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Drugs That Can Cause an Acute Angle Closure Crisis

Home / Basic Ophthalmology Review / Ocular Adverse Effects of Systemic Medications

Title: Drugs That Can Cause an Acute Angle Closure Crisis

Author: Shane Nau M.S., 4th Year Medical Student, University of Colorado School of Medicine

Figure: Nicholas Henrie, 1st Year Medical Student, University of Utah School of Medicine

Ultrasound Images: Roger Harrie, MD

Overview: Glaucoma is a type of optic neuropathy that, without proper treatment, can lead to progressive visual loss and even blindness. Though glaucoma has numerous subtypes, there are two major categories worth discussing here: Chronic Open-Angle (COAG) and Acute Angle Closure (AACG) or acute angle closure crisis. These categories can be differentiated by evaluating the iridocorneal angle, which is open in COAG but closed off or very narrow in AACG.  Chronic open-angle glaucoma has an insidious onset—typically over the course of years. AACG presents abruptly and is considered an ophthalmic emergency.

Numerous medications include in their listed sided effects, “Glaucoma,” or “vision changes,” or “seeing halos or rainbows around lights.”  These are most commonly referring to medications that can induce AACG or increase the risk of an individual already at risk of having such an attack.   To understand why the following drugs can cause an AACG event, we must review the pathway of aqueous fluid in the eye. Aqueous fluid is produced by the ciliary body, enters the posterior chamber then moves anterior to the lens and flows through the pupil into the anterior chamber. From there it drains through the trabecular meshwork at the iridocorneal angle—where the cornea meets the iris. AT this point, the fluid moves through the trabecular meshwork to the Canal of Schlemm where it returns to venous circulation. Because the eye is continually producing aqueous fluid, the drainage pathway is critical for intraocular pressure (IOP) maintenance. Importantly, significantly elevated IOP, even for a short time, can lead to optic nerve ischemia, retinal vein thrombosis, or corneal damage. Drugs cause AACG events through two primary mechanisms: 1) Pupillary block: obstruction of aqueous flow between the lens and pupil, thereby increasing pressure in the posterior chamber, 2) Non-pupillary block: forward movement of the iris-lens diaphragm, ciliary body, or choroid. Both mechanisms result in a posterior chamber-anterior chamber pressure gradient causing anterior billowing of the iris that narrows the iridocorneal angle. The following text categorizes the medications that can induce AACG by the mechanism of angle closure (pupillary block vs. non-pupillary block) and then further by the drug class (i.e. cholinesterase).

Autonomic mechanisms of Angle Closure: The autonomic nervous system (ANS) plays a significant role in the acute closure of the iridocorneal angles. The ANS innervates, and thus, structurally and functionally affects a variety of ocular tissues. Based on the aforementioned aqueous flow pathway and anatomy, it becomes clear that structural changes within the eye that narrow the lens-iris space or iridocorneal angle can increase the likelihood of angle closure. As a reminder, the parasympathetic nervous system increases iris sphincter constriction (pupil constriction) and ciliary muscle contraction whereas the sympathetic nervous system dilates the pupil, inhibits ciliary muscle contraction, and can either increase or decrease aqueous humor production. The effects of both the sympathetic and parasympathetic nervous system vary based on the specific receptor types being acted on. For this reason, sympathomimetics, alpha-2 agonists, B-blockers, and cholinergic agonists can all be used as glaucoma medications to decrease intraocular pressure—despite their different and often antagonistic drug classes. Classically, maneuvers or pharmacological agents that cause mydriasis (a sympathetic nervous system response) are known to be a risk factor for inciting acute angle closure crises.

Drugs that cause pupillary block angle closure: Anticholinergic agents (i.e. Tropicamide eye drops, Ipratropium inhaler, Promethazine & Ranitidine-antihistamines, periocular Botulinum Toxin), drugs with anticholinergic side effects (i.e. Imipramine-other TCA’s, Fluoxetine-other SSRI’s, Fluphenazine-other antipsychotics), adrenergic agents (i.e. Phenylephrine eye drops, IV Ephedrine, Epinephrine, intranasal Naphazoline, Salbutamol), Amphetamines (i.e. MDMA, intranasal Cocaine), and Marijuana are all associated with pupillary block glaucoma. Notably, Marijuana has only been reported as an inciting agent in one patient.

