Week 1 - Case File - Emergency Medicine, Section - Head, Eyes, Ears, Nose, & Throat, Case Study - Acute Angle-Closure Glaucoma

Discipline: Nursing

Type of Paper: Question-Answer

Academic Level: Undergrad. (yrs 3-4)

Paper Format: APA

Pages: 4 Words: 1000


A 63-year-old woman presents to the emergency department (ED) with severe left eye pain, redness, and blurred vision for 3 hours. Her right eye is asymptomatic. She denies preceding trauma, photophobia, ocular discharge, increased tearing, prior similar events, or past eye surgery. She is farsighted and sometimes wears nonprescription reading glasses. Other symptoms include seeing colored halos around the light fixtures in the ED, having a headache over her left brow, some nausea, and one episode of vomiting. She denies dizziness, weakness, imbalance, abdominal pain, and chest pain.

On examination, her blood pressure is 138/80 mm Hg, and the other vital signs are normal. She is alert and in obvious discomfort but can tolerate ambient light. She has no periorbital signs of trauma. The left conjunctiva has ciliary flush (circumferential reddish ring around the cornea) but no discharge or visible foreign body. Visual acuity is 20/30 in the right eye but only finger counting in the left eye. Visual fields are grossly intact. Gentle palpation of the closed left eye reveals that it is much firmer than the right. Her left pupil is 5 mm, fixed, and unreactive. Her right eye appears normal; the pupil is 3 mm and briskly reactive. She does not experience pain in the left eye when direct light is applied to the right eye (absent consensual photophobia). When a penlight is shone temporally across each eye, the beam does not reach the nasal side. Extraocular movements are intact and nonpainful. The left cornea is slightly cloudy, which makes fundoscopy difficult. The right fundus appears normal. Her temporal arteries are pulsatile and nontender. The rest of the physical examination, including the remainder of the neurologic examination, is normal.


What is the next diagnostic step?

What is the most likely diagnosis?

What is the best next therapeutic step?

Answers to Case 49: Acute Angle-Closure Glaucoma

Summary: A 63-year-old woman presents with

  • Acute onset of left eye redness, pain, and markedly decreased visual acuity

  • A left eye that feels firmer to palpation compared to the right eye

  • A cloudy left cornea with a fixed and dilated pupil

Next diagnostic step: Measure intraocular pressures (IOP) in both eyes using tonometry and perform a slit-lamp examination to assess for inflammatory changes and the presence of red blood cells or white cells in the anterior chamber.

Most likely diagnosis: Acute angle-closure glaucoma.

Best next therapeutic step: Preserve vision by lowering the IOP as quickly as possible. Consult ophthalmology emergently.



  1. List the vision-threatening causes of a painful red eye. (EPA 2, 10)

  2. Describe the basic treatment modalities and disposition options for vision-threatening causes of a painful red eye. (EPA 4)

  3. Recognize the clinical signs, symptoms, and complications of acute primary angle-closure glaucoma. (EPA 2, 3, 10)

  4. Describe the key treatment modalities and their potential complications for acute angle-closure glaucoma. (EPA 4, 12)


This case is an example of acute angle-closure glaucoma (AACG), a true ophthalmologic emergency characterized by rapidly elevated IOP. In AACG, elevated IOP compromises blood flow to the optic nerve and leads to the loss of retinal ganglion cells, which can result in permanent vision loss. This patient likely has underlying narrow anterior chamber angles (congenital structural narrowing) that, combined with being in dim lighting causing her pupils to dilate, limited the outflow of aqueous humor as the cornea and iris came together (ie, pupillary block). Careful questioning eliminated the use of prescribed medications or over-the-counter drugs as additional potential triggers of AACG.


  • ACUTE ANGLE-CLOSURE GLAUCOMA: A rapid increase in intraocular pressure due to outflow obstruction of aqueous humor. This is a medical emergency.

  • CONJUNCTIVITIS: Inflammation of the conjunctiva, leading to an injected “red eye.”

  • CONSENSUAL PHOTOPHOBIA: Pain when a light is directed to the unaffected eye, which is suggestive of an iritis (anterior uveitis).

