Angle Closure Glaucoma

History of present illness

A male in his 60s with multiple medical comorbidities presents to a community hospital with approximately three days of progressively worsening left eye pain, redness, vision loss, and a reported sensation of a foreign body in the eye. The patient had bilateral cataract surgeries one month previously with a normal recovery time. He states that he visited an eye clinic yesterday complaining of mild eye pain and blurriness and was told he had “increased pressure” in the left eye. He was started on timolol drops. He presents now with acutely worsening pain and vision loss as well as a new unilateral, infraorbital headache with associated nausea. He states that he is only able to detect light and shadows in the affected left eye. He denies any trauma, fevers, or changes in medications. 

Physical exam

On examination, he is noted to have an atraumatic face with no periorbital deformities, edema or erythema. Examination of the affected left eye (OS) notes injected sclera, mildly cloudy cornea, minimally reactive 4mm pupil and a small hyphema appreciated on pen light examination. His extra-ocular movements are intact and he can count fingers at 1.5 feet. The right eye (OD) is grossly unremarkable with reported baseline acuity. Slit lamp and fluorescein testing were not performed. Tonometry reveals increased intraocular pressure (IOP) of 51mmHg OS, 36mmHg OD (normal pressure 10-21mm Hg). Cardiopulmonary, abdominal, and neurologic examinations are benign. 

hospital course

Based on this initial presentation, the patient was transferred to a tertiary hospital for emergent ophthalmology evaluation given the concern for acute angle closure glaucoma. He was seen by ophthalmology in the emergency department and started on timolol, brimonidine, and dorzalamide drops as well as oral acetazolamide, with interval improvement in his pain and IOP. Repeat tonometry revealed significant improvement after therapy with a pressure of 41mmHg OS. Slit lamp examination showed deep anterior chambers and no detectable cupping of the optic nerve head. He was instructed to continue therapy to reduce his IOP as well as treatment for hyphema including topical steroids, tropicamide (a mydriatic agent), strict cessation of anticoagulation and instructions to elevate head of bed. He was discharged in stable condition with next-day follow-up with ophthalmology.  The patient was seen daily in clinic for the next three days and noted to have no further pain, stable IOP and no progression of his visual symptoms. He was given follow up at an outside eye clinic thereafter and subsequently lost to follow up.


This is a medically complex patient presenting with unilateral, painful vision loss with increased IOP, which was concerning for possible acute angle closure glaucoma, one of the few true ophthalmologic emergencies. The following discussion will outline the pathophysiology, presentation and management of acute angle closure glaucoma, as well as brief overview of the spectrum of glaucomatous disorders. 

Glaucoma is a form of optic neuropathy that involves atrophy of the optic nerve head, leading to visual field loss and irreversible blindness. While glaucoma is traditionally thought of as a disorder of increased intra-ocular pressure (IOP), there are forms of glaucoma that present with normal IOP (normal pressure glaucoma), as well as patients with elevated IOP who do not develop glaucoma (ocular hypertension). Thus, increased IOP is neither necessary nor sufficient for glaucoma development. Glaucomatous damage to the optic nerve preferentially affects the central disc, sparing the margins, which creates a characteristic ‘scooped out’ appearance to the disc on fundoscopy. The exact mechanism of optic neuropathy is unclear, but may involve direct pressure, ischemic insults or immune mediated processes.  
Glaucomatous disorders are categorized in several ways, including whether the angle of the iris and cornea is open or closed. Open angle glaucoma is typically painless and progressive over many years, whereas angle closure can cause vision loss in a matter of hours. Glaucoma can also be categorized by time of onset as acute, subacute and chronic variants exist. Both open and closed glaucoma can be divided into primary and secondary variants. Secondary glaucoma has numerous individual subtypes, in which elevated IOP is caused by mechanisms such as developmental anomalies, ocular neoplasms, surgical complications, glucocorticoid use, trauma, uveitis, neovascularization from diabetic complication, and medication side effects. The anti-epileptic medication topiramate is most famously known for causing acute angle closure secondary to choroidal hemorrhage, which typically occurs within the first two weeks of therapy.[2] Notably, acute angle closure can result from blood or inflammation affecting the angle itself, leading to fibrosis and closure of the trabecular network. One specific entity, uveitis-glaucoma-hyphema-syndrome, implicates mechanical friction and irritation from implanted lenses as the cause of inflammation and bleeding, leading to hyphema and secondary glaucoma. 