Drugs that cause non-pupillary block angle closure: Cholinergic agents (i.e. Pilocarpine & Carbachol eye drops), Sulfa-based agents (i.e. Topiramate, Acetazolamide, Hydrochlorothiazide, Bactrim), Anticoagulants (i.e. Heparin), cycloplegics agents (i.e. Atropine eye drops), Dopamine receptor agonists (i.e. Cabergoline), and NSAID’s (i.e. Mefenamic Acid).

Recognition & Management: Before management of an AACG event can be initiated, clinicians must recognize its clinical features: red eye, acute-onset reduction in vision, ocular or periocular pain, headache, and colored haloes. Notable physical exam signs include: elevated IOP (>21 mmHg is abnormal, but the IOP is frequently in the 30’s or 40’s), a shallow anterior chamber, a cloudy cornea, and a pale cupped optic disc (in the case of longstanding elevated IOP). Once recognized or suspected, ophthalmology should be consulted immediately. Management focuses on decompressing the pressure gradient between the posterior and anterior chambers of the eye. This makes sense as each AACG mechanism leads to anterior billowing of the iris secondary to this pressure gradient. The specific treatment is dependent on the suspected offending drug and its associated mechanism of angle closure. Treatment options include: stopping the offending agent, administering drugs that may reverse angle closure (i.e. Miotics), reduce IOP (i.e. Beta-blockers, Alpha-adrenergic agonists, Acetazolamide, and Hyperosmotic agents), or reduce inflammation (i.e. Prednisolone), and performing a laser peripheral iridotomy—the creation of a small hole in the iris to bypass the natural aqueous flow.


Achiron A, Sharif N, Haddad F. Drug-induced Acute Angle Closure Glaucoma. American Academy of Ophthalmology, EyeWiki. June 2015. Accessed June 25, 2018.

Ah-kee EY, et al. A review of drug-induced acute angle closure glaucoma for non-ophthalmologists. Qatar Medical Journal. 2015; 1: 6.

Lachkar Y, Bouassida W. Drug-induced acute angle closure glaucoma. Current opinion in ophthalmology 2007; 18: 129-33

Root, Timothy. OphthoBook. Introduction to Glaucoma. Accessed June 26, 2018.

Tripathi RC, Tripathi BJ, Haggerty C. Drug-induced glaucomas: mechanism and management. Drug safety 2003; 26: 749-67.


Figure 1.  Bottom: Labeled diagram of the eye.  The anterior part of the eye is highlighted and enlarged in the top figures. Top-Right: In healthy patients, the ciliary processes of the ciliary body secrete the aqueous humor into the posterior chamber.  The fluid then flows up through the pupil into the anterior chamber maintaining pressure in both chambers.  The fluid drains out of the anterior chamber through trabecular meshwork and into the canal of Schlemm.  Top-Left: A closed angle, demonstrated by the more narrow angle, shallow anterior chamber and obstruction of aqueous outflow.

Image 1: Anterior chamber ultrasound in a Moran Eye Center patient in acute angle closure crisis. Note: narrow iridocorneal angles (<25 degrees), a shallow anterior chamber (1 mm), an anteriorly bowed iris plane, and anteriorly rotated ciliary bodies.

Image 2: Anterior chamber ultrasound in a control patient with a normal open angle. Note: normal iridocorneal angles (~40 degrees), a normal depth anterior chamber (2.5-3.5mm), a flat iris plane, and the absence of anteriorly rotated ciliary bodies.

Red Flag Symptoms of Unilateral Vision Loss

Home / Basic Ophthalmology Review / Visual Acuity and Vision Loss

 Title: Red Flag Symptoms of Unilateral Vision Loss

Author: Troy Teeples, 4th year medical student, University of Utah School of Medicine; Griffin Jardine, MD

Photographer: James Gilman, CRA, FOPS

Date: 8/7/2018

Keywords/Main Subjects: Unilateral vision loss, monocular vision loss, red flags, headache, painful eye, pain with eye movement, floaters, flashes, atherosclerosis, central retinal artery occlusion, central retinal vein occlusion, giant cell arteritis, acute angle closure glaucoma, optic neuritis, keratitis, retinal detachment, vitreous hemorrhage, amaurosis fugax


Acute, monocular vision loss is a frightening experience for patients and may have long-term consequences depending on the etiology. The key to providing efficient, effective care is a careful history, a focused physical exam and knowing when to seek help from an ophthalmologist. The goal of this section is to help identify red flag signs and symptoms during a work up of unilateral vision loss in order to able to 1) efficiently narrow a differential diagnosis and 2) know when to urgently consult ophthalmology.

