Moran CORE

Open source ophthalmology education for students, residents, fellows, healthcare workers, and clinicians. Produced by the Moran Eye Center in partnership with the Eccles Library

Search Moran CORE

How to Assess Whether a Globe is Ruptured

Home / Basic Ophthalmology Review / Trauma

Title: How to Assess Whether a Globe is Ruptured
Author: Johnny Lippincott, 4th Year Medical Student, University of Mississippi Medical Center

Location: Medical Student Education Outline > II. Anatomical Approach to Eye Disease > Trauma > 2. How to assess whether a globe is ruptured


Introduction: An open globe or ruptured globe is an eyeball with a full-thickness defect in part of the eye’s wall, and is a true ophthalmic emergency. “Full-thickness” means all layers of the eye are disrupted. An open globe therefore allows communication between the eye’s interior and the environment. The danger of this communication is two-way: the eye’s internal contents can extrude, and environmental factors (e.g., pathogens) may enter.

If there is any concern that a patient may have an open globe, the top priority is avoiding further damage to the eye. This means special precautions must be taken immediately to assess whether this is the case. Until the integrity of the globe is confidently established, do not place external pressure of any sort on the eye of concern. Doing so can squeeze ocular contents through the defect and possibly cause permanent loss of vision or loss of the eye itself. Do not: patch the eye, measure intraocular pressure (e.g., with a Tonopen®), or allow the patient to rub the eye.


Patients may present with an open globe after various forms of trauma, from work- and sports-related injuries to falls and motor vehicle accidents. Particularly important history includes:

Signs of an Open Globe

A simple penlight is useful in grossly assessing the integrity of the globe.


Figure 1: Prolapsed iris through a corneal laceration with a very irregular pupil visible retina through the pupil.  The conjunctiva is boggy and the entire globe appears deflated or slightly collapsed or simply “not round.”

Image 2: Fundus photo of an inferior choroidal rupture versus scleral rupture with a vitreous tracking to the wound.

Pathognomonic signs:

Three necessary tools for this test are 1) anesthetic eye drops (e.g., proparacaine HCl 0.5%), 2) fluorescein strip, and 3) cobalt blue light source with slit lamp/magnification. After numbing the eye with drops, gently paint dye across the wound. Looking under magnified cobalt blue light, either gross leakage from the defect or paling of the fluorescein dye wound indicate an active leak (indicating dilution of dye with intraocular fluid).

Suggestive signs:

Treatment & Plan

Salient orders in the event of a suspicious or confirmed open globe include:


  1. Castellarin, A. A., & Pieramici, D. J. (2006). Open globe management. Comprehensive ophthalmology update8(3), 111-124.
  2. 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.
  3. Harlan Jr, J. B., & Pieramici, D. J. (2002). Evaluation of patients with ocular trauma. Ophthalmology Clinics of North America15(2), 153-161.
  4. Seidel Test. Retrieved August 21, 2017, from

Wet versus Dry Macular Degenerative Changes

Home / Basic Ophthalmology Review / Retina

Title: Wet versus Dry Macular Degenerative Changes

Author: Nina Boal, MSIV, Thomas Jefferson University

Photographer: James Gilman, CRA, FOPS

Location: Medical Student Education Outline > II. Anatomical Approach to Eye Disease > RETINA> 2. Wet versus Dry Macular degenerative changes


Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in industrialized countries among people 50 years or older [1]. It is a degenerative disease of the macula (central portion of the retina), that results in central vision loss. Clinically, it is divided into dry (atrophic) or wet (exudative or neovascular). The risk of progressing from dry AMD to wet AMD is estimated at 1 to 4.7 percent in one year and 13 to 18 percent at three years [2].

Dry age-related Macular Degeneration

Macular changes in dry AMD are characterized by subretinal drusen deposits, atrophy of the retinal pigment epithelium (RPE), pigment epithelial detachments, and subretinal pigment epithelial clumping. There is an absence of neovascularization [3]. Dry AMD affects 85 to 90 percent of everyone with AMD [4].

Figure 1. Drusen in Dry AMD

Figure 2. Geographic atrophy in Dry AMD

Wet age-related Macular Degeneration

In wet (or neovascular) AMD, abnormal vessels grow into the subretinal space from the choroidal circulation. These vessels can leak and lead to subretinal hemorrhage, seen in figure 3, and subretinal fluid collections, indicating choroidal neovascularization. The goal is to recognize these new vessels before they bleed and cause a hemorrhagic detachment of the retinal pigment epithelium. Wet AMD is less common than dry AMD, affecting only 10 to 15 percent of people with AMD. However, it accounts for more than 80% of patients with severe visual loss or legal blindness [4].

