Posts filed under Ophthalmology

Optic Neuritis

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Written by: Steve Chukwulebe, MD (NUEM PGY-4) Edited by: Victor Gappmaier, MD (NUEM Alum ‘18) Expert commentary by: Shira Simon, MD, MBA


Case:

31-year-old female, with no significant past medical history, presents to the emergency department with a mild headache and blurry, decreased vision in the right eye for the past 2 days. Other historical elements include that the patient has been experiencing pain with eye movement.  However, she denies difference in color perception. She also denies any trauma to the eye, recent fevers, chills, malaise, exposures, or travel. The left eye is unaffected.

 

Exam:

Normal vitals and a well appearing female of stated age

Ocular exam reveals normal appearing eyes without chemosis, proptosis, conjunctival injection, scleritis, icterus, or foreign bodies

Non-dilated funduscopic exam is unremarkable

Visual acuities are OD: 20/40 and OS: 20/20 

Tonometry reveals right and left eye pressures are < 20 mmHg 

Slit lamp exam is without cells or flare 

Fluorescein stain is without any corneal uptake

CN 3-12 are intact, and no focal neurologic deficits on exam

 

Differential Diagnosis [1,2]: 

Painless Vision Loss

  • Central retinal artery occlusion

  • Central retinal vein occlusion

  • Retinal detachment

  • Vitreous detachment/vitreous hemorrhage

  • Tumor/Mass

  • Stroke 

Painful Vision Loss

  • Acute angle closure glaucoma

  • Scleritis

  • Anterior uveitis (iritis)

  • Optic neuritis

  • Keratitis

  • Corneal abrasion/trauma

  • Temporal arteritis

The challenge in diagnosing optic neuritis is to exclude other causes of acute monocular vision loss.  Therefore, a normal appearing eye, slit lamp exam, fluorescence stain, and intraocular pressures eliminates scleritis, uveitis, keratitis/abrasion, and glaucoma respectively [5].  Additionally, the history is less suggestive of other urgent and emergent ocular pathologies such as retinal detachment and central retinal artery occlusion.

Some physical exam findings more specific to optic neuritis include:

  • Afferent pupillary defect

  • Optic disk swelling and papilledema, which can be seen by ultrasound [6]

  • Decreased perception in the saturation of deep red colors

  • Decreased visual acuities ranging from 20/25 to 20/190, and even no light perception[4]

  • Eye pain, especially with eye motion, is seen in 92 percent of patients

  • Loss of color vision out of proportion to the decrease in visual acuity

  • Retro-orbital headache

Further diagnostics may include an MRI of the brain and orbits, but is not necessary for the diagnosis of optic neuritis [5].  MRI can help characterize the disease burden and assess the risk for the development of multiple sclerosis [7].

Given the patient’s age and constellation of symptoms, both neurology and ophthalmology consultation were performed with the leading concerning diagnosis being optic neuritis. The patient was admitted for further evaluation with a dilated ocular exam, MRs of the brain, and treatment.

 

Pathophysiology and Clinical Disease:

Optic neuritis is an inflammatory and demyelinating process that usually presents with monocular vision loss [3-4].  While there are many causes for optic neuritis, the demyelinating lesions seen in optic neuritis are similar to those that have been associated with multiple sclerosis.  Patients are typically women between the ages of 20-40.  Patients often develop progressive symptoms over a period of a few hours to several days.

 

Treatment and Timing:

Typical treatment is high dose intravenous steroids for three days. Another treatment regimen that has been described is intravenous methylprednisolone (250 mg four times per day) for three days, followed by oral prednisone (1 mg/kg per day) for 11 days, and then a four-day taper [8, 9]. 

If the diagnosis is uncertain, then is it acceptable to delay treatment for an MRI or specialist consultation the following morning?

The Optic Neuritis Treatment Trial described treatment of optic neuritis with high dose intravenous methylprednisolone.  The initial multicenter trial enrolled 457 patients from July 1, 1988, through June 30, 1991.  They ultimately randomized 389 patients with acute optic neuritis (and without known multiple sclerosis) to receive intravenous methylprednisolone (250 mg every six hours) for 3 days followed by oral prednisone (1 mg per kilogram of body weight) for 11 days, oral prednisone (1 mg per kilogram) alone for 14 days, or placebo for 14 days.  They then assessed the neurologic status of the subjects for a period of two to four years and published their results in 1993.  Also by following the subjects longitudinally, the authors were able to reanalyze the data and publish again in 2003. From the initial study, it was learned that high the steroids hastened the recovery of visual function, but did not affect long term visual outcomes when compared to both placebo and oral prednisone [10, 11, 12] after six months, and ten-year follow-up.  It was found that a 3-day course of methylprednisolone reduced the rate of development of multiple sclerosis over a 2-year period [12]. Multiple sclerosis developed within the first two years in 7.5 percent of the IV methylprednisolone group vs. 14.7 percent of the oral prednisone group vs. 16.7 percent of the placebo group.  The adjusted rate ratio for the development of definite multiple sclerosis within two years in the intravenous methylprednisolone group was 0.34 as compared with the placebo group and 0.38 as compared with the oral-prednisone group.  However, after a 5-year period the treatment effect was no longer significant for the same group of patients.