  • SLIT LAMP EXAMINATION: Uses a special device with a high intensity light source focused on a thin sheet in conjunction with a binocular microscope to view the anterior and posterior aspects of the eye.

Approach to Acute Angle-Closure Glaucoma


Globally, the highest prevalence rates of acute angle-closure glaucoma (AACG) occur in Chinese and Inuit populations. African Americans have much higher rates of primary open-angle glaucoma (POAG) with resultant blindness, but they have lower rates of AACG. Persons between the ages of 55 and 65 years have the highest incidence of AACG; women are affected more than men (3:1). AACG is likely to occur in 33% to 50% of a patient’s first-degree relatives, so patients should inform their family members if they are diagnosed.

Risk Factors

Risk factors for narrow angle closure include older age, age-related lens thickening and enlargement, anterior lens shift, hyperopia (far-sightedness with a shortened eyeball), and a relatively shallow anterior chamber. There is a 75% risk of a similar attack in the fellow eye if left untreated. Also, medications that cause pupil dilation and pupillary block can trigger AACG, including anticholinergics, tricyclic antidepressants, adrenergic agonists, and topical mydriatics. Nonpupillary block leading to bilateral acute angle closure has been associated with sulfur-containing drugs such as topiramate, hydrochlorothiazide, furosemide, and even acetazolamide. AACG can occur with stress, fatigue, dim lighting, or sustained work at close range. Many over-the-counter sympathomimetics or anticholinergics can cause AACG.


The major mechanism of AACG or primary angle-closure glaucoma is pupillary block of the trabecular meshwork outflow pathway. Normally, aqueous humor is produced by the ciliary body in the posterior chamber and diffuses through the pupil into the anterior chamber where it is drained via the trabecular meshwork. A balance exists between aqueous humor production and outflow to maintain a normal intraocular pressure (IOP). However, some individuals are predisposed to angle closure secondary to anatomic (angle crowding) and environmental factors such as drugs. Many other forms of glaucoma have a far more insidious presentation but still lead to a significant loss of vision.

Clinical Presentation

It is important to recognize AACG quickly since a delay in the diagnosis and treatment may result in permanent loss of vision. Patients with AACG have elevated IOP, optic nerve changes, and progressive visual field loss that begins in the periphery. It is always important to examine the asymptomatic eye for anterior chamber depth (the angle is usually also narrow) and elevated pressure. Common signs and symptoms include mild to intense eye pain, blurry vision, nausea, vomiting, abdominal pain, diaphoresis, and frontal headache. The symptoms of headache, nausea, vomiting, or abdominal pain may lead providers to focus on neurologic or gastrointestinal etiologies; however, AACG must always be considered if primary symptoms of acute, painful red eye with vision loss are present. The hallmarks of the physical examination include:

  • Fixed, dilated, mid-position pupil

  • Diffuse conjunctival injection

  • Corneal edema (clouding) (Figure 49-1)

  • Shallow anterior chamber (Figure 49–2)

  • Slit-lamp examination that may reveal mild cell and flare but no hyphema or hypopyon (blood or pus in the anterior chamber)

  • IOP elevated up to 80 mm Hg (normal is 9-21 mm Hg)

Figure 49–1.

Acute angle-closure glaucoma. The pupil is mid-dilated and fixed, and the cornea is cloudy. (Reproduced, with permission, from Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine. 6th ed. New York, NY: McGraw-Hill; 2004:1460.)

Figure 49–2.

Glaucoma. A. A physiologic block normally occurs where the posterior surface of the iris touches the lens. B. When this block is increased, the iris, as a result, bows forward (iris bombé) and the angle is narrowed and pressure increases. C. As pressure increases, the angle becomes blocked. (Reproduced, with permission, from Knoop KJ, Stack LB, Storrow AB, Thurman R, eds. Acute angle-closure glaucoma. In: The Atlas of Emergency Medicine. 5th ed. New York, NY: McGraw-Hill; 2021.)