Figure 3A. Subretinal hemorrhage in Wet AMD

Figure 3B. Fluorescein dye retinal angiography of patient with wet AMD, area of leakage corresponds to hemorrhage in figure 3A


The main symptom of AMD is loss of central vision, but initially AMD may be asymptomatic. Patients with dry AMD describe a gradual loss of vision in the center of their visual field. Patients with wet AMD may describe a more acute visual distortion or loss of central vision as fluid or blood accumulates under the retina.


Figure 4 Amsler Grid


Treatment of Dry AMD

 There is no proven effective treatment for dry AMD, however these patients may eventually develop wet AMD [3]. To prevent this progression, patients can be advised to stop smoking and take a combination of vitamins and minerals that make up the AREDS formula (Age-Related Eye Disease Study). A combination of antioxidant vitamins plus zinc was shown to protect the eye from further damage from AMD in patients who had more extensive dry and wet AMD [5,6].

Treatment of Wet AMD

In addition to the use of antioxidants and zinc, treatment of wet AMD attempts to stop and prevent neovascularization through:

 Summary Table


85 to 90% of patients with AMD 10 to 15% of patients with AMD
Absence of neovascularization Choroidal neovascularization– subretinal hemorrhage and subretinal fluid collections
Drusen, RPE atrophy, pigment epithelial detachments, subretinal pigment epithelial clumping Drusen, RPE atrophy, pigment epithelial detachments, subretinal pigment epithelial clumping
Slow progression Rapid loss of central vision over weeks to months
Mild to Severe central vision loss More severe vision loss or legal blindness

–          Monitor progression to wet AMD with Amsler grid

–          Smoking cessation

–          AREDS antioxidants and zinc supplements (more effective for extensive dry AMD)


–          Smoking cessation

–          AREDS antioxidants and zinc supplements

–          Anti-VEGF therapy

–          If anti-VEGF therapy does not work consider PDT or thermal laser photocoagulation

Faculty Reviewer: Griffin Jardine, MD


  1. Hyman L. Epidemiology of eye disease in the elderly. Eye (Lond) 1987; 1 ( Pt 2):330.
  2. Bressler NM. Age-related macular degeneration is the leading cause of blindness… JAMA 2004; 291:1900.
  3. Lietman MW. Manual for eye examination and diagnosis. 9th Hoboken, NJ: John Wiley & Sons Inc.; 2017.
  4. Jager RD, Mieler WF, Miller JW. Age-related macular degeneration. N Engl J Med 2008; 358:2606.
  5. Age-Related Eye Disease Study Research Group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch Ophthalmol 2001; 119:1417.
  6. Tan JS, Mitchell P, Kifley A, et al. Smoking and the long-term incidence of age-related macular degeneration: the Blue Mountains Eye Study. Arch Ophthalmol 2007; 125:1089.
  7. Solomon SD, Lindsley K, Vedula SS, et al. Anti-vascular endothelial growth factor for neovascular age-related macular degeneration. Cochrane Database Syst Rev 2014.

Identifier: Moran_CORE_24645

The Motility Exam

Home / Basic Ophthalmology Review / Extraocular Motility

Title: The Motility Exam

Author: Eric Peterson, MSIV, BS

Date: N/A

Keywords/Main Subjects: Ocular Motility Exam;

Diagnosis: None

Description of Image:

The ocular motility exam can be a simple yet profoundly important part of the ophthalmic exam. Six extraocular muscles act to move the eye up/down, left/right and intort/excyclotort. These six muscles control the eye in a complex combination of agonist and antagonist cooperation.  Interestingly, the extraocular muscles have the densest ratio of motor neurons to muscle fibers of any muscle in the body, thus facilitating the tremendously fine motor control and impeccable alignment of the eyes.

The actions of the eye muscles are most easily assessed by utilizing the H motility pattern as seen in Figure 1. These six cardinal positions along with primary gaze are particularly useful when assessing ocular motility because each cardinal position is primarily obtained by the action of one muscle. For example, elevation of the eye from primary gaze is accomplished by actions of both the superior rectus and the inferior oblique. However, elevation of the abducted eye is primarily accomplished by the superior rectus, while elevation of the adducted eye is primarily accomplished by the inferior oblique. Similarly, depression in abduction isolates the inferior rectus while depression in adduction isolates the superior oblique.  Figure 2 demonstrates each of the nine positions with captions describing the muscle(s) being used to obtain that particular position.

When testing motility, assess the eye alignment in primary gaze (consider using the Hirschberg test) and then have the patient move the eyes in an “H” pattern, as shown in Figure 1. Using your finger, a light or a toy, trace an “H” pattern in front of the patient while instructing them to hold their head still.  Be sure to alternate between observing the left and right eye in each gaze during the exam.


