Mild pain, decreased vision, and rainbows around lights. Rare condition. Often a history of previous episodes. Usually unilateral in young to middle-aged patients.

• Inflammatory open-angle glaucoma: Significant amount of aqueous cells and flare. Synechiae may be present. See 9.7, INFLAMMATORY OPEN-ANGLE GLAUCOMA.
• Pigmentary glaucoma: Acute increase in IOP, often after exercise or pupillary dilation, with pigmented cells in the anterior chamber. See 9.10, PIGMENT DISPERSION SYNDROME/PIGMENTARY GLAUCOMA.
• Neovascular glaucoma: Abnormal blood vessels along the pupillary margin, the TM, or both. See 9.14, NEOVASCULAR GLAUCOMA.
• Fuchs heterochromic iridocyclitis: Asymmetry of iris color, mild iritis usually present in the eye with the lighter-colored iris. IOP increase is rarely as acute. See 12.1, ANTERIOR UVEITIS (IRITIS/IRIDOCYCLITIS).
• Others: Herpes simplex or varicella zoster keratouveitis, toxoplasmosis, and others.

Mechanism unknown, but possible association with a viral etiology (e.g., CMV).

Tends to be very responsive to topical steroids and aqueous suppressants.

1. Topical β-blocker (e.g., timolol 0.5% daily or b.i.d.), topical α2 agonist (e.g., brimonidine 0.1% to 0.2% b.i.d. to t.i.d.), and topical CAI (e.g., dorzolamide 2% b.i.d. to t.i.d.).
2. Short course (1-week) of topical steroids (e.g., prednisolone acetate 1% q.i.d.) may decrease inflammation. Longer use may cause an IOP elevation. Oral indomethacin (e.g., 75 to 150 mg p.o. daily) or topical nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., ketorolac q.i.d.) may also be effective.
3. Consider a systemic CAI (e.g., acetazolamide 500 mg sequel p.o. b.i.d.) if IOP is significantly increased and unresponsive to topical therapy (rare).
4. Hyperosmotic agents (e.g., mannitol 20% 1 to 2 g/kg i.v. over 45 minutes) or anterior chamber paracentesis can be considered when the IOP is determined to be dangerously high for the involved optic nerve (see Appendix 13, ANTERIOR CHAMBER PARACENTESIS).
5. Consider a cycloplegic agent (e.g., cyclopentolate 1% t.i.d.) if the patient is symptomatic.

1. Patients are seen every few days at first and then weekly until the episode resolves. Attacks usually subside within a few hours to a few weeks.
2. Medical or surgical therapy may be required depending on baseline IOP between attacks.
3. If the IOP decreases to levels not associated with disc damage, no treatment is necessary.
4. Steroids are tapered rapidly if they are used for 1 week or less and slowly if they are used for longer.
5. Both eyes are at risk for the development of chronic open-angle glaucoma. Patients should be followed as if the diagnosis is POAG. See 9.1, PRIMARY OPEN-ANGLE GLAUCOMA.