Angle-closure glaucoma (ACG) is an uncommon but emergent condition; although far less common than open-angle glaucoma, it has a much greater chance of causing permanent vision loss due to its acute nature. Individuals of Northern European descent have a 0.1% incidence of acute ACG, while those of Inuit or Eskimo descent have up to 40 times this rate. ACG is also more common in persons aged 55-70, women, those of Asian descent, individuals with hyperopia / smaller eyes, and those with a family history of the disease. People who have had ACG in one eye are also more likely to get it in the other eye. Many drugs, including anticholinergic agents, tricyclic antidepressants, selective serotonin reuptake inhibitors, and adrenergic agonists, can precipitate ACG by shifting the lens iris diaphragm anteriorly.

An attack of acute ACG occurs when there is a sudden obstruction of aqueous humor outflow through the drainage angle of the eye, causing a rapid increase in intraocular pressure (IOP). Primary angle closure may be caused by pupillary block or angle crowding or both. Pupillary block occurs when the increased iris convexity brings the iris into apposition with the trabecular meshwork, thereby blocking drainage of the aqueous fluid. With angle-crowding mechanism, anteriorly positioned ciliary processes push the iris anteriorly so that the peripheral iris lies against the trabecular meshwork. Secondary angle closures are associated with angle blockage from other ocular diseases such as iris neovascularization, uveitis, trauma, tumors, ectopic lens, cataract, or lens protein leakage.

Patients often present with acute onset of extremely painful, decreased vision associated with a red eye and a mid-dilated pupil. Headache, seeing rainbow-colored halos around lights, nausea, and vomiting are also commonly present. There may be a recent history of physiologic (ie, being in a dark room) or pharmacologic pupillary dilation.