Figure 1- Cardinal Gaze Positions

Figure 2- “H” pattern for ocular motility assessment

Format: image

References: none

Faculty Approval by: Griffin Jardine

Copyright Statement: Eric Peterson, ©2016. For further information regarding the rights to this collection, please visit: URL to copyright information page on Moran CORE

Disclosure (Financial or other): none


Home / Basic Ophthalmology Review / Trauma

Title: Hyphema

Author: Bryan Thiel, MS4 – University of Central Florida College of Medicine


Grade I Hyphema with cells visible floating in the anterior chamber

Grade III hyphema or 60% fill hyphema with ciliary flush or conjunctival injection

Post-surgical hyphema after a cataract extraction and intra-ocular lens placement.


Hyphema refers to the presence of red blood cells in the anterior chamber of the eye. This is not to be confused with hypopyon which refers to the presence of white blood cells in the same compartment. Hyphemas most commonly arise secondarily to blunt trauma to the globe due to shearing of the small vessels supplying the iris, ciliary body and trabecular meshwork. The severity of the hyphema can either be measured by the depth of settled red blood cells at the base of the anterior chamber or graded on a scale of zero to four as below (Table 1).

Table 1. Grading System of Hyphemas


Grade 0 or “microhyphema” Rare cells visible only in slit lamp examination, no layering of cells
Grade I Layering of cells at base of anterior chamber, measuring less than ⅓ the total space
Grade II Layering of cells at the base of the anterior chamber, measuring between ⅓ and ½ the total space
Grade III Layering of cells at the base of the anterior chamber, measuring greater than ½ the total space but not occupying its entirety
Grade IV Layering of cells that occupy the entire total space of the anterior chamber, also called “8-ball” or “black ball” hyphema


Patients will not  typically present with complaints of “seeing red” or having “blood in the eye” but rather will have had recent trauma to the globe with symptoms including pain, photophobia and blurred vision. It is imperative to confirm the mechanism of injury, medication use (i.e. anti-platelets, anti-thrombotics) and family history of sickle cell disease or coagulopathy, as these may contribute to the severity of the bleed. A comprehensive eye exam is mandatory in every case of hyphema looking for other sequela of trauma such as ruptured globe, traumatic optic neuropathy or retinal detachments.


While trauma is the most common source of hyphemas, it is important to keep a broad differential as this symptom may be an early indicator for the following conditions:

Post-surgical hyphema: Surgical manipulation of the anterior structures of the eye may result in bleeding.


Currently, there is no designated protocol for medical management of hyphemas. Medicinal eye drops such as corticosteroids (e.g. prednisolone acetate) and cycloplegics (cyclopentolate or atropine) are most commonly used.  Fibrinolytics, such as aminocaproic acid (ACA) and tranexamic acid (TA), have been extensively discussed in the literature, however sensitivity analyses have demonstrated that these medications minimally reduce the risk of secondary bleeding. Therefore, these drugs have fallen out of favor for treating hyphemas. Patients with hyphemas may develop sudden jumps in their intraocular pressure (IOP) putting them at risk for glaucomatous optic nerve damage and significant discomfort.  Therefore, IOP needs to be monitored daily for several days following the injury.

For cases of elevated IOP, first-line therapy includes the use of pressure-reducing medications.  Of note, carbonic anhydrase inhibitors like dorzolamide are contraindicated in patients with sickle cell disease or trait, due to their effect on lowering pH which can induce sickling. All patients should be questioned about their sickle cell status and if there is any possibility the patient could have sickle cell disease, hemoglobin analysis testing should be ordered to ascertain disease status of the patient.

Due to the inherent association of hyphema with trauma, inflammation is classically seen in addition to red blood cells. Thus, topical steroids, in addition to cycloplegics, are commonly prescribed to reduce inflammation and the risk of development of iris synechiae (iris scarring to lens or cornea). It is important to keep in mind that once symptoms of inflammation have resolved, topical steroids should be tapered to reduce the risk of steroid-induced glaucoma.

In addition to medication, preventative measures such as placing strict activity restrictions, maintaining an elevated position of the head and using an eye shield are highly recommended to encourage settling of red blood cells and to reduce risk of secondary bleeds.  Patients with non-resolving clots, corneal blood staining, or uncontrolled elevated IOPs may benefit from surgical evacuation of the clot or blood from the anterior chamber.  All hyphema patients are at lifelong risk of glaucoma due to the damage to the trabecular meshwork from the injury and/or blood and need regular IOP checks for life.


