Primary acute angle-closure glaucoma (acute angle-closure crisis) results from closure of a preexisting narrow anterior chamber angle. The predisposing factors are shallow anterior chamber, which may be associated with farsightedness or a small eye (short axial length); enlargement of the crystalline lens with age; and inheritance, such as among Inuits and Asians. Closure of the angle is precipitated by pupillary dilation and thus can occur from sitting in a darkened theater, during times of stress, following nonocular administration of anticholinergic or sympathomimetic agents (eg, nebulized bronchodilators, atropine for preoperative medication, antidepressants, bowel or bladder antispasmodics, nasal decongestants, or tocolytics), or, rarely, from pharmacologic mydriasis (see Precautions in Management of Ocular Disorders, below). Subacute primary angle-closure glaucoma may present as recurrent headache.
Secondary acute angle-closure glaucoma, for which the mechanism may differ between cases, does not require a preexisting narrow angle. Secondary acute angle-closure glaucoma may occur in anterior uveitis, with dislocation of the lens, with hemodialysis, or due to various drugs (see Adverse Ocular Effects of Systemic Drugs, below). Symptoms are the same as in primary acute angle-closure glaucoma, but differentiation is important because of differences in management.