Red Flags from History and Physical Exam

There are key elements that need to be addressed when working up a patient with unilateral vision loss. Providers should look for the following associated symptoms and signs in order to guide the decision-making process.


When a patient over the age of 60 complains of a headache and unilateral vision loss, Giant Cell Arteritis (GCA) should be immediately considered given the potential for permanent vision loss. Ask the patient about a history of polymyalgia rheumatica, scalp tenderness, jaw claudication and other constitutional symptoms such as fever, malaise, weight loss or anorexia. If GCA is suspected, order an ESR, CRP and CBC looking for an elevated platelet count.  If there is a high enough suspicion for GCA, don’t wait for the lab results to initiate high-dose systemic corticosteroids. An ophthalmologist should be consulted to evaluate the cause of the vision loss, specifically looking for a central retinal artery occlusion. The patient should then be schedule for a diagnostic temporal artery biopsy within the next week as an outpatient.

Red, Painful Eye

There are several causes of monocular vision loss accompanied by a red, painful eye.  After inquiring about recent trauma and ruling out a ruptured globe, check the patient’s intraocular pressure (IOP) with a Tono-pen® to evaluate for Acute Angle Closure Glaucoma, as this may lead to permanent vision loss if not treated appropriately. Patients will present with a red, painful eye as well as a headache, and nausea/vomiting. They may also complain of halos around lights. Physical exam will reveal a steamy (hazy) cornea, a dilated pupil that is not reactive to light, and an IOP greater than 40 typically. Consult an ophthalmologist if suspected.

Keratitis or corneal ulcers may also present with a red, painful eye and unilateral decreased or blurry vision. Patients may complain of excessive tears or discharge, and photophobia. Ask about contact lens wear, autoimmune conditions such as rheumatoid arthritis and look for corneal whitening or loss of corneal clarity and consult an ophthalmologist if concerned.

Pain with eye movement

Optic neuritis will present with acute vision loss, typically over the course of < 1 week. The majority of these patients will have pain with eye movement and decreased color vision. They may have a history of demyelinating symptoms or a known diagnosis of multiple sclerosis. On exam, a relative afferent pupillary defect (APD) will be seen during a swinging flashlight test.

Floaters and flashes

Another combination of concerning symptoms are flashes and floaters in combination with monocular vision loss. Flashes and floaters of acute onset are concerning for a retinal detachment. Patients are commonly myopic (short-sighted) and may additionally complain of vision loss as a “curtain drawn” over their vision. A retinal detachment is painless but a surgical emergency and a vitreoretinal specialist should be consulted.

A vitreous hemorrhage may also present as painless monocular vision loss associated with floaters. Patients should be questioned regarding a history of trauma, ocular surgery, diabetes, sickle cell anemia, leukemia and high myopia, all of which may precipitate a vitreous hemorrhage.

Atherosclerosis Risk Factors

If a patient presents with painless, temporary monocular vision loss with subsequent restoration of sight, then amaurosis fugax should be high on the differential. A thorough history should include atherosclerotic risk factors such as diabetes mellitus, smoking, CAD, and HTN. Fundoscopy may reveal Hollenhorst plaques (cholesterol emboli).

Central Retinal Artery Occlusion (CRAO) and Central Retinal Vein Occlusion (CRVO) are nearly impossible to distinguish by history alone. Patients will present with acute, painless monocular vision loss without other associated symptoms. These diagnoses are made with fundoscopy revealing a “blood and thunder” appearance in CRVO along with diffuse hemorrhages and cotton wool spots (figure 1). No emergent treatment is particularly effective in reversing the changes, but there are several long-term sequelae and corresponding treatments so these patients should be referred to an ophthalmologist for close follow-up.

CRAO, on the other hand, does have a few emergent treatment options and is an ophthalmologic emergency. It can by recognized on fundoscopy by diffuse ischemic retinal whitening and a cherry red fovea along with boxcar segmentation of blood in the retinal veins (figure 2). Consult an ophthalmologist immediately if suspected and within the first several hours of the vision loss.