  1.  Gharaibeh A, Savage HI, Scherer RW, Goldberg MF, Lindsley K. Medical interventions for traumatic hyphema. The Cochrane database of systematic reviews.2013(12):Cd005431.
  2.  Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of Traumatic Hyphema. Survey of Ophthalmology. 2002;47(4):297-334.

Identifier: Moran_CORE_24622

Ocular Adverse Effects of Systemic Medications: Amiodarone

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

Title: Ocular Adverse Effects of Systemic Medications: Amiodarone
Author: Emily Ross, 4th Year Medical Student, Indiana University School of Medicine
Location: Med Student Outline > II. Anatomical Approach to Eye Disease > Ocular Adverse Effects of Systemic Medications > 3. Amiodarone

Overview: Amiodarone is a Class III antiarrhythmic medication that slows repolarization of the myocardium which increases the action potential duration and the refractory period, thus slowing the cardiac conduction rate. It is used to treat certain tachyarrhythmias. Long-term use is associated with the following ocular adverse effects.

Image 1: Corneal Verticillata

Corneal verticillata: Also known as vortex keratopathy, occurs in almost all patients who take amiodarone and is related to the dosage of the medication and duration of treatment. It is the most common and most well-known ocular adverse effect of amiodarone. On slit lamp exam, one can see corneal deposits in a whorl-like pattern in the inferior cornea bilaterally (see image 1). The deposits are usually a gray or golden-brown color and accumulate in the basal layer of the corneal epithelium. This is a benign condition and patients usually do not have any visual complaints.  Rarely, they report colored rings around lights, haloes and glare which are worse at night. The condition is reversible with discontinuation of the drug. Notably other medications may also cause corneal verticillata including chloroquine and hydroxychloroquine, indomethacin, and phenothiazines and is also seen in Fabry’s disease.

Lens opacities can occur in the anterior cortex of the lens. These are due to pigment deposition and are small and yellowish-white in color. They do not reverse with discontinuation of amiodarone but rarely cause any visual disturbance.

Optic neuropathy is a very rare but serious side effect of long-term amiodarone use. It tends to progress slowly with resulting vision loss. Patients taking amiodarone should have yearly check-ups with an ophthalmologist to monitor for development of optic neuropathy as discontinuing the drug stabilizes the patient’s vision.


Ophthalmology AA of. 2017-2018 Basic and Clinical Science Course Lens and Cataract. S.I.: American Academy of Ophthalmology; 2017.
Ophthalmology AA of. 2017-2018 Basic and Clinical Science Course External Disease and Cornea. S.I.: American Academy of Ophthalmology; 2017.
 Graff JM. Verticillata: 54-year-old white male with a known history of atrial fibrillation and hypertension on amiodarone., February 21, 2005; Available from
Mantyjarvi M, Tuppurainen K, Ikaheimo K. Ocular side effects of amiodarone. Survey of Ophthalmology. 1998 Jan-Feb;42(4):360-6.
Giardina E, Zimetbaum P. Monitoring and management of amiodarone side effects. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. (Accessed on September 14, 2017.)

Identifier: Moran_CORE_24549

Bacterial Corneal Ulcer

Home / Basic Ophthalmology Review / Cornea

Name: Paul D Chamberlain, 4th year medical student, Baylor College of Medicine; Dr. Amy Lin, Associate Professor, University of Utah Moran Eye Center.
Topic: Bacterial Corneal Ulcer

The cornea is the “window” of the eye and consists of five layers (from anterior to posterior): the epithelium, anterior limiting lamina (i.e. Bowman’s layer), stroma, endothelial basement membrane (Descemet’s membrane), and endothelium (image 1). Like ulcers elsewhere in the body, a corneal ulcer is a complete disruption of the epithelial cell layer with an inflammatory response.  Unlike other areas of the body, the cornea is dehydrate and avascular which both contribute to its impressive clarity and transparency.  The avascular nature of the cornea, however, poses a challenge for the body to fight off infections due to an impaired ability for the immune system to access the infection.  For this reason, corneal infections require topical antibiotics and urgent attention.

Image 1

Corneal ulcers are generally due to bacterial infection, and occur most frequently in patients wearing contact lenses, especially if worn through the night. Bacterial corneal ulcers may also develop secondary to corneal abrasions, blepharitis, or ocular trauma and can be fungal, parasitic, viral or sterile (auto-immune) in addition to bacterial.  Patients typically complain of decreased vision, severe pain, redness, or light sensitivity. On physical exam the patient will have injected conjunctiva with a dense collection of inflammatory cells in the cornea called an “infiltrate” (image 2).  Marginal corneal ulcers are more commonly multiple and in the periphery of the cornea (where it meets the sclera). These may be due to an immune reaction to staphyloccal toxins from chronic blepharitis (eyelid infection).  In severe corneal ulcers, there can be a hypopyon, or dense collection of white blood cells in the anterior chamber (image 4).