Therefore, in a scenario when a provider may delay high dose steroids for a neurology and ophthalmology consultation, or for an MRI, it can be inferred that this delay will not affect long term outcomes for the patient. However, given that early treatment hastens symptom recovery and delays progression to multiple sclerosis, it may be beneficial to start high dose IV steroids in the emergency department in patients if optic neuritis is the suspected diagnosis.


Expert Commentary

This is a very good review of optic neuritis. There are just a few, additional nuanced points I’d like to mention, as well as some tips on counseling the patient.

  • Visual field changes: A central visual field deficit is commonly seen with this entity. It is most easily detected on formal visual field testing in the ophthalmology clinic (Humphrey or Goldmann visual fields), though some patients may report this on their own in the acute care setting.

  • Optic nerve swelling: In the ONTT, only 35% of patients had disc swelling (65% had normal appearing optic nerve heads on fundoscopy), so evaluating with ultrasound would not be revealing in most cases.

  • MRI for diagnosis: MRI is actually very important for the diagnosis of optic neuritis, as inflammation of a different part of the optic nerve (other than the nerve head) can only be visualized radiographically. MRI of the orbits and brain should be obtained with thin slices through the orbits, with fat suppression, and gadolinium (in addition to FLAIR sequences to look for demyelination).

  • Differential diagnosis: While this article talks about optic neuritis from demyelination related to possible MS, it’s important to bear in mind that there are other causes of optic neuritis: autoimmune disease (e.g., lupus), infections (e.g., syphilis or Lyme), other inflammatory conditions (e.g., sarcoidosis), other demyelinating processes (like neuromyelitis optica), or it can be idiopathic.

When counseling the patient about prognosis, it may be helpful to remember the “10-20-40-60” rule. I had been taught this, and it helps quickly summarize the ONTT prognostic statistics (that are outlined very nicely in this article). The “10-20-40-60 rule” mnemonic reminds us that at 10 years: there is a 20% chance of developing MS after an episode of idiopathic optic neuritis if there were no white matter lesions found on MRI; a 40% chance regardless of MRI findings; and, a 60% chance if 1+ white matter lesions are found on MRI.

It is also helpful to let the patient know that visual recovery is often excellent. Most patients return fairly close to their baseline vision within 3-5 weeks, although they may note some lingering difficulties with contrast sensitivity and color vision. An afferent pupillary defect may also persist.

 

Shira Simon, MD, MBA

Assistant Professor of Ophthalmology and Neurology

Northwestern Medicine


How to Cite This Post

[Peer-Reviewed, Web Publication] Chukwulebe S, Gappmaier V. (2019, March 11). Optic Neuritis. [NUEM Blog. Expert Commentary by Simon S]. Retrieved from http://www.nuemblog.com/blog/optic-neuritis


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Resources

  1. Dargin JM, Lowenstein RA. The painful eye. Emerg Med Clin North Am. 2008;26(1):199-216, viii.

  2. Vortmann M, Schneider JI. Acute monocular visual loss. Emerg Med Clin North Am. 2008;26(1):73-96, vi.

  3. The clinical profile of optic neuritis. Experience of the Optic Neuritis Treatment Trial. Optic Neuritis Study Group. Arch Ophthalmol. 1991;109(12):1673-8.

  4. UpToDate

  5. Germann CA, Baumann MR, Hamzavi S. Ophthalmic diagnoses in the ED: optic neuritis. Am J Emerg Med. 2007;25(7):834-7.

  6. Teismann N, Lenaghan P, Nolan R, Stein J, Green A. Point-of-care ocular ultrasound to detect optic disc swelling. Acad Emerg Med. 2013;20(9):920-5.

  7. Beck RW, Arrington J, Murtagh FR, Cleary PA, Kaufman DI. Brain magnetic resonance imaging in acute optic neuritis. Experience of the Optic Neuritis Study Group. Arch Neurol. 1993;50(8):841-6.

