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Scleritis in Emergency Medicine Clinical Presentation

  • Author: Theodore J Gaeta, DO, MPH, FACEP; Chief Editor: Robert E O'Connor, MD, MPH  more...
 
Updated: Dec 29, 2015
 

History

Pain

Severe, constant, deep, boring, or pulsating pain is noted.

Pain worsens with movement of the eye.

Pain is worse at night and may awaken the patient.

Pain may be referred to the eyebrow, temple, or jaw. Occasionally, the configuration of the pain pattern corresponds to the course of the trigeminal nerve.

Onset

Scleritis is subacute, a more gradual onset occurs than is seen in episcleritis.[10]

Duration of symptoms

Scleritis generally persists from months to years, whereas episcleritis usually resolves within weeks.

Associated symptoms

See the list below:

  • Erythema of the eye is a defining symptom with anterior scleritis.
  • Lacrimation
  • Photophobia
  • Discharge is ordinarily not part of the clinical picture of scleritis.

Less prevalent symptoms include the following:

  • Fever
  • Nausea/vomiting
  • Headache
  • Similar previous episodes

Both eyes are affected in slightly more than one half of cases.

Prior history

See the list below:

  • Underlying systemic disease[12]
  • Trauma
  • Ocular surgery
  • Glaucoma
  • Exposure to irritants/chemicals
  • Previous use of eye drops
  • Medications
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Physical

As with any eye complaint (except chemical injury), begin with vision testing. Visual acuity may be normal or decreased with all forms of scleritis. Visual impairment is most pronounced with posterior scleritis.[16]

Additionally, a complete physical examination, particularly of the skin, joints, heart, and lungs, may be obligatory when an underlying complicating illness is suspected.

Ensure that the eye examined is supported by satisfactory lighting, inspecting for breadth and degree of injection, as well as the presence of bluish hue signifying attenuation of the sclera. Prominent findings may include photophobia, tearing without discharge, tenderness of the eye, and purplish red, edematous, engorged blood vessels. Deeper sclera blood vessels appear darker, follow a radial pattern, and do not move when manipulated with a cotton swab. Administration of topical phenylephrine 2.5-10% causes blanching of the more superficial episcleral vessels but does not change the engorgement of deeper sclera vessels and can help differentiate between scleritis and episcleritis.

Perform a slit lamp/biomicroscopic examination to judge the depth and breadth of involvement. Determine whether there is diffuse or segmental involvement. Widespread injection of the conjunctival and deep scleral vessels is characteristic of diffuse anterior scleritis. Localized elevation of the sclera is representative of nodular anterior scleritis. Nodules in anterior scleritis are immobile, differing from the non-mobile nodules that can be seen in episcleritis. Scleral thinning is suggested when the choroid pigment becomes a blue-violet hue best seen in natural lighting. Global perforation typically results in an abnormal shape of the pupil and/or uveal or vitreous prolapse. Use of a red-free filter (green light) helps identify avascular areas of the sclera. Corneal changes are present in up to 50% of cases. Examination of the eyelids for possible blepharitis or conjunctivitis should be performed.

Assessment of the anterior chamber for possible narrowing, hyphema, or hypopyon. Angle narrowing can be seen in acute angle-closure glaucoma. Hyphema can be seen with trauma and/or bleeding disorders. Hypopyon may be seen in uveitis/iritis.

External findings associated with posterior scleritis include restriction of eye movements, sensitivity to palpation, and proptosis. Dilation of the fundus may be necessary to identify posterior scleritis. Posterior scleritis may simulate amelanotic choroidal. Funduscopic examination of the patient with posterior scleritis may also reveal papilledema, choroidal folds, and retinal hemorrhage or detachment.[15]

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Causes

Scleritis coexists with a serious systemic disease in almost one half of cases; the underlying problem is frequently a connective tissue disorder.[12]

Rheumatoid arthritis is the underlying disease for approximately one sixth of patients suffering from scleritis, and approximately 1% of patients with rheumatoid arthritis will develop scleritis at some point in the course of the disease. Scleritis associated with RA is due to the development of a rheumatoid nodule on the sclera and is associated with an increased risk of mortality.[12]

Other connective tissue and autoimmune diseases seen with scleritis include the following:[12]

  • Systemic lupus erythematosus (SLE)
  • Polyarteritis nodosa
  • Seronegative spondyloarthropathies - Ankylosing spondylitis, psoriatic arthritis, reactive arthritis
  • Wegener granulomatosis
  • Relapsing polychondritis[17]
  • Sarcoidosis
  • Inflammatory bowel disease
  • Sjörgen syndrome

Additional maladies that may accompany scleritis include the following:

  • Syphilis[18]
  • Post herpes zoster ophthalmicus
  • Tuberculosis
  • Gout
  • Lyme disease
  • Foreign body
  • Hypertension
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Contributor Information and Disclosures
Author

Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: American College of Emergency Physicians, New York Academy of Medicine, Society for Academic Emergency Medicine, Council of Emergency Medicine Residency Directors, Clerkship Directors in Emergency Medicine, Alliance for Clinical Education

Disclosure: Nothing to disclose.

Coauthor(s)

Diana Valcich, MD Attending Physician, Department of Emergency Medicine, North Shore LIJ Hospital System

Diana Valcich, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Gino A Farina, MD, FACEP, FAAEM Professor of Emergency Medicine, Hofstra North Shore-LIJ School of Medicine at Hofstra University; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center

Gino A Farina, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Heart Association, Medical Society of Delaware, Society for Academic Emergency Medicine, Wilderness Medical Society, American Medical Association, National Association of EMS Physicians

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Jerome FX Naradzay, MD, Loice Swisher, MD, and Jonathan Adler, MD, to the development and writing of this article.

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