Image 2

Image 4

Critical to the management of corneal ulcers is assessing the depth of involvement of the cornea and assessing for potential perforation (image 3). This is accomplished with the seidel test. In the seidel test, a small amount of fluorescein dye is placed on the area of ulceration. Using a UV light (either in a slit lamp or with a wood’s lamp) the examiner looks to see if the dye begins to drain down from the ulcer and becomes less bright, indicating that it is being diluted by fluid leaking from the eye. If there is leakage, this is considered “seidel positive.”

Image 3

Corneal ulcers are an ocular emergency and patients should be referred to an ophthalmologist immediately, as a delay in treatment may result in corneal perforation, endophthalmitis (infection of the entire eye), and/or permanent corneal scarring and subsequent visual impairment. Central corneal ulcers are generally more serious than marginal corneal ulcers. Patients should not be given topical analgesics such as proparacaine for pain relief as continued use horrifically damaging to the eye. To help with pain control, the patient should be prescribed topical parasympatholytics such as atropine or cyclopentolate to reduce ciliary muscle spasm. Culturing the infection on presentation prior to starting treatments also helps guide management in complex or unusual cases.


Leitman MW. (2017).  Manual for Eye examination and Diagnosis 9th Ed. Hoboken, NJ: John Wiley & Sons, Inc.

Identifier: Moran_CORE_24538

Preseptal vs Orbital Cellulitis

Home / Basic Ophthalmology Review / Orbit

Name: Paul D Chamberlain, 4th year medical student, Baylor College of Medicine; Reese Feist, Chief Resident, University of Utah Moran Eye Center.
Topic: Preseptal vs Orbital Cellulitis
Terminology and Anatomy

Differentiating orbital from preseptal cellulitis is extraordinarily important given that orbital cellulitis has the potential to cause a compartment syndrome within the eye socket resulting in irreversible vision loss to the affected eye.  The orbital septum is a membranous sheath extending from the periosteum of the orbit to the tarsal plate located in the eyelid, and is the key anatomical structure in differentiating preseptal from orbital cellulitis. The orbit (eye socket) is the bony structure in which the globe (eyeball) is housed, and it also contains extraocular muscles, fat, and the blood vessels and nerves that supply these structures. Orbital cellulitis (Image 1), also called post-septal cellulitis, is inflammation of the soft tissues (muscles, fat, and connective tissue) of the orbit most commonly from infection.  It is important to remember that in orbital cellulitis, the globe itself is not infected or inflamed. Because the orbit is surrounded by the frontal, ethmoid, and maxillary sinuses, infection often results from extension of a sinus infection.

In comparison, pre-septal cellulitis (Image 2), also known as peri-orbital cellulitis, is an infection of the eyelids and surrounding soft tissues that are anterior to the orbital septum. Both orbital cellulitis and preseptal cellulitis are more common in children, and preseptal cellulitis is much more common that orbital cellulitis.

A patient with orbital cellulitis. Note: orbital cellulitis can take on a variety of clinical manifestations and this image should not be taken as a gold standard to which an examiner compares a patient.


A patient with preseptal cellulitis.

Clinical Manifestations

A number of signs may alert the examiner to the presence of orbital cellulitis (table 1). Patients typicall present with erythema and edema of the eyelids.  In orbital cellulitis, they erythema and edema can abruptly stop at the arcus marginalis, where the orbital septum inserts into the periosteum.  Preseptal cellulitis typically expands beyond this landmark.  Patients may present with eye pain, especially with eye movements due to irritation of inflamed muscles.  Partial or complete ophthalmoplegia (inability to move the eye in one or more directions) and associated diplopia (double vision) due to inflammation of extraocular muscles or associated cranial nerves. In orbital cellulitis, inflammation and/or an orbital abscess can displace the globe, often pushing it forward or outward which is called proptosis. The presence of proptosis is a medical emergency to evaluate for compartment syndrome. The eyelids can be swollen and in severe cases swollen shut. Eyelids being swollen shut can be present in either orbital or preseptal cellulitis, and is not as helpful in distinguishing between the two.  Visual acuity may be decreased but is often unaffected, and a normal visual acuity should not rule out orbital cellulitis. There is often a history or sinusitis or dental abscess. However, there may be no clear source of inflammation, and it may not even be infectious, as with idiopathic orbital inflammatory syndrome.