Initially, the management goal of AACG is to decrease IOP by decreasing aqueous production and increasing outflow. An ophthalmologist should be consulted in the ED. Treatment modalities to decrease IOP include aqueous suppressants, osmotic agents, and miotic agents. After the corneal edema subsides, the definitive treatment is a laser peripheral iridectomy performed by an ophthalmologist. In some resource-limited countries, the definitive treatment is lens removal.

Decreasing Aqueous Humor Production

First, IOP is lowered by decreasing aqueous humor production with agents such as topical beta-blockers (timolol 0.5%), an alpha-2-agonist (brimonidine 0.1%), and/or a carbonic anhydrase inhibitor (acetazolamide 500 mg orally or intravenously). Of note, patients with sulfa allergies may not tolerate acetazolamide.

Osmotic Agents

Osmotic agents, such as mannitol and glycerol, can be used instead of acetazolamide to dehydrate the vitreous humor; the result is decreased intraocular fluid volume and thus decreased IOP. Mannitol may induce hypotension in patients with poor cardiac function; glycerol should be avoided in diabetic patients.

Miotic Agents

Miotics such as pilocarpine 1% to 2% enhance trabecular outflow by constricting the pupil and disrupting the corneal-iris apposition. However, their use is controversial. Topical beta-blockers and acetazolamide should be administered prior to the administration of pilocarpine since the ischemic iris sphincter may be unresponsive to pilocarpine at extremely high intraocular pressures (greater than 50 mm Hg).

Other Pharmacologic Agents

Administration of prednisolone acetate 1% eye drops should be considered, especially if the AACG is bilateral. The patient should also receive analgesic and antiemetic medications.

Approach to Red Eye

Differential Diagnosis of Red Eye

In addition to AACG, vision-threatening and painful causes of a red eye include severe conjunctivitis, keratitis, corneal ulcer, anterior uveitis, endophthalmitis, orbital cellulitis, scleritis, and temporal arteritis (Table 49–1). Causes of acute vision loss are outlined in Table 49–2. Examination with the slit lamp and fluorescein staining are required for all patients with a red or painful eye.






Bacterial Conjunctivitis

Gonococcal conjunctivitis (the most serious form of bacterial conjunctivitis) usually presents with an intensely red eye and copious purulent discharge, and it carries an increased risk of corneal ulcer and perforation. In contrast, chlamydial conjunctivitis generally presents with a more chronic clinical course, and although the conjunctivae are very red, there is typically scant discharge. It is important to recognize this diagnosis since the incidence of sexually transmitted chlamydial conjunctivitis is increasing.

Viral Conjunctivitis

Most conjunctivitis is viral and is often caused by adenovirus species. Epidemic keratoconjunctivitis (EKC) can be especially severe and contagious. Patients have profound conjunctival redness and swelling (chemosis), watery discharge, and lymphadenopathy. Many coronavirus disease 2019 (COVID-19) patients also present with conjunctivitis.

Distinguishing Bacterial from Viral Conjunctivitis

Distinguishing between bacterial and viral conjunctivitis can be challenging. A recent literature review suggests that a bacterial etiology is more likely if the patient has a diffusely red conjunctiva that renders the tarsal (eyelid) vessels indistinguishable, a purulent discharge, and bilaterally matted eyelids in the morning (morning gluing). A bacterial etiology is less likely if the eye redness is not noticeable at 20 ft or if the eyelids are not matted in the morning (see Table 49–3 for features of bacterial vs viral conjunctivitis).


Bacterial conjunctivitis is usually treated with topical broad-spectrum antibiotics (eg, erythromycin or trimethoprim-polymyxin B), whereas viral conjunctivitis is self-limited and typically resolves in 2 to 3 weeks.



Corneal inflammation, or keratitis, may be due to viral or bacterial infection, contact lenses, trauma, or ultraviolet (UV) light (eg, sunlight, welding, or UV lighting). Slit-lamp examination should be performed. The most important pathogens to identify are herpes simplex virus (HSV) and herpes zoster virus (HZV) because, if untreated, corneal ulceration and scarring may occur.