Of the many glaucoma variants, acute angle closure glaucoma (ACG) is the most emergent to diagnose and treat. Primary acute angle closure glaucoma is due phenomenon known as pupillary block. In pupillary block, the lens is pushed anteriorly into contact with the posterior aspect of the iris, occluding the normal anterograde flow of aqueous humor from the ciliary body, through the pupil and into the anterior chamber. The increasing pressure physically distorts the peripheral iris anteriorly, causing it to come into contact with the cornea, which obstructs the trabecular meshwork and Schlemm's canal at the angle and prohibits the normal drainage from the anterior chamber. Acute ACG typically presents dramatically with acute painful vision loss and can lead to irreversible damage within hours. 

Primary acute ACG typically occurs due to anatomical predisposition in individuals with a narrow anterior chamber. Risk factors include advanced age, female gender, and those of Asian or Inuit descent.[3] Redundant folds of a dilated iris can contribute to obstruction of an anatomically narrow angle.  Therefore, acute angle closure may be triggered by events that cause mydriasis, including dim illumination (leading to the classic presentation of an elderly female from a movie theater), emotional stress (increased sympathetic tone), or use of anti-cholinergic or adrenergic medications. 

Figure 1. anatomy of the eye. courtesy of wikimedia commons.

Presentation of acute angle closure glaucoma is often dramatic. Patients may complain of sudden, severe eye pain and vision changes. In the early stages, this may be described as a halo effect around lights. Peripheral vision is often affected prior to complete vision loss, though peripheral vision disturbances can go unnoticed by the patient. Frequently associated symptoms include eye redness, headache (classically unilateral and periorbital), nausea, vomiting, and photophobia.[3] Rarely, acute ACG can present as painless vision loss.[4]

Exam findings in acute ACG may include a unilaterally affected eye with: hyperemic conjunctiva greater near the cornea (ciliary flush); corneal hazing secondary to edema from elevated IOP; a mid-dilated sluggish or fixed pupil from ischemic paralysis of the iris sphincter muscles; and an appreciably tense and tender globe on palpation.[1] Tonometry is an essential tool to evaluate for elevated IOP, as well as trend response to therapy. IOP in acute angle closure is often greater than 45mmHg, and may be as high as 60-80mmHg.[4] Visual acuity with both near and distant fields may be decreased. Confrontational testing of visual fields is important to detect loss of peripheral vision, as many patients may be unaware of peripheral vision loss, even in advanced disease. 

Fundoscopy may reveal characteristic cupping of the optic disc; however, dilating the eye may worsen symptoms and is typically discouraged if concern for angle closure is present. Slit lamp examination should be performed, as the presence of cell and flare would suggest a secondary etiology of angle closure, which would change management.[1] Angle depth can be calculated using various techniques on slit lamp, although this is typically beyond the expertise of ED providers. A simple technique to screen for narrowing of the angle by an anterior bowing iris is to illuminate the iris with a penlight held at the temporal side, aimed nasally. When the iris bows anteriorly, the concavity is capable of casting a shadow on the nasal side of the iris. Thus, if the penlight illuminates only the temporal iris, narrowing of the angle is likely present. A flat iris will illuminate symmetrically. While uncommon practice for ED providers, the use of a refractive lens to directly visualize the angles (gonioscopy) is an essential tool for consulting ophthalmologists.[1] 

Some ED clinicians promote a role for point of care ultrasound in evaluation of acute glaucoma, particularly in the setting of malfunctioning tonometry or atypical presentation. A midline view of the anterior chamber with a high frequency linear probe can be used to measure the distance of the anterior chamber (normal 2-3mm), and case reports of ultrasound diagnoses have been published.[3] Primary acute angle closure is almost always unilateral. Bilateral symptoms of acute angle closure should raise concern for drug-induced glaucoma or alternative diagnoses. Other disorders to consider in the differential of acute angle closure include the many variants of secondary angle closure, migraine, cluster headaches, iritis, and retrobulbar hematoma.[5] 

Acute management of acute ACG in the ED is targeted at reducing the intraocular pressure. There are three mechanisms by which this is achieved: prevention of aqueous humor production, decreasing the volume of vitreous humor and increasing aqueous humor outflow. Reduction of aqueous humor production at the ciliary body decreases pressure build up. Beta-blockers (timolol drops), Alpha-2 adrenergic agonists (apraclonidine or brimonidine drops), and carbonic anhydrase inhibitors (both topical dorzolamide or systemic acetazolamide) decreases humor production, and can all be given in concert to maximize effect. In refractory or severe cases, osmotic diuresis with IV mannitol decreases volume of vitreous humor in the eye, further decreasing pressure. Some sources recommend topical prostaglandins (latanoprost 0.005%), which are believed to increase flow through the trabecular meshwork via an undetermined mechanism.[5] 

In cases of primary AACG from pupillary block, topical muscarinic acetylcholine receptor agonists (1-2% pilocarpine) can be used as miotic agents, constricting the pupil and reducing obstruction of the angle by the peripheral iris. Ischemic paralysis of the iris that occurs at higher pressure (often >50mmHg) typically prevent pupillary constriction. Thus, pilocarpine is started after other modalities have reduced IOP to <40mmHg.[1]  Conversely, many secondary causes of AACG benefit from cycloplegic agents (e.g. tropicamide 0.5-1%) to increase pupillary flow. Additionally, topical steroids are often added to decrease inflammation and corneal edema.[5] 

Table 1. Medications used for angle closure glaucoma.

No random controlled trials or comparisons of therapy have been conducted on closed angle glaucoma, so treatment is based on mechanism-based therapies and expert opinion. Most sources recommend using maximal medical therapy, unless contraindicated.[1,4,5] A typical regimen consists of timolol, brimonidine, and dorzolomide drops every fifteen minutes for three doses, as well as 500mg intravenous or oral acetazolamide. IOP should be rechecked frequently to assess for response. Intravenous mannitol may be added if IOP and vision do not improve after one hour. The use of miotic or mydriatic agents is more complex, as indications for each depend on the specific etiology of AACG, which may not be apparent immediately upon presentation. 

Pupillary constriction will benefit most cases of pupillary block, but will worsen some secondary causes of AACG and limit fundoscopic exam. Conversely, cycloplegics are used for many secondary causes, but may also potentiate primary pupillary block.[1] Thus, it may be preferable to initiate these therapies in consultation with an ophthalmologist. In cases of secondary AACG, treatment to decrease aqueous humor should still be initiated immediately, followed by therapy for any reversible underlying causes.[5] Cessation of potentially precipitating medications, including anticholinergics, is typically advised. In all cases, treatment should be initiated along with emergent ophthalmology consultation, including transfer to a tertiary care facility if required.[4]

Definitive management of acute angle closure glaucoma requires surgical intervention. Traditional first line surgery is laser iridiotomy, which creates a patency in the peripheral iris to allow anterograde flow of aqueous humor around an occluded pupil, thus preventing the potential for pupillary block. More recently, immediate laser surgery has been promoted as initial management in the acute setting, though corneal edema is a relative contraindication for laser therapy.[1] More commonly, iridiotomy is performed after stabilization with medical therapy after corneal hazing has resolved. Alternative operative approaches include surgical opening of the trabecular meshwork, or placement of a shunt into the anterior chamber for drainage of humor.[1] While definitive management of angle closure glaucoma mandates consultation with a specialist, emergency providers can salvage a patient's vision through early identification and medical management of this ophthalmologic emergency.

Authored by aaron murphy-crews, md

posted by Matthew Scanlon, MD


  1. Yanoff, M., Duker, J. S., & Augsburger, J. J. Ophthalmology, 2014. Saunders Elsevier, 1084-1089.
  2. Leibowitz, H. M. (2000). The red eye. New England Journal of Medicine, 343(5), 345-351.
  3. Rose, J., Cuevas, D., Dawson, M. Diagnosis at a Glance: Bedside Ultrasound Diagnosis of Acute Angle Closure Glaucoma Emergency Medicine. 2016 March;48(3):131-132
  4. Tintinalli, J. E., Stapczynski, J. S., & Ma, O. J. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide . 2011.
  5. Ehlers, J. P., & Shah, C. P. (Eds.). (2008). The Wills eye manual: office and emergency room diagnosis and treatment of eye disease. Lippincott Williams & Wilkins.

Figure 1. Courtesy of on 8/24/17.