Preseptal cellulitis is much more common than orbital cellulitis and also presents with eye pain and erythema of the eyelid and surrounding skin and soft tissue. The inflammation may be great enough to tightly close the eyelids as well (image 3), and they should be opened for a visual inspection. Pre-septal cellulitis does not cause loss of vision and if visual acuity is decreased it is likely because of a poor exam or a more severe infection. Preseptal cellulitis may also arise from sinusitis, but may also arise secondary to local trauma, foreign body, or bug bite (Image 4).

Preseptal cellulitis with mechanical ptosis or droopy eyelid due to edema and erythema of the eyelids.  Note that there is no proptosis and the erythema doesn’t abruptly stop at the orbital rim, making it clinically less likely to be orbital cellulitis.

A patient with preseptal cellulitis secondary to a bug bite.

Orbital cellulitis.  Note the bullous, edematous conjunctiva (conjunctival chemosis), proptosis and the delineation of swelling around the orbital rim.  This patient underwent an urgent lateral canthotomy/cantholysis.

Table 1: Comparison of clinical, historical, and diagnostic characteristics of preseptal and orbital cellulitis.

Characteristic Preseptal Cellulitis Orbital Cellulitis
Eye pain May be present Yes
Eyelid erythema and/or tenderness Yes Yes
Pain with eye movements No May be present
Ophthalmoplegia ± diplopia No May be present*
Proptosis No May be present*
Vision loss No May be present*
RAPD No May be present*
Fever Usually not present Usually present
Intraocular Pressure (IOP) Normal May be elevated*
Resistance to Retropulsion None Present*
History of sinusitis May be present, but often not Present more often than not
CT or MRI imaging Shows inflammation only anterior to the orbital septum Show post-septal involvement of the inflammation.
Blood Cultures Very rarely has bacteremia Bacteremia may be present
*Emergent signs and symptoms that might warrant immediate lateral canthotomy/cantholysis

Work-up and Treatment

As previously discussed, the first step is to determine whether a patient has orbital cellulitis, which requires orbital imaging, admission, blood cultures and IV antibiotics.  Begin with a thorough ophthalmologic exam, with particular attention to visual acuity, pupillary testing for a relative afferent pupillary defect (RAPD), intraocular pressure, and assessment of proptosis and eye motility. In cases of question, Computed tomography (CT) with and without contrast of the orbits and sinuses should be ordered to look for evidence of post-septal involvement.  If a diagnosis of orbital cellulitis is made, the patient needs to be immediately assessed monitored for signs of compartment syndrome and optic neuropathy which would warrant an emergent lateral canthotomy/cantholysis.  This procedure allows for anterior expansion of orbital contents which relieves pressure within the orbit in restores blood flow to those structures.  Even after initiating antibiotics the swelling may increase for the first 24-48 hours, so frequent re-evaluation is warranted.  Immediate surgery may be indicated if there is evidence of a subperiosteal abscess, orbital abscess, or extension of the infection into the cranium.  Consider consulting an otolaryngologist for management of sinus disease.

Patients whose history and examination are consistent with preseptal cellulitis without symptoms of orbital cellulitis may be treated as an outpatient with oral antibiotics. Patients with preseptal cellulitis who are appropriately treated typically recover completely without any permanent sequelae. If treated appropriately, patients with orbital cellulitis also often have good outcomes. However, failure to diagnose and treat orbital cellulitis in a timely manner may result in permanent vision loss.  An ophthalmologist should be consulted in all cases of orbital or preseptal cellulitis.  However, assessing for vision threatening orbital cellulitis should not be postponed until an ophthalmologist is available as an irreversible ischemic optic neuropathy can occur in less than 90 minutes.


Amin N, Syed I, Osborne S. Assessment and management of orbital cellulitis. British Journal of Hospital Medicine. 2016; 77(4):216-20.
Hauser A, Fogarasi S. Periorbital and orbital cellulitis. Pediatrics in Review. 2010; 31(6):242-9.
Meara DJ. Sinonasal disease and orbital cellulitis in children. Oral Maxillofacial Surgery Clinics of North America. 2012; 24(3):487-96.
Rashed F, Cannon A, Heaton PA, Paul SP. Diagnosis, management and treatment of orbital and periorbital cellulitis in children. Emergency Nurse. 2016; (24(1):30-5.

Identifier: Moran_CORE_24521

Dry Eye Disease

Home / Basic Ophthalmology Review / Lids/Lashes

Title: Dry Eye Disease

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

Description: Dry eye disease is a very common condition and is one of the most common causes of eye discomfort in the general population. Dry eye disease is typically split into two categories: evaporative dry eye and decreased aqueous production1. Recently, increased interest in dry eye disease and the importance of the ocular surface has paved the way to newer treatment modalities. Being equipped with the awareness of the signs and symptoms will help clinicians manage these patients appropriately.  It is important to recognize the risk factors, common signs and symptoms of dry eye disease so that patients can be appropriately treated.

