eMedicine Specialties > Ophthalmology > Sclera

Episcleritis: Treatment & Medication

Author: Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Contributor Information and Disclosures

Updated: Jun 18, 2009

Treatment

Medical Care

  • Episcleritis is a self-limiting disease producing little or no permanent damage to the eye. Therefore, many, if not most, patients with episcleritis will not require any treatment. However, some patients with mild symptoms demand treatment and may benefit from the use of artificial tears.
  • Occasionally, a clear history of an exogenous sensitization can be obtained, and removal of this agent will prevent recurrent attacks.
  • Ocular therapy  
    • Simple episcleritis often requires no treatment. Artificial tears are useful for patients with mild-to-moderate symptoms. Patients with severe or prolonged episodes may require artificial tears and/or topical corticosteroids.
    • Nodular episcleritis is more indolent and may require local corticosteroid drops or anti-inflammatory agents.
    • Topical ophthalmic 0.5% prednisolone, 0.1% dexamethasone, or 0.1% betamethasone daily may be used.
  • Systemic therapy
    • If nodular episcleritis is unresponsive to topical therapy, systemic anti-inflammatory agents may be useful.
    • Flurbiprofen (100 mg tid) is usually effective until inflammation is suppressed.
    • If there is no response to flurbiprofen, indomethacin should be used; 100 mg daily and decreased to 75 mg when there is a response.
    • Many patients who do not respond to one nonsteroidal anti-inflammatory agent (NSAID) may respond to another NSAID.

Activity

Sunglasses may be useful for patients with sensitivity to light.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.


Dexamethasone sodium phosphate (Ocu-Dex)

Suppresses the inflammatory response to a variety of agents and probably delays healing. Used for steroid responsive inflammatory conditions of the palpebral and bulbar conjunctiva, cornea, and anterior segment of the globe; when the inherent hazard of steroid use is accepted; and corneal injury from chemical or thermal burns or penetration of foreign bodies has occurred. Duration of treatment will vary from a few days to several weeks, according to therapeutic response.

Adult

Instill 1-2 gtt in conjunctival sac qh during the day and q2h during the night as initial therapy; further reduction in dosage to 1 gtt 3-4 times daily may suffice to control symptoms

Pediatric

Not established

Documented hypersensitivity; most viral diseases of the cornea and conjunctiva, including epithelial herpes simplex keratitis (dendritic keratitis), vaccinia, and varicella; mycobacterial infections of the eye; fungal diseases of the ocular structures; may increase intraocular pressure (monitor patients with glaucoma)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Prolonged use may increase hazard of secondary ocular infection; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use (obtain fungal cultures when appropriate); may increase intraocular pressure; may cause cataract


Prednisolone acetate 1% (Pred Forte)

Sterile ophthalmic suspension that is a topical anti-inflammatory agent for treating steroid responsive inflammation of palpebral and bulbar conjunctiva as well as cornea and anterior segment. Shake well prior to use. Do not discontinue therapy prematurely.

Adult

Instill 1-2 gtt bid/qid into conjunctival sac; during initial 24-48 h, dosage may be increased in frequency, prn

Pediatric

Not established

Documented hypersensitivity; most viral diseases of the cornea and conjunctiva, including epithelial herpes simplex keratitis (dendritic keratitis), vaccinia, and varicella; mycobacterial infections of the eye; fungal diseases of the ocular structures

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Fungal infections of the cornea are prone to develop coincidentally with long-term local corticosteroid use; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use (obtain fungal cultures when appropriate); if used for 10 d or longer, monitor intraocular pressure; steroid use in episcleritis may increase the risk of recurrence

Nonsteroidal anti-inflammatory agents

Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.


Flurbiprofen (Ansaid)

May inhibit cyclooxygenase enzyme, which, in turn, inhibits prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities. Available in 50- and 100-mg doses.

Adult

100 mg PO tid until suppressed

Pediatric

Not established

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Category D in third trimester of pregnancy; may cause gastrointestinal disturbances and fluid retention and should not be used in patients with congestive heart failure; can mask symptoms of infection; other adverse effects, such as platelet aggregation and liver dysfunction, exist with long-term use but should not be a factor in a relatively short duration of treatment


Indomethacin (Indocin, Indochron E-R)

Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis. For use with episcleritis that has been nonresponsive to topical treatment.

Adult

100 mg PO qd; decrease to 75 mg when a response is seen

Pediatric

Not established

Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; may cause gastrointestinal disturbances; should not be used in patients with congestive heart failure; other adverse effects, such as platelet aggregation and liver dysfunction, exist with long-term use but should not be a factor in a relatively short duration of treatment

More on Episcleritis

Overview: Episcleritis
Differential Diagnoses & Workup: Episcleritis
Treatment & Medication: Episcleritis
Follow-up: Episcleritis
References

References

  1. Boniuk M. The ocular manifestations of ophthalmic vein and aseptic cavernous sinus thrombosis. Trans Am Acad Ophthalmol Otolaryngol. Nov-Dec 1972;76(6):1519-34. [Medline].

  2. Foster CS, Maza MS. The Sclera. Springer-Verlag; 1994:96-102.

  3. Lim L, Suhler EB, Smith JR. Biologic therapies for inflammatory eye disease. Clin Experiment Ophthalmol. May-Jun 2006;34(4):365-374. [Medline].

  4. Lin CP, Shih MH, Su CY. Scleritis. Surv Ophthalmol. May-Jun 2006;51(3):288-9; author reply 289. [Medline].

  5. Minas TF, Podos SM. Familial glaucoma associated with elevated episcleral venous pressure. Arch Ophthalmol. 1968;80:202-213. [Medline].

  6. Roy FH. Ocular Differential Diagnosis. Vol 1. 7th ed. Baltimore: Williams & Wilkins; 2002.

  7. Watson PG. Episcleritis. In: Current Ocular Therapy. 5th ed. 809.

  8. Watson PG, Hayreh SS. Scleritis and episcleritis. Br J Ophthalmol. 1976;60:163-192. [Medline].

  9. Watson PG, Hazelman BL. The Sclera and Systemic Disorders. Philadelphia: WB Saunders; 1976.

  10. Williams CP, Browning AC, Sleep TJ. A randomised, double-blind trial of topical ketorolac vs artificial tears for the treatment of episcleritis. Eye. Sep 2004;[Medline].

Further Reading

Keywords

simple episcleritis, nodular episcleritis, episcleral tissue, inflammation, conjunctiva, sclera

Contributor Information and Disclosures

Author

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

Medical Editor

Andrew A Dahl, MD, Director of Ophthalmology Teaching, Mid-Hