Medical Concepts: Acute Angle Closure Glaucoma

In Medical Concepts by Stephanie Cargnelli2 Comments

A 62 year old woman presents to your Emergency Department with a chief complaint of severe right eye pain. Upon further questioning, she reveals reduced vision in the affected eye and colored halos around lights. She reports a diffuse headache and two episodes of vomiting. A quick physical exam reveals significant conjunctival injection and a fixed, mid-dilated pupil. Does your differential contain acute angle closure glaucoma?

What is Acute Angle Closure Glaucoma?

Acute angle closure glaucoma is a condition characterized by raised intraocular pressure due to impaired outflow of aqueous humor from the posterior chamber of the eye.1  In a normal eye, the aqueous humor is produced in the posterior chamber by the ciliary process and proceeds to flow through the pupil to the anterior chamber and out through the trabecular meshwork into Schlemm’s canal.2 In acute angle closure glaucoma, the flow to the trabecular meshwork is blocked by contact between the lens and the iris resulting in accumulation of aqueous humor in the posterior chamber. This is referred to as “pupillary block.”3 As pressure in the posterior chamber rises, the iris is pushed further forward and causes the angle between the peripheral iris, trabecular meshwork, and cornea to close, hence the name acute angle closure glaucoma.

acute angle closure glaucoma

With permission from Weinreb RN, Aung T, Medeiros FA. The Pathophysiology and Treatment of Glaucoma. JAMA. 2014;311(18):1901-1911.

Clinical Presentation

As a result of the associated systemic symptoms, acute angle closure glaucoma carries a significant risk of being incorrectly diagnosed. A thorough history and physical examination with documented raised intraocular pressure is imperative for diagnosis.


Patients with acute angle closure glaucoma present with abrupt onset of pain in the affected eye. In addition patients may present with blurred vision, frontal headache, nausea and vomiting, photophobia, and colored halos around lights.4 Nausea and vomiting occurs as a result of autonomic stimulation, while blurred vision and colored haloes are a result of corneal edema.5  The onset is often precipitated by dilation of the pupil. When the pupil is mid-dilated, the contact between the iris and the lens is maximal and the iris thickens, which worsens pupillary block.6 Patients often describe onset of ocular pain when transitioning from a light to dark environment. Medications that dilate the pupil have the potential to precipitate an attack; these include adrenergic agents, drugs with anticholingeric effects, sulfa-based drugs, tricyclic antidepressants, anticonvulsants, and antiparkinsonian drugs.7 Other risk factors for acute angle closure glaucoma include a family history of the condition, being of Asian descent, female gender, hyperopic eyes, eyes with shallow anterior chambers, thick lens, and narrow irido-corneal angles. 6  As people age, their anterior chamber becomes more shallow and the lens thickens and moves anteriorly, 5  which makes this condition rare below the age of forty, with the peak incidence occurring in the sixth and seventh decades of life.8

Physical Examination

Patients with acute angle closure glaucoma present with conjunctival injection and a fixed, mid-dilated pupil measuring 5-6 mm in diameter.9 Due to the elevated intraocular pressure, the eye may feel hard to the touch. The visual acuity is often reduced. Raised intraocular pressure is necessary for the diagnosis of this condition, and is measured using a Tonopen. A pressure that exceeds 21 mmHg characterizes elevated intraocular pressure, however the pressure may exceed 60-80 mmHg. 2  Fundoscopic examination is often difficult due to the presence of corneal edema; however, one of the most notable features is a pale, cupped optic disc. Cupping occurs due to atrophy of the optic nerve fibers that results in the central cup of the optic nerve appearing enlarged. The normal cup-to-disc ratio is 0.3, but a patient with glaucoma will have a ratio of 0.6 or greater.10 Finally, a slit lamp examination is required for a complete eye examination in patients suspected of having acute angle closure glaucoma. Slit lamp examination will reveal a shallow anterior chamber and a cloudy cornea due to edema. 10  Gonioscopy, a procedure used to measure the depth of the anterior chamber, will be conducted by the Ophthalmologist.

acute angle closure glaucoma

Images from Glaucoma RCSI


Treatment and Disposition

Prompt treatment is required for this condition, as the increased intraocular pressure can lead to optic nerve damage and vision loss. Immediate consultation with an Ophthalmologist is required. Pharmacological treatment options include:

Topical Agents

  1. Miotics – Pilocarpine is the miotic agent of choice. It acts on the muscarinic receptors of the iris, causing it to contract and leading to constriction of the pupil and the movement of the iris away from the angle. 5  This subsequently facilitates the opening of the trabecular meshwork and the outflow of aqueous humor. Be aware that pilocarpine may be ineffective at causing the iris to contract in the early stages of an acute attack because the elevated intraocular pressure can cause pressure-induced ischemic paralysis of the iris. 2  It is effective only once the pressure in the affected eye is reduced, leading to controversy regarding when pilocarpine should be administered. Some experts recommend initiating pilocarpine only after the intraocular pressure falls below 40 mmHg, while others recommend initiating it immediately upon diagnosis. Most experts recommend immediate administration to ensure availability once the ischemic paralysis has resolved.8
  2. Beta-blockers – These agents act by reducing the production of aqueous humor and reduce the intraocular pressure by 10-20%. 5  The same pulmonary and cardiac contraindications that apply to the use of oral beta-blockers also apply to topical beta-blockers, as they can cause systemic side effects including bronchoconstriction and bradycardia. As such, topical beta-blockers should be avoided in patients with asthma, chronic obstructive pulmonary disorder, and patients with second and third degree heart blocks.
  3. AlphaAdrenergic Agonists – Topical Clonidine is the agent of choice. It lowers the intraocular pressure by reducing the production of aqueous humor and by increasing the aqueous outflow.
  4. Steroids Prednisolone Acetate is the steroid most commonly used in the treatment of angle closure glaucoma. These agents help to reduce intraocular inflammation and in doing so, help to minimize the damage to the optic nerve.

Systemic Agents

  1. Carbonic Anhydrase Inhibitors – Acetazolamide is the typical agent used, and functions by reducing the production of aqueous humor through the inhibition of the enzyme carbonic anhydrase. These agents are contraindicated in patients with a sulfonamide allergy, sickle cell anemia, renal failure, and Addison’s disease. In addition, it is important to be aware that these agents may cause a metabolic acidosis, since this enzyme normally causes the dehydration of carbonic acid. As such, caution must be exercised in people with diabetes, liver disease, and COPD. 5
  2. Hyperosmotic Agents – Depending on the agent used, these can be administered either orally or intravenously. These agents decrease the intraocular pressure by causing an osmotic diuresis and reducing the vitreous volume. They should be used with caution in patients with cardiac, pulmonary, and renal issues.

table for glaucoma article

Given the potentially vision compromising nature of this condition, all of these medical treatments should be initiated upon diagnosis. Intraocular pressure should be reassessed hourly to monitor response to treatment. While these pharmacological agents are often effective at lowering the intraocular pressure, patients will often require more definitive management with laser treatment, or occasionally, surgical treatment.

This post was copyedited by Rob Carey (@_RobCarey) and uploaded by Jesse Leontowicz (@jleontow)


Goel M, Picciani R, Lee R, Bhattacharya S. Aqueous humor dynamics: a review. Open Ophthalmol J. 2010;4:52-59. [PubMed]
Tintinalli J E, Cline D, Ma O John, et al. Tintinalli’s Emergency Medicine Manual 7/E. McGraw Hill Professional; 2012.
Gandhewar R, Kamath G. Acute glaucoma presentations in the elderly. Emerg Med J. 2005;22(4):306-307. [PubMed]
Pokhrel P, Loftus S. Ocular emergencies. Am Fam Physician. 2007;76(6):829-836. [PubMed]
Castaneda-Diez R, Mayorquin-Ruiz M, Esponda-Lamoglia C, Albis-Donado O. Current Diagnosis and Management of Angle-Closure Glaucoma. Glaucoma – Current Clinical and Research Aspects. November 2011. doi: 10.5772/18123 [Source]
Lai J, Gangwani R. Medication-induced acute angle closure attack. Hong Kong Med J. 2012;18(2):139-145. [PubMed]
Lachkar Y, Bouassida W. Drug-induced acute angle closure glaucoma. Curr Opin Ophthalmol. 2007;18(2):129-133. [PubMed]
Jackson J, Carr L, Fisch B, Malinovsky V, Talley D. Optometric Clinical Practice Guideline: Care of the Patient With Primary Angle Closure Glaucoma. St Louis, MO: American Optometric Association; 1994.
Marx J, Hockberger R, Walls R. Rosen’s Emergency Medicine: Concepts and Clinical Practice . 8th ed. Elseveir Saunders Inc; 2014.
Nickson C. Blind, Aching and Vomiting. LITFL: Life in the Fast Lane Medical Blog. Published January 18, 2012. Accessed September 25, 2016.

Reviewing with the Staff

Acute angle closure glaucoma is an important cause of headache in the adult, and can be missed if not included in your differential diagnosis. While some of the physical examination findings are admittedly difficult to appreciate, measurement of the patient’s IOP with the Tonopen is simple and essential to making the diagnosis. The pharmacologic treatments listed in the article can temporize the patient, especially if you are in a centre without quick access to an Ophthalmologist, however their administration should not delay transfer and definitive management. Acute angle-closure glaucoma is an ophthalmological emergency, and the most important thing you can do is to recognize it and arrange for emergent definitive management.

Dr Ashley Krywenky MD FRCPC
Emergency Medicine Physician and Simulation Instructor for Residency Education | Department of Emergency Medicine, The Ottawa Hospital
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Stephanie Cargnelli

Stephanie Cargnelli

Stephanie Cargnelli is a Family Medicine resident at the University of Toronto with a special interest in Emergency Medicine. She enjoys teaching and has a passion for research. When she's not working, she can be found horseback riding and playing soccer.
Stephanie Cargnelli

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  • Danica K

    First off, I would like to say great job on the article! Really great summary of some key points.

    As an Ophthalmology resident I can attest that this diagnosis is often missed and the emergency physician has the potential to make a great save and quality-of-life improvement for the patient. A few tips and corrections from my point of view.
    (It goes without saying that none of this is to be taken as medical/legal advice.)

    – I often find patients simply present to emergency with a unilateral headache as opposed to true eye pain. If a
    patient presents with severe unilateral eye pain it is more of a slam-dunk however I would urge you to always be cautious of this potential diagnosis in anyone who presents with a headache.

    – The key to the diagnosis as you mentioned really is the intraocular pressure (IOP). Most emergency rooms will have a Tonopen or an iCare machine however these seem to go missing often. I am not sure why there is such a black market in tonometers however I do believe that M.D. often stands for “Make Do” and therefore it is brilliant of you to have mentioned that the eye may feel hard to touch. If the eyes feel approximately the same it certainly does not rule out elevated intraocular pressure however if one feels rock hard and one feels fairly normal then you are much more confident in your diagnosis. Also, it is critical to check the IOP bilaterally. If your tonometer gives you 57 in each eye, it’s more than likely the tonometer is wonky. I’ve never heard of a case of simultaneous bilateral angle closure.

    – While it is true that an IOP of 21 mmHg is one standard deviation above the mean in a population, there are people walking around with pressures of 26 who do not have glaucoma. Additionally, patients who may be on steroids or other reasons to have an IOP spike usually do not have pain until it is significantly elevated (usually in the high 30s to low 40s). This will obviously be different for every patient however this has been my experience of the absolute lowest value for a patient seen with eye pain which was attributed to an intraocular pressure rise.

    – Also, I am certainly not a glaucoma subspecialist but a normal cup to disc ratio is not necessarily 0.3. Someone may have a cup to disc ratio of 0.0 or 0.7 (physiologic cupping) and it still may be normal. While I appreciate this is not something of great relevance to an emergency doctor I do feel it is worthwhile mentioning as if you are doing fundoscopy and see a large cup it does not necessarily equate one to one with glaucoma. Additionally, a patient may have glaucoma with a cup to disc ratio of 0.4 and it does not necessarily need to be larger than 0.6 as indicated in your article.

    – An easy way to assess chamber depth is to look at the slit lamp with the beam of light from the side as you have described in your article. You will notice the beam of light is split in two and the space between the beams can
    give you an indication of the anterior chamber depth. Though less ideal, this process can also be performed with a direct ophthalmoscopes.

    – One request I usually make of emergency providers is that they please do a set of electrolytes for the patient prior to sending them from the emergency department. This is because patients may be seen in a private office or at an eye institute which does not have as much access to the lab and if we are to use acetazolamide, mannitol, or glycerin it is helpful to have a baseline set of labs.

    Again, thanks for your article! Job well done and appreciate others taking the time to learn about this important topic.

  • Danica K

    Also I just noticed the section on ‘Reviewing with Staff”: while I completely agree I would not want waiting an hour or more for drops to come down from pharmacy to delay patient transfer, if you have any of the above mentioned drops on hand in emergency and there are no other contraindications, I would definitely suggest putting them in. Transfer to whichever centre has the proper equipment to deal with the issue may take a significant amount of time and any drops are only likely to help somewhat and unlikely to hurt. If in doubt, ask your friendly neighbourhood ophthalmologist on the phone!