Patients with dry eye can present with a variety of signs and symptoms. Symptoms of fluctuations in vision, discomfort, burning or a foreign body sensation are common2. Patients may demonstrate conjunctival injection and eyelid swelling/inflammation, or blepharitis.

Firstly, take a careful history as environmental factors and diet can significantly contribute to dry eye disease2.  Ask the patient about the use of ceiling/direct fans, humidifiers, water intake, contact lens wear, time outdoors, direct sun exposure and daily activities. Patients who work long hours on near tasks such as a computer frequently blink less and are subsequently at-risk for dry eye3,4.  Some medications may also contribute to dry eyes, such as antihistamines, pain relievers, certain anti-hypertensives, decongestants, hormones, antidepressants, antipsychotics, chemotherapeutics and acne medications2. Diet is another significant contributor; studies suggest that patients who supplement with omega-3-based vitamins report less dry-eye related symptoms.5

When a patient presents with an irritated red eye, it is important to be cognizant of dry eye disease and gather a full history to prevent unnecessary treatments with extensive or prolonged antibiotic regiments. If you suspect a patient is suffering from dry eye disease, encourage them to seek out an eye care provider and manage any modifiable risk factors in the meantime.


  1. The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5(2):75-92.
  2. Lemp MA. Advances in understanding and managing dry eye disease. American Journal of Ophthalmology. 2008;146(3):350-356. doi:10.1016/j.ajo.2008.05.016.
  3. Tsubota K, Nakamori K. Dry Eyes and Video Display Terminals. N Engl J Med. 1993;328(8):584-584. doi:10.1056/NEJM199302253280817.
  4. Tsubota K. Tear dynamics and dry eye. Progress in Retinal and Eye Research. 1998;17(4):565-596.
  5. Korb DR, Blackie CA, Finnemore VM, Douglass T. Effect of Using a Combination of Lid Wipes, Eye Drops, and Omega-3 Supplements on Meibomian Gland Functionality in Patients With Lipid Deficient/Evaporative Dry Eye. Cornea. 2015;34(4):407-412. doi:10.1097/ICO.0000000000000366.

Identifier: Moran_CORE_24492

3rd Nerve Palsy

Home / Basic Ophthalmology Review / Extraocular Muscles / Motility

Title: 3rd Nerve Palsy
Author: Patrick Commiskey, 4th Year Medical Student, University of Michigan Medical School
Description: The 3rd cranial nerve (CN III), or oculomotor nerve, is a motor nerve responsible for many eye-related functions. The third cranial nerve innervates four of the six extraocular muscles: medial rectus, superior rectus, inferior rectus, and inferior oblique. Parasympathetic nerve fibers originating from the Edinger-Westphal nucleus travel circumferentially with CN III to the pupil. causing pupillary constriction when activated. The levator palpebrae superioris muscle, which is the primary muscle in elevating the eyelid is innervated by the superior division of CN III.

A complete lesion of CN III would result in ipsilateral ptosis (droopy eyelid) and a “down and out” eye due to denervation of most extraocular muscles leaving the lateral rectus (innervated by CN VI, abducts) and superior oblique (innervated by CN IV, depresses) unopposed.  A dilated pupil (mydriasis) resulting from disruption of the parasympathetic fibers are the result of denervation of the sphincter pupillae.

Understanding the anatomy of CN III is important to deciphering important the etiology of a CN III palsy. Most lesions of the 3rd cranial nerve are from vascular insults causing ischemia and can be attributed to known vascular risk factors such as diabetes or hypertension.  These presentations typically have ptosis, a down-and-out eye but a normal pupil.  However, a compressive or space-occupying lesion such as an aneurysm or tumor would cause disruption of the parasympathetic fibers because of their superficial location on the outside of CN III. In fact, an acutely “blown” pupil in conjunction with the above mentioned ptosis and motility deficits may be an ominous sign of a growing aneurysm. Retrospective review studies have shown that we cannot completely rely upon the pupil to differentiate vascular from compressive causes because numerous exceptions have occurred. Therefore, a “blown” pupil is treated emergently and requires neuro-imaging, but the lack of this sign does not exclude an acute space-occupying pathology.

Additional etiologies of 3rd nerve palsy to consider include Myasthenia Gravis, Thyroid disease, internuclear ophthalmoplegia, orbital tumor or pseudotumor, and temporal arteritis (giant cell arteritis).