  8. Beck RW, Cleary PA, Anderson MM, et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med. 1992;326(9):581-8.

  9. Sellebjerg F, Nielsen HS, Frederiksen JL, Olesen J. A randomized, controlled trial of oral high-dose methylprednisolone in acute optic neuritis. Neurology. 1999;52(7):1479-84.

  10. Beck RW, Gal RL, Bhatti MT, et al. Visual function more than 10 years after optic neuritis: experience of the optic neuritis treatment trial. Am J Ophthalmol. 2004;137(1):77-83.

  11. Beck RW, Trobe JD, Moke PS, et al. High- and low-risk profiles for the development of multiple sclerosis within 10 years after optic neuritis: experience of the optic neuritis treatment trial. Arch Ophthalmol. 2003;121(7):944-9.

  12. Beck RW, Cleary PA, Trobe JD, et al. The effect of corticosteroids for acute optic neuritis on the subsequent development of multiple sclerosis. The Optic Neuritis Study Group. N Engl J Med. 1993;329(24):1764-9.

Posted on March 11, 2019 and filed under Ophthalmology.

Anatomic Approach to Ocular Complaints

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Written by: Philip Jackson, MD (NUEM PGY-3) Edited by: Jesus Trevino, MD (NUEM PGY-4) Expert commentary by: Rehan Hussain, MD


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Expert Commentary

Thank you for this excellent diagram, which demonstrates a thorough and systematic approach to the most common ocular complaints one would encounter in the ED.  In assessing a painful red eye, there is so much value in determining whether the discomfort is relieved with topical anesthetics, as you can reliably confine the pathology to the cornea or conjunctiva in those cases. However, a red eye associated with deep achy pain that is not relieved with tetracaine could be caused by scleritis, which is highly associated with autoimmune disease.  If cells and flare are visible in the anterior chamber, uveitis is more likely.  Any history of a recent eye procedure should prompt you to consider endophthalmitis, which can be visually devastating, and warrants urgent ophthalmology referral. 

In diagnosing conjunctivitis, you did a great job of highlighting the importance of a good history in determining the etiology . I would add that asking about sexual history can be valuable, as gonorrhea can present with copious purulent discharge, and chlamydia can present with chronic follicular conjunctivitis. Both would warrant systemic antibiotics and treatment of partners, in addition to eyedrops. 

Acute angle closure glaucoma is a diagnosis that should be considered in almost all cases of unilateral headache. It can mimic migraine, since both may present with nausea, vomiting, and visual disturbances. Checking the eye pressure is the most important step to making the diagnosis. 

Finally, acute onset of floaters and/or flashes always warrants an ophthalmology consult to rule out retinal detachment. Ultrasound is a useful tool to differentiate retinal detachment from posterior vitreous detachment (PVD) and vitreous hemorrhage. PVD and vitreous hemorrhages tend to move freely when the eye moves, whereas retinal detachment is anchored to the nerve but still flaps with eye movement.   

Once again, this diagram serves as a very helpful flowchart to trouble-shoot eye complaints in the ED.

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Rehan M. Hussain, MD
Vitreoretinal Surgery Fellow

Bascom Palmer Eye Institute

University of Miami Health System


How To Cite This Post

[Peer-Reviewed, Web Publication]   Jackson P, Trevino J (2018, October 22). Anatomic approach to ocular complaints.  [NUEM Blog. Expert Commentary by Hussain R]. Retrieved from http://www.nuemblog.com/blog/ocular-complaints


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Open Globe Injury

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Written by: Justine Ko, MD (NUEM PGY-1) Edited by: Hashim Zaidi, MD (NUEM PGY-3)  Expert commentary by:  Rehan Hussain, MD


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Expert Commentary

Hi Drs. Ko & Zaidi,

Thank you for this great review on emergency management of open globe injuries. The presentation of open globe injuries can vary widely depending on the mechanism of injury, and so can the final visual outcome. For obvious ruptured globes with peaked pupils or extruding intraocular contents, I am glad you emphasized that it is best to avoid any manipulation of the eye to prevent further extrusion of contents or increase the risk of infection. Cover the eye with a shield, start topical and systemic antibiotics, and consult ophthalmology so they can arrange surgery in a timely manner. The patient must be kept NPO to avoid delaying surgery unnecessarily. Definitely don’t check the eye pressure if you already know it is a ruptured globe.