  • HSV: The clinical diagnosis of HSV is made by identifying multiple arborizing dendritic epithelial ulcers with terminal bulbs. HSV almost always stains with fluorescein, with the classic dendritic pattern. HSV corneal infections can also present in a more diffuse disciform or ulcerative pattern.

  • HZV: These dendrites taper at their ends and are typically associated with periorbital dermatomal vesicular eruptions or lesions at the tip of the nose (Hutchinson sign of nasociliary involvement).

Severe keratitis can progress to a corneal ulcer, which may be visible to the unaided eye as a white defect. Distinguishing an ulcer from a corneal abrasion is clinically significant and can be challenging. Ulcers can be distinguished from abrasions on slit-lamp examination by the hazy/cloudy stroma that lies beneath the ulcer in contrast to the clear stroma deep to most abrasions.

Anterior uveitis

Also known as iritis, anterior uveitis is associated with pain, blurred vision, photophobia (direct and consensual), circumcorneal redness, and anterior chamber cells and flare. A hypopyon (layer of white cells) may be visible along the inferior rim of the anterior chamber. The affected pupil is smaller, irregular, and minimally reactive. IOP can be elevated. Etiologies include:

  • Idiopathic

  • Infectious (eg, tuberculosis, syphilis, HSV/HZV, toxoplasmosis, cytomegalovirus [CMV]), Lyme disease)

  • Autoimmune (eg, sarcoidosis, collagen vascular diseases, human leukocyte antigen [HLA] B27 associated)

  • Medications (eg, sulfas)

  • Posttraumatic

Uveitis due to HSV and HZV is common in patients with human immunodeficiency virus (HIV). Treatment is complicated and may or may not involve topical corticosteroids, which increase the risk of glaucoma, cataracts, or reactivation of herpes simplex infections. For this reason, consultation with an ophthalmologist is strongly recommended.


Endophthalmitis is inflammation of the vitreous humor and can be endogenous, secondary to hematogenous spread from a distant site, or exogenous from inoculation after penetrating trauma. Traumatic endophthalmitis usually develops within 3 days of penetrating injury, retained foreign body, or ocular surgery. Hallmark features include decreased vision, eye pain, hypopyon, anterior chamber cells and flare, an absent red reflex, and a hazy vitreous. In addition, varying degrees of eyelid swelling, chemosis (conjunctival swelling), and severe conjunctival injection will be present. Causative organisms include Bacillus cereus, coagulase-negative Staphylococcus, Streptococcus, gram-negative rods, and fungi. Any patient presenting with a hypopyon requires an emergent ophthalmology consult. Orbital computed tomography (CT) or ultrasound B-scan microscopy (UBM) may help diagnose a foreign body. Systemic and intravitreal antibiotics will be necessary to preserve any remaining vision.

Orbital cellulitis

Orbital cellulitis is an infection deep to the orbital septum and is usually associated with blurred vision, diplopia, conjunctival injection, lid swelling, proptosis, fever, toxicity, and limited or painful ocular motility. An orbital CT (axial and coronal cuts) is diagnostic and will often reveal sinusitis (often ethmoid). Admission and parenteral antibiotics are indicated. Preseptal or periorbital cellulitis is a superficial infection and a far less serious entity, but it can be difficult to distinguish from orbital cellulitis. In general, these patients appear less toxic, have less pain, and can be treated with oral antibiotics.

Subconjunctival Hemorrhage

Subconjunctival hemorrhages are caused by blood collecting between the conjunctiva and sclera. Despite their appearance, they are painless and do not affect vision. These hemorrhages are often spontaneous or may be associated with minor trauma, including coughing and sneezing. If a patient with subconjunctival hemorrhage from blunt trauma complains of pain or vision changes, providers should continue evaluating for hyphema, globe rupture, or retrobulbar hemorrhage. Patients should be informed that the redness (bruise) might take weeks to completely resolve.