  1. Jacobson DM , BrosteSK. Early progression of ophthalmoplegia in patients with ischemic oculomotor nerve palsies.Arch Ophthalmol.1995;113(12):1535–1537.
  2. Trobe JD . Managing oculomotor nerve palsy.Arch Ophthalmol.1998;116(6):798.

Identifier: Moran_CORE_ID: 24487

Leukocoria (in children)

Home / Basic Ophthalmology Review / Pupillary Exam

Title: Leukocoria (in children)

Author:  Spencer Fuller, MSIV – UC San Diego School of Medicine, MPH

Definition: In contrast to the normal red reflex, leukocoria is defined as a yellow, pale, white, or otherwise abnormal reflection of light observed in the pupil of one or both eyes.

Presentation: The asymmetric “white pupil” is either caught by family members (often in photos with asymmetric red reflexes from the flash) or incidentally by a practitioner on routine direct ophthalmoscopy.  Every well child check—especially the newborn baby check in the nursery—should include an examination of the pupils. Patients in whom leukocoria is observed should be promptly referred to an ophthalmic specialist for diagnosis and management.

Differential Diagnosis:

The differential diagnosis of leukocoria in children is broad and includes hereditary, developmental, inflammatory, neoplastic and miscellaneous conditions [1]:


This patient with leukocoria eventually was diagnosed with Retinoblastoma and underwent enucleation.

Jordan, Michael (2014). 2 year Old with Leukocoria. Moran Eye Center Grand Rounds

Image of a stage 2 demarcation line commonly seen in ROP

Fundus photo of the mass lipid exudation from leaky, telangiectatic vessels in Coat’s disease

Diagnosis: The following modalities may be used by ophthalmic specialists to determine the cause of leukocoria:

  1. Direct ophthalmoscopy
  2. Slit lamp biomicroscopy and indirect ophthalmoscopy
  3. Retinal fundus photography
  4. Fluorescein Angiography
  5. Orbital/Head imaging often aids to narrow the differential diagnosis
    1. B-scan ultrasonography
    2. Optical coherence tomography (OCT)
    3. MRI of the head and orbits (CT scans are avoided in case of malignancy to avoid radiation exposure)

Management: Management of leukocoria varies and is dependent on the specific cause.  Though retinoblastoma is the most feared cause of the leukocoria, many referrals for an asymmetric or abnormal red reflex turn out to be nothing.  Nonetheless, a timely referral for a dilated eye exam is still vital.  In the infant to toddler age range it is important to ask about a family history of retinoblastoma or congenital cataracts along with taking a careful birth and delivery history.  In the case of a congenital cataract (which may be unilateral or bilateral), the timing of cataract surgery is amongst the most important factors in eventual visual outcomes.  Unilateral cataracts are ideally removed at six weeks of ages and bilateral cataracts by eight to ten weeks.  Missing this window can cause irreversible deprivational amblyopia, or permanent blindness in one or both eyes.

From: American Academy of Pediatrics. (2008). Red reflex examination in neonates, infants, and children. Pediatrics, 122(6), 1401-1404.

See Red handout from the American Academy of Pediatrics:


  1. Stagg, B., Ambati, BK. et al. (2014) Diagnostic Ophthalmology. Amirsys Publishing, Inc., Manitoba, Canada.
  2. Shields, J. A., Shields, C. L. (2008). Retinoblastoma: Introduction, Genetics, Clinical Features, Classification. In Intraocular Tumors: An Atlas and Textbook (pp. 293-318). Lippincott Williams & Wilkins, Philadelphia, PA.
  3. Shields, J. A., Shields, C. L. (2008). Retinoblastoma: Diagnostic Approaches. In Intraocular Tumors: An Atlas and Textbook (pp. 319-326). Lippincott Williams & Wilkins, Philadelphia, PA.
  4. Shields, J. A., Shields, C. L. (2008). Lesions That Can Simulate Retinoblastoma. In Intraocular Tumors: An Atlas and Textbook (pp. 353-366). Lippincott Williams & Wilkins, Philadelphia, PA.
  5. Balmer, A., & Munier, F. (1999). Leukokoria in a child: emergency and challenge. Klinische Monatsblatter Fur Augenheilkunde, 214(5), 332-335.
  6. Haider, S., Qureshi, W., & Ali, A. (2008). Leukocoria in children. Journal of pediatric ophthalmology and strabismus, 45(3), 179-180.
  7. American Academy of Pediatrics. (2008). Red reflex examination in neonates, infants, and children. Pediatrics, 122(6), 1401-1404.

Identifier: Moran_CORE_24126