For the less obvious ruptured globes, which may sometimes mimic a corneal or conjunctival abrasion, it is imperative to perform a Seidel test carefully. This involves placing a wet fluorescein strip (not the pre-made drop) over the suspected entry site, looking at it under the cobalt blue light of the slit lamp, and checking to see if a stream of aqueous fluid is coming out of the injury site (it can be either quick or a slow stream). Fluorescein staining in absence of a stream of fluid indicates that only an abrasion is present. When in doubt, consult ophthalmology for confirmation. Other slit lamp findings that may be present include subconjunctival hemorrhage, chemosis, corneal abrasion, hyphema, flat anterior chamber, iris defects, foreign body in the anterior chamber, or traumatic cataract.

For imaging workup, CT of the ORBITS is preferable, as it allows for 1 mm sections that increase the likelihood of detecting small intraocular foreign bodies (IOFB) that might be missed with a standard head CT. MRI should be avoided as it is slow, costly, and can cause movement of metallic IOFBs, causing further damage to the eye. Gentle ultrasound over the closed eyelids could be used in absence of availability of CT, but I prefer to avoid it since puts pressure on the eye.

The patient and family members are often times distraught over the injury, and appropriate counseling is an essential part of the encounter. They frequently ask if they will be permanently blind. I avoid making any predictions on the final visual outcome, as it is difficult to predict and can lead to either unmet expectations or unnecessary anxiety. I say that the goal is to save the eye at this time, and we will follow closely to see how the vision turns out. Sometimes patients do very well if the extent of injury is not severe, but on other occasions patients require multiple surgeries to correct associated retinal detachment, vitreous hemorrhage, or lens dislocation. If appropriate antibiotic therapy is not initiated, there is an increased risk of developing endophthalmitis, which portends a poor visual prognosis.

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Rehan Hussain, MD

Vitreoretinal Surgery Fellow,  Bascom Palmer Eye Institute, Univeristy of Miami

 

 


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How to cite this post

[Peer-Reviewed, Web Publication]  Ko J,  Zaidi H  (2018, Feb 26). Open Globe Injury.  [NUEM Blog. Expert Commentary By Hussain R]. Retrieved from http://www.nuemblog.com/blog/globe-rupture. 


Resources

  1. Alteveer, J and Lahmann B. 2010. “An Evidence-Based Approach To Traumatic Ocular Emergencies.” Emergency Medicine Practice, 12(5): 1-24. 2017.

  2. “Emergency Management of Traumatic Eye Injuries | 2001-07-01 | AHC Media: Continuing Medical Education Publishing.” 2017. Accessed October 6. https://www.ahcmedia.com/articles/71714-emergency-management-of-traumatic-eye-injuries.

  3. Guluma K, Lee JE. Ophthalmology. In: Gausche-Hill M, Hockberger R, Walls R, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed. Philadelphia, Pa: Elsevier, Inc. 2018:790-819.e3.

  4. Bord, Sharon P., and Judith Linden. 2008. “Trauma to the Globe and Orbit.” Emergency Medicine Clinics of North America, Ophthalmologic Emergencies, 26 (1): 97–123. doi:10.1016/j.emc.2007.11.006.

  5. “Trauma: Open-Globe Injuries.” 2015. American Academy of Ophthalmology. November 4. https://www.aao.org/pediatric-center-detail/open-globe-injuries.

  6. Harlan JB, Pieramici DJ. Evaluation of patients with ocular trauma. Ophthalmol Clin N Am. 2002;15:153-161. (Review article)

  7. Ahmed, Y, A M Schimel, A Pathengay, M H Colyer, and H W Flynn. 2012. “Endophthalmitis Following Open-Globe Injuries.” Eye 26 (2): 212–17. doi:10.1038/eye.2011.313.

  8. Arey, Mark L., V. Vinod Mootha, Anthony R. Whittemore, David P. Chason, and Preston H. Blomquist. 2007. “Computed Tomography in the Diagnosis of Occult Open-Globe Injuries.” Ophthalmology 114 (8): 1448–52. doi:10.1016/j.ophtha.2006.10.051.

A Visual Guide to Acute Angle Closure Glaucoma

Glaucoma is one of the leading causes of preventable blindness. While most cases are due to chronic open-angle glaucoma, acute angle-closure glaucoma is an ophthalmic emergency. This week we present a visual guide to successful management of these patients in the emergency department. 

Color Coded Clarity

The American Academy of Ophthalmology (AAO) has been attempting to reduce errors in ophthalmic drops since the mid-90’s with the advocacy of a uniform color coded system for topical ocular medications. This standardized color system would then theoretically help patients and providers identify medications correctly and reduce errors both inpatient and outpatient.