Blunt trauma to the eye may result in a hyphema (blood in the anterior chamber) and associated symptoms of painful, blurred vision. With a hyphema, blood may be visible to the unaided eye if it layers, or it may only be seen with the slit lamp in the anterior chamber (microhyphema) on maximum magnification. Complications include staining of the cornea by the red cells (producing a partially opaque cornea), elevated IOP secondary to red blood cells occluding the trabecular outflow tract, and rebleeding. Initial treatment consists of head elevation, an eye shield to prevent additional trauma, mydriatics to paralyze the ciliary body allowing the iris to rest, pain medication, antiemetics, and consultation. Retrobulbar hematoma must also be considered in the setting of blunt eye trauma. If hematoma is suspected, the IOP should be evaluated, an orbital CT obtained, and preparations made for lateral canthotomy if the pressure is significantly elevated.


In scleritis, the conjunctival, episcleral, and scleral vessels are inflamed, either diffusely or focally. Unlike episcleritis, which usually involves a milder pain, symptoms of scleritis include severe eye pain, redness, and decreased vision. It is also often associated with an underlying systemic disorder, such as a connective tissue disease, autoimmune disorder, HSV, HZV, HIV, Lyme disease, or syphilis. Rheumatoid arthritis is the most common systemic etiology, and HZV is the most common infectious cause. In contrast to episcleral vessels, scleral vessels do not blanch with topical vasoconstrictors or move under cotton swabs. Additionally, the entire sclera may have a bluish or violaceous hue and may be very tender upon palpation.

Treatment of scleritis involves treating the underlying disorder, which may involve systemic corticosteroids, immunosuppressive therapy, and nonsteroidal anti-inflammatory drugs (NSAIDs). This is always done after consultation with an ophthalmologist. Ultrasound may be useful in the assessment of posterior scleritis.

Clinical Pearls

  • Vision-threatening causes of red eye include acute angle-closure glaucoma, anterior uveitis, endophthalmitis, corneal ulcer, corneal infection, chlamydial/gonococcal conjunctivitis, orbital cellulitis, hyphema, retrobulbar hemorrhage, and scleritis.

  • Subconjunctival hemorrhages should be painless and do not affect vision. In the setting of blunt trauma, continue evaluating for hyphema, hypopyon, globe rupture, endophthalmitis, or retrobulbar hemorrhage if the patient complains of pain or vision changes because emergent ophthalmologic consultation would then be indicated.

  • Visual acuity, penlight pupil assessment, slit-lamp examination, fluorescein staining, measurement of intraocular pressure, and fundoscopy are essential elements of a thorough evaluation of the red eye.

  • Beware of systemic complications from topical ophthalmologic medications. Complications such as bradycardia and bronchospasm due to topical beta-blockers are common.


Ah-kee  EY, Egong  E, Shafi  A,  et al. A review of drug-induced acute angle closure glaucoma for non-ophthalmologists. Qatar Med J. 2015;1:6.

Bagheri  N, Wajda  BN, eds. The Wills Eye Manual. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2016.

Chan  PP, Pang  JC, Tham  CC. Acute primary angle closure—treatment strategies, evidences and economical considerations. Eye (Lond). 2019;33(1):110–119.

Flores-Sanchez  BC, Tatham  AJ. Acute angle-closure glaucoma. Br J Hosp Med. 2019;80(12):C174–C179.

Gilani  CJ, Yang  A, Yonkers  M,  et al. Differentiating urgent and emergent causes of acute red eye for the emergency physician. West J Emerg Med. 2017;18(3):509–517.

Liu  Y, Rhee  DJ. Acute bilateral angle closure. JAMA Ophthalmol. 2013;131(9):1231–1232.

Tabbut  M, Bates  A, Marple  G,  et al. Point-of-care ultrasound in the evaluation of the acutely painful eye. J Emerg Med. 2019;57(5):705–709.

Tarff  A, Behrens  A. Ocular emergencies: red eye. Med Clin N Am. 2017;101:615–639.

Question 1 of 3


A 45-year-old man complains of the acute onset of right eye redness with circumcorneal injection (ciliary flush), blurred vision, and pain with bright lights. On examination, his pupil is small and minimally reactive. Cell and flare are noted on slit-lamp examination. There is no fluorescein uptake. He also has pain in the affected eye when light is directed in the unaffected eye (consensual photophobia). Which of the following is the most likely diagnosis?


Acute angle-closure glaucoma (AACG)


Acute anterior uveitis


Herpes zoster virus infection


Corneal abrasion

You will be able to view all answers at the end of your quiz.

The correct answer is B. You answered B.


B. Acute anterior uveitis. Anterior uveitis usually presents as photophobia, blurred vision, a painful red eye, and an indirect consensual light reflex. A ciliary flush and cells with flare are noted on slit-lamp examination. AACG (answer A) usually presents as a painful red eye with a cloudy cornea, shallow anterior chamber, and mid-dilation of the pupil. Slit-lamp exam will not reveal any cells in the anterior chamber. Both herpes zoster virus keratitis (answer C) and corneal abrasion (answer D) will have positive fluorescein uptake.


Question 2 of 3


A 48-year-old woman with diabetes presents with 1 day of right eye pain, foreign body sensation, redness, and decreased vision. She underwent an artificial lens implant procedure in the right eye 2 days ago but missed her follow-up appointment. Visual acuity is to hand movement only in the right eye and is 20/30 in her left eye. The right pupil is 3 mm and sluggishly reactive, and the left pupil is 3 mm and briskly reactive. The right eye has a prominent ciliary flush and a hazy cornea; a right hypopyon is also present. The left conjunctivum and cornea are normal. Cell and flare are noted in the right eye. There is no fluorescein uptake. The right fundus cannot be visualized, and the red reflex is absent due to corneal haziness. Which of the following is the most appropriate next step?


Prescribe a topical ophthalmic steroid medication and have the patient return to the emergency department (ED) in 24 hours.


Prescribe a topical ophthalmic antibiotic medication and have the patient return to the ED in 12 hours.


Arrange an emergent ophthalmology consultation.


Check the blood glucose, and if it is elevated, recommend an urgent visit to her doctor.

You will be able to view all answers at the end of your quiz.

The correct answer is C. You answered C.


C. Arrange an emergent ophthalmology consultation. An emergent ophthalmology consult is appropriate for possible endophthalmitis in a diabetic patient with recent eye surgery and a hypopyon. This patient will require hospital admission with intravenous and intravitreal antibiotics. A topical steroid (answer A) is used for some rare inflammatory conditions of the eye in the absence of infection. Topical ophthalmic antibiotic medication (answer B) is used for various types of bacterial conjunctivitis and is insufficient for this likely very serious infection; delay of 12 hours can mean loss of vision. An urgent primary care physician appointment for elevated glucose (answer D) is warranted when there are systemic symptoms of hyperglycemia; in this case, the complaint is dealing with vision.


Question 3 of 3


A 39-year-old man with a history of migraines presents to the ED with a headache over both brows, nausea, and blurry vision for the past 6 hours. He recently started taking topiramate for his migraines. His current headache began gradually but is slightly worse than usual. The presence of blurry vision is new. He denies trauma or fever. Visual acuity is 20/200 in both eyes, and the pupils are each 4 mm and minimally reactive. The conjunctivae are injected, and the anterior chambers are clear but shallow. There is no fluorescein uptake. Fundoscopy is normal. The neurologic exam is nonfocal. Which of the following is the most important next diagnostic test?


Computed tomography (CT) of the head without contrast


CT of the orbit


Magnetic resonance imaging (MRI) of the head



You will be able to view all answers at the end of your quiz.

The correct answer is D. You answered D.


D. Tonometry. AACG is an uncommon but significant side effect of topiramate, an anticonvulsant and antimigraine medication. Patients typically present with bilateral blurry vision, headache, nausea, and vomiting. However, eye redness is minimal or absent, unlike most cases of AACG. Topiramate-induced AACG is usually bilateral and occurs within several weeks of beginning the medication or within several hours if the dosage is doubled. When AACG is suspected, tonometry to measure the intraocular pressure should be performed. Imaging of the head (answer A, CT without contrast, and answer C, MRI) would be indicated if the patient had neurologic deficits or if the intraocular pressures were normal. CT of the orbit (answer B) would be indicated if there were anatomic abnormalities of the orbit on exam.