acute Angle Closure Glaucoma
• Anterior Uveitis
• Hyphema
• Angle Recession Glaucoma
• Lens Induced Glaucoma
• Pseudoexfoliation Syndrome and Pseudoexfoliative Glaucoma
• Axenfeld-Rieger Syndrome
• Neovascular Glaucoma
• Pars Planitis
• Choroidal Rupture