Images or video:

Figure 1: A color fundus photo of the left eye with diffuse retinal hemorrhages in all four quadrants (“blood and thunder”) and optic nerve edema, consistent with a central retinal vein occlusion.

Figure 2: A color fundus photo of the right eye demonstrating diffuse, ischemic retinal whitening; arterial attenuation and a “cherry red spot” at the fovea—pathognomonic in the context of retinal whitening and sudden, painless vision loss for a central retinal artery occlusion.



  1. Farris W, Waymack JR. Central Retinal Artery Occlusion. [Updated 2017 Dec 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan-. Available from: Accessed 6/19/2018.
  2. Khazaeni B, Khazaeni L. Glaucoma, Acute Closed Angle. [Updated 2017 Apr 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan-. Available from: Accessed 6/20/2018.
  3. Ness T, Bley TA, Schmidt WA, Lamprecht P. The diagnosis and treatment of giant cell arteritis. Dtsch Arztebl Int 110: 376-385, 2013.
  4. Patel A, Nguyen C, Lu S. Central Retinal Vein Occlusion: A Review of Current Evidence-based Treatment Options. Middle East Afr J Ophthalmol. 2016 Jan-Mar;23(1):44-8. PubMed PMID: 26957838.

Faculty Approval by: Griffin Jardine, MD


Copyright statement: Copyright Troy Teeples, ©2018. For further information regarding the rights to this collection, please visit:


How to Use the Direct Ophthalmoscope

Home / Basic Ophthalmology Review / Direct Ophthalmoscope

Title: How to Use the Direct Ophthalmoscope
Authors: Tania Padilla Conde, 4th Year Medical Student, University of South Dakota Sanford School of Medicine; Christopher Bair, MD and Michele Burrow, MD
Date: 08/10/2018
Videographer: Ethan Peterson
LOCATION: Medical Student Education Outline > I. Introduction to the Eye Exam > Direct Ophthalmoscope > Using a Direct Ophthalmoscope – VIDEO
Learning Objectives

  1. Understand the utility of the direct ophthalmoscope
  2. Identify key anatomical structures visible with the direct ophthalmoscope
  3. Learn the parts and settings of the direct ophthalmoscope
  4. Learn the exam technique of the direct ophthalmoscope

Understand the utility of the direct ophthalmoscope

The direct ophthalmoscope allows you to look into the back of the eye to look at the health of the retina, optic nerve, vasculature and vitreous humor. This exam produces an upright image of approximately 15 times magnification.

Instrument Parts

Light Settings

Exam Technique

  1. Wash your hands.
  2. Introduce yourself to the patient and explain what you are going to do.
  3. Position the patient so that the ophthalmoscope is held directly at the level of the patient’s eye.
  4. Turn on the ophthalmoscope and set the light to the correct aperture.
  5. Dim the lights.
  6. Instruct the patient to focus on an object straight ahead on the wall.
  7. To exam the patient’s RIGHT eye, hold the ophthalmoscope in your RIGHT hand and use your RIGHT eye to look through the instrument.
  8. Place your left hand on the patient’s head and place your thumb on their eyebrow.
  9. Hold the ophthalmoscope about 6 inches from the eye and 15 degrees to the right of the patient.
  10. Find the red reflex.
  11. Move in closer, staying nasally until you see the optic nerve.
  12. Rotate the diopter lens until the optic nerve comes into focus.
  1. Measure the cup to disc ratio.
  2. Scan slightly up, down, right and left to look at the vessels.
  3. Move out temporally to find the macula and fovea.
  4. Repeat the same technique on the other eye.


  1. “Examination of the optic nerve at the slit-lamp biomicroscope with a handheld lens – EyeWiki.” Accessed July 17, 2018.
  2. “3.5V Standard Ophthalmoscope.” Accessed July 17, 2018.–traditional-direct/35v_standard_ophthalmoscope.html

Faculty Approval by: Griffin Jardine, MD

Copyright statement: Copyright Tania Padilla Conde, ©2018. For further information regarding the rights to this collection, please visit: URL to copyright information page on Moran CORE


Disclosure (Financial or other): None

Herpetic Disease of the Cornea

Home / Basic Ophthalmology Review / Cornea

Name: Austin D. Bohner, 2nd Year Medical Student, University of Utah, School of Medicine

Figure 1: A herpetic dendrite highlighted with a fluorescein stain.

Herpetic disease of the cornea from herpes simplex virus (HSV), also known as HSV keratitis, is a major cause of corneal scarring and blindness worldwide.1 Correct identification of HSV keratitis is important as misdiagnosis can result in a delay in treatment—or worse, inappropriate treatment with topical glucocorticoids which can exacerbate HSV infections.2

Diagnosis of HSV keratitis is based on clinical history and physical examination. Laboratory tests are usually not necessary, with slit lamp findings being typically sufficient. The exam findings include conjunctival injection near the limbus, a decrease in corneal sensation and characteristic dendritic lesions of the cornea that stain with fluorescein (see image 1).3 When deeper stromal tissue is involved corneal edema may also be found in addition to the above.

HSV-1 accounts for the majority of ocular HSV keratitis infections and is endemic in human populations, with the majority of people being exposed to the virus by middle age. The virus is transmitted through direct contact of mucosal membranes. The bulk of ocular disease is represented by reactivation of the virus from its latency in sensory neurons (usually the trigeminal nerve ganglion in ocular cases) rather than from primary infection. History of HSV infection and reactivation can be useful in making a clinical diagnosis. Most ophthalmic HSV cases occur unilaterally, with recurrences affecting the same eye. Ocular HSV reactivation has been associated with sun exposure, stress, ultraviolet laser treatment, topical ocular medication (epinephrine, beta-blockers and prostaglandins), and immunosuppression drugs such as glucocorticoids.

HSV Keratitis warrants prompt referral to an eye care specialist, as the treatment varies based on the depth of the involvement of the cornea as well as integrity of the overlying epithelium.  Topical and oral antiviral medications are frequently used and can shorten the duration of the disease though each has its limitations.4

Antiviral Dose Additional Notes
Trifluorothymidine 1% (trifluridine, Viroptic) One drop every two hours (8-9 doses daily) Treatment time is limited by epithelial toxicity
Topical Ganciclovir 0.15% gel (Zirgan) one drop five times daily until epithelial healing occurs and then three times daily for one week Less corneal epithelial toxicity, maybe better tolerated for long term use compared to trifluridine
Topical Acyclovir 3% Available in Europe but not in the US
Oral acyclovir 400mg five times daily. Avoids epithelial toxicity, though acyclovir resistant strains of HSV exist


  1. Liesegang TJ. Herpes simplex virus epidemiology and ocular importance. Cornea. 2001;20(1):1-13.
  2. Benz MS, Glaser JS, Davis JL. Progressive outer retinal necrosis in immunocompetent patients treated initially for optic neuropathy with systemic corticosteroids. Am J Ophthalmol. 2003;135(4):551-553.
  3. Teng CC. Images in clinical medicine. Corneal dendritic ulcer from herpes simplex virus infection. N Engl J Med. 2008;359(17):e22.
  4. A controlled trial of oral acyclovir for iridocyclitis caused by herpes simplex virus. The Herpetic Eye Disease Study Group. Arch Ophthalmol. 1996;114(9):1065-1072.


Home / Basic Ophthalmology Review / Red Flag Symptoms

Title: Diplopia

Author: DanHung Nguyen


Diplopia is commonly referred to as “double vision”, or when patients report seeing two images instead of one. The ability to fuse the two distinct images from each eye is a complex one requiring both a central or sensory component as well as a neuromuscular or motor component.  What is most concerning about sudden onset diplopia is that it can be the first manifestation of a systemic, muscular, or neurological disorder.

The first step in evaluating a patient with diplopia is a thorough history, including:

Physical exam:

Summary of Common Causes of Sudden-Onset Diplopia


  1. “Diplopia (Double Vision).” April 13, 2017.
  2. “Red Flags in Neuro-ophthalmology.” Accessed September 17, 2017.
  3. Root, Timothy. OphthoBook., 2012.

Identifier: Moran_CORE_24945

Copyright statement: Copyright 2018. Please see terms of use page for more information.

Performing the Confrontational Visual Field Exam

Home / Basic Ophthalmology Review / Confrontational Visual Fields

Title: Performing the Confrontational Visual Field Exam

Author: Brian Kirk, 4th Year Medical Student, University of Utah School of Medicine


The visual field encompasses all that can be seen when fixated on a single point. This includes the central vision and the peripheral vision. There are several methods for measuring the visual field. Some common ways include using specialized instruments (i.e. Humphrey Visual Field Machine) that are capable of sensitive measurements that can detect small defects throughout the entire visual field. Another less sensitive but highly specific test is known as the confrontational visual field exam1. This is a simple and quick way to assess the peripheral vision of the patient without the use of expensive specialized equipment. It is useful as there are a variety of conditions that can affect the peripheral vision such as glaucoma, retinal detachment, stroke, vascular occlusions within the eye and certain brain tumors.

Performing the exam:

  1. Have the patient remove their hat or anything that could interfere with their peripheral vision.
  2. Sit approximately three to four feet away and directly in front of the patient. If possible, adjust your seat height until you are at eye level with the patient.
  3. Ask the patient to gently cover their left eye with their left hand and instruct the patient to fix their gaze directly on your left eye throughout the test.
  4. While the patient is focusing on your eye, close your right eye and maintain fixation on the patients open eye. Raise your hand to the inferior temporal edge of your peripheral vision halfway between yourself and the patient, while holding up 1, 2, or 5 fingers. Using only 1, 2, and 5 fingers helps to make the number more easily distinguished by the patient. Ask the patient how many fingers are seen.
  5. Repeat step 4, testing all four visual quadrants of the left eye: Inferior temporal, inferior nasal, superior temporal, and superior nasal.
  6. Repeat steps 3, 4, and 5 for the patient’s right eye.


  1. Johnson LN, Baloh FG. The accuracy of confrontation visual field test in comparison with automated perimetry J Natl Med Assoc. 1991 Oct; 83(10): 895–898. When compared to automated perimetry confrontational field testing was found to have an overall sensitivity of 50% and a specificity of 93.4% when examining 512 patients with both tests.

Identifier: Moran_CORE_24944

Copyright statement: Copyright 2018. Please see terms of use page for more information.


Home / Basic Ophthalmology Review / Conjunctiva / Sclera

Title: Scleritis

Author: Trey Winter, 1st Year Medical Student, University of Utah

Description: Scleritis is a disorder characterized by the inflammation of the sclera that can radiate to the cornea, episclera, and uveal tract. This inflammation can be destructive, painful, and potentially blinding. It is commonly associated with other systemic diseases such as rheumatoid arthritis.

Scleritis is divided into two main types, anterior scleritis and posterior scleritis. Anterior scleritis is further divided into three categories: diffuse anterior scleritis, nodular anterior scleritis, and necrotizing anterior scleritis.

Diffuse anterior scleritis- the most common, best prognosis.

Scleromalacia or corneal thinning from prior scleritis.

Necrotizing anterior scleritis- least common, most dangerous.

Nodular anterior scleritis- 2nd most common, often recurrent.

Presentation: Scleritis most commonly presents with severe, constant eye pain that worsens at night and in the morning. Movement of the eye is generally painful as the muscles controlling eye movement insert into the sensitized sclera. Patients with scleritis also present with ocular redness, headaches, photophobia, and watering of the eye.

The key sign of scleritis during ocular examination is an injection (an apparent increase in size and number of blood vessels on the sclera), associated with violaceous discoloration of the eye and tenderness to palpation. Although the injection can span multiple layers, involvement of the deep episcleral vascular plexus is what distinguishes scleritis from other, less severe conditions.

Diagnosis: It is important to note that the diagnosis of scleritis involves two aspects: the primary diagnosis of scleritis and the evaluation for a systemic disorder associated with scleritis.

Scleritis can be diagnosed and classified largely based on the information in the history and from the ophthalmologic exam. The ophthalmoscopy and slit-lamp examinations are used to detect deep scleral injection. Tenderness to palpation (done by gently pressing on the eyelid over the area of inflamed sclera) is highly specific to scleritis. A less common but occult form of scleritis known as “posterior scleritis” can present with a normal appearing external eye but instead present with choroidal and posterior scleral thickening on ultrasound.

The most important differential diagnosis is between scleritis and episcleritis. Episcleritis is an inflammation limited to the episclera (the layer superficial to the sclera) and is typically not emergent or vision-threatening. Both conditions present with similar symptoms including redness of the eye and pain. The phenylephrine test can be used to help distinguish these conditions by administering phenylephrine topically to the eye. In cases of episcleritis, the phenylephrine will blanch the eye due to vasoconstriction of the episcleral vessels. The deeper and larger inflamed vessels from sclerits will remain red after administration of the phenylephrine.

A large percentage of true scleritis cases have an underlying, associated systemic inflammatory condition. Here is a truncated list with a brief review of each disease:

Complications: Scleritis can lead to permanent ocular complications in severe cases.

Complications from scleritis include:

Management/Treatment: Treatment of scleritis usually begins with nonsteroidal anti-inflammatory drugs (NSAIDS), especially for diffuse anterior scleritis and nodular anterior scleritis. NSAIDS reduce the stiffness, swelling, and pain associated with scleritis. For necrotizing anterior scleritis and posterior scleritis, glucocorticoids or the combination of glucocorticoids and immunosuppressive agents are administered. In severe cases, patients need surgery to prevent rupture and retain vision.

Treatment is individualized based on the patient’s symptoms and the severity of the symptoms. As mentioned above, it is imperative not to forget a careful history and systemic work-up for any underlying, associated systemic inflammatory conditions.


  1. Benson WE. Posterior scleritis. Survey of Ophthalmology 1988; 5:297.
  2. Fong LP, Sainz de la Maza M, Rice BA, et al. Immunopathology of scleritis. Ophthalmology 1991; 98:472.
  3. Jabs DA, Mudun A, Dunn JP, Marsh MJ. Episcleritis and scleritis: clinical features and treatment results. Am J Ophthalmol 2000; 130:469.
  4. McCluskey PJ, Watson PG, Lightman S, et al. Posterior scleritis: clinical features, systemic associations, and outcome in a large series of patients. Ophthalmology 1999; 106:2380.
  5. Okhravi N, Odufuwa B, McCluskey P, Lightman S. Scleritis. Survey of Ophthalmology 2005; 50:351-363.
  6. Tuft SJ, Watson PG. Progression of scleral disease. Ophthalmology 1991; 98:467.
  7. Watson PG, Hayreh SS. Scleritis and episcleritis. British Journal of Ophthalmology 1976; 60:163-191.
  8. Albini TA, Rao NA, Smith RE. The Diagnosis and Management of Anterior Scleritis. International Ophthalmology Clinics 2005; 45:191-204.

Identifier: Moran_CORE_24943

Copyright statement: Copyright 2018. Please see terms of use page for more information.


Home / Basic Ophthalmology Review / Diagnostic Use of Eye Drops

Topic: Proparacaine

Name and Title: Brian Walker, 4th year Medical Student, McGovern Medical School at UTHealth

Location: (Medical Student Education Outline > I. Introduction to the Eye Exam > Diagnostic use of Eye Drops > Proparacaine)


Proparacaine (Alcaine, Parcaine) is a topical ophthalmic anesthetic. This eye-drop provides 10-20 minutes of eye surface anesthesia or numbing for diagnostic and operative procedures but NEVER as a therapeutic treatment for eye pain, as repeated use can be severely toxic to the eye.


  1. Imming P., Sinning C., Meyer A. Drugs, their targets and the nature and number of drug targets. Nat Rev Drug Discov. 2006 Oct; 5(10):821-34.
  2. Lexicomp Online®, Lexi-Drugs®, Hudson, Ohio: Lexi-Comp, Inc.; September 11, 2017.
  3. T., Levent T., Inci M.A. Toxic keratopathy associated with abuse of topical anesthetics and amniotic membrane transplantation for treatment. Int J Ophthalmol. 2015; 8(5): 938–944.

Identifier: Moran_CORE_24941

Copyright statement: Copyright 2018. Please see terms of use page for more information.


Home / Basic Ophthalmology Review / Lens

Title: Cataracts

Author: Tanner Ferguson, 4th year medical student, University of South Dakota Sanford School of Medicine

IMAGES: Photography by James Gilman, CRA, FOPS, Moran Eye Center


Figure 1: Retroillumination reveals a posterior subcaspular cataract centrally with vacuoles peripherally.

Figure 2: This central opacity would be visually significant due to its central location. Note the zonular fibers seen at the edge of the lens.

Figure 3: An unusual feathery pattern of cataract that accentuates the embryonal “Y” suture.

Figure 4: A slit lamp photo with a tangential beam of light highlighting a cross section of a more typical nuclear cataract with its accompanying yellowing.


Cataracts are an opacity or clouding of the crystalline lens in the eye1. Cataracts are extremely common and being able to recognize the common signs and symptoms is helpful for all clinicians. This introduction will provide a brief summary of the anatomy of the lens, risk factors for cataract formation and the symptoms associated with cataracts. For more detailed information of cataracts, please see our lens/cataract section of the CORE curriculum.


Normally, the human lens is a transparent, flexible biconcave disk that sits posterior to the iris (colored part of the eye) and is suspended circumferentially by zonular fibers from the ciliary body muscle. The lens is made up of three main parts: capsule, cortex and nucleus. The ciliary muscle contracts/relaxes to alter the shape of the lens to change its refractive power. This is particularly helpful for accommodation, or focusing on near objects, when contraction of the ciliary muscle changes the shape of the lens to bring near objects into focus. For more on accommodation, please see the Presbyopia topic (link).


The development and progression of cataract formation is dependent on numerous factors. Specific factors that can accelerate cataract formation include diabetes, steroids, trauma and intraocular surgery2,3. When cataracts do develop, patients may remain asymptomatic for some time. Symptoms typically differ depending on the type of cataract formation and its location within the lens. When they become visually significant, the common symptoms include difficulty driving at night, “starbursts” around lights, difference in color perception, cloudy vision or a change in eye glasses prescription4. Patients may even suggest their vision has improved, a phenomenon known as “second sight”, which occurs due to the change in refractive index of the lens with cataract formation5. Patients should be referred for cataract surgery when the cataract is affecting their visual needs.

Posterior Capsular Opacification

It’s also important to recognize a minor complication that many patients experience after cataract surgery. Although the capsule of the lens is typically polished and cleaned during cataract surgery, a small film can develop on the posterior capsule that is visually significant to patients, known as posterior capsular opacification (PCO). It can occur months to years after the initial procedure and is treated with an Nd:YAG laser capsulotomy, an office-based procedure.1,6 This is sometimes referred to as a “second cataract,” though this term is inaccurate as it is not a recurrence of the original cataract.


  1. Olson RJ, Braga-Mele R, Chen SH, et al. Cataract in the Adult Eye Preferred Practice Pattern®. Ophthalmology. 2017;124(2):P1-P119. doi:10.1016/j.ophtha.2016.09.027.
  2. West SK, Valmadrid CT. Epidemiology of risk factors for age-related cataract. Survey of Ophthalmology. 1995;39(4):323-334.
  3. Klein BE, Klein R, Lee KE, Danforth LG. Drug use and five-year incidence of age-related cataracts: The Beaver Dam Eye Study. Ophthalmology. 2001;108(9):1670-1674.
  4. Crabtree HL, Hildreth AJ, O’Connell JE, Phelan PS, Allen D, Gray CS. Measuring visual symptoms in British cataract patients: the cataract symptom scale. British Journal of Ophthalmology. 1999;83(5):519-523.
  5. Brown NA. The morphology of cataract and visual performance. Eye (Lond). 1993;7 ( Pt 1)(1):63-67. doi:10.1038/eye.1993.14.
  6. Fong CS-U, Mitchell P, Rochtchina E, Cugati S, Hong T, Wang JJ. Three-year incidence and factors associated with posterior capsule opacification after cataract surgery: The Australian Prospective Cataract Surgery and Age-related Macular Degeneration Study. American Journal of Ophthalmology. 2014;157(1):171-179.e171. doi:10.1016/j.ajo.2013.08.016.

Identifier: Moran_CORE_24940

Copyright statement: Copyright 2018. Please see terms of use page for more information.


Ophthalmic Pathology for Medical Students

Basic Ophthalmology Review / Additional Resources

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Title: Ophthalmic Pathology for Medical Students
Author: Nick Mamalis, MD, Professor of Ophthalmology, Director of Ocular Pathology, Moran Eye Center
Date: 01/18/2018
Keywords/Main Subjects: Ocular Pathology
Diagnosis: NA
Brief Description: A comprehensive overview of ocular pathology for medical students.
Format: PDF
Series: Medical Student Education Outline
References: Pathologic Basis of Disease, 7th Edition, pp 1421-47.
Identifier: Moran_CORE_24888
Copyright statement: Copyright 2018. Please see terms of use page for more information.