The clinical presentation of angle closure glaucoma stems from sudden increases in intraocular pressure (IOP), with possible triggers being dim lighting or use of drugs that induce pupillary dilation (eg. anticholinergics), ciliary body swelling (eg. topiramate) [1]. Moreover, anterior placement of the lens (most commonly caused by the gradual development of cataract) [2], myopia, hyperopia, a shallow anterior chamber, but also advanced age and female gender have all been established as potential risk factors for this type of glaucoma [3] [4]. Only about a third of cases develop an acute exacerbation of IOP changes, however, but increased IOP may not cause marked eye-related symptoms in the beginning [5]. Unfortunately, patients frequently report when profound visual deficits have already occurred, especially in chronic forms, thus reducing the chance of total sight repair [4] [5]. Most prominent symptoms of acute angle closure glaucoma are blurred vision, redness of the eye, ocular discomfort, colored halos around lights and frontal headaches accompanied by nausea and vomiting. Gastrointestinal complaints and headaches may mislead the physician by suggesting a gastrointestinal or central nervous system origin of symptoms [1] [3], and it is not uncommon for glaucoma patients to undergo detailed gastrointestinal or CNS workup prior to their diagnosis [2]. In some patients, a prolonged (chronic) clinical course may be observed, distinguished by ocular discomfort and headaches that are alleviated with sleep [1]. In the setting of a delayed diagnosis, irreversible blindness can occur rapidly, which is why early recognition is detrimental in achieving good outcomes [4].

Patients must be promptly evaluated through a detailed examination of the eye [5]. IOP of more than 30 mmHg (physiological range is between 10 and 23 mmHg) is encountered in virtually all patients suffering from glaucoma, while other findings include a fixed mid-dilated pupil (4-6 mm) that reacts poorly to direct illumination, a hazy cornea that may be edematous, hyperemia of the conjunctiva and a shallow anterior chamber [3]. The presence of adhesions between the iris and the angle structure, termed peripheral anterior synechiae (PAS), can cause obstruction of the trabecular meshwork and are frequently encountered in angle closure glaucoma patients as well [3]. These findings can be confirmed either by performing gonioscopy or through a slit-lamp examination [5], while more specialized techniques have been developed to confirm angle closure. Ultrasound biomicroscopy, which is able to acquire real-time images of structures that potentially cause obstruction of the canal, and anterior segment optical coherence tomography, used to evaluate the anterior chamber, are imaging methods that are recommended for glaucoma workup by more skilled ophthalmologists [5].

1. Porter RS, Kaplan JL. Merck Manual of Diagnosis and Therapy. 19th Edition. Merck Sharp & Dohme Corp. Whitehouse Station, N.J; 2011.
2. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 18e. New York, NY: McGraw-Hill; 2012.
3. Pokhrel PK, Loftus SA. Ocular emergencies. Am Fam Physician. 2007;76(6):829.
4. Azuara-Blanco A, Burr J, Ramsay C, Cooper D, Foster PJ, Friedman DS, et al. Effectiveness of early lens extraction for the treatment of primary angle-closure glaucoma (EAGLE): a randomised controlled trial. Lancet. 2016;388(10052):1389-1397.
5. Weinreb RN, Aung T, Medeiros FA. The Pathophysiology and Treatment of Glaucoma: A Review. JAMA. 2014;311(18):1901-1911.