History
Classically, affected patients are in their sixth decade of life, suffer from hyperopia, and have no history of glaucoma. Most commonly, they present with periorbital pain and visual deficits. [11] The pain is described as piercing and is associated with an ipsilateral headache. Patients note blurry vision and see halos, or rings of light, around objects.
Careful investigation can elucidate a precipitating factor, such as dim light or medications (eg, anticholinergics, sympathomimetics).
It is not uncommon for patients with PACG to present with non-ocular complaints, such as an isolated headache, thereby increasing the likelihood that they are initially evaluated for a subarachnoid hemorrhage, or treated for migraines. Several case reports detail patients presenting with abdominal pain and vomiting, leading to a diagnosis of gastroenteritis and delayed definitive treatment. [12]
Physical
Initial evaluation of a patient with concern for AACG should include an exam of the external eye, the pupils, a direct or slit-lamp ophthalmoscopic exam, an assessment of ocular motility, visual fields, and visual acuity, and a measurement of the IOP. All of these tend to be affected in AACG.
Patients complaining of blurred vision may reveal to have decreased visual acuity in the affected eye, often with the ability to only detect hand movement. They may even be unable to identify numbers and letters on distance charts or near cards.
Slit-lamp evaluation may reveal corneal edema, synechiae, segmental iris atrophy, or an irregular pupillary shape or pupillary function, although the exam may be limited by the presence of a cloudy cornea, which is commonly present.
Other findings may include ciliary flush, or corneal and scleral injection.
Increased IOP (IOP > 21 mm Hg, but often 20 mm Hg and more) and ischemia result in pain on eye movement, a mid-dilated nonreactive pupil, and a firm globe. Clinicians must take a comprehensive history and perform a thorough physical examination to ensure that this time-sensitive diagnosis is not missed.
Causes
Anatomic variants with a higher propensity for the development of AACG include a shallow anterior chamber, anteriorly situated lens, short axial eye length, thick iris, overdeveloped iris dilator muscles, and a narrow angle. [3]
Precipitating factors include drugs (ie, sympathomimetics, anticholinergics, antidepressants [SSRIs], anticonvulsants, sulfonamides, cocaine, botulinum toxin), [13, 14, 15, 16, 17] dim light, and rapid correction of hyperglycemia (leading to lens swelling).
Case reports have identified AACG associated with carotid-cavernous sinus fistula, trauma, prone surgical positioning, and giant cell arteritis. [17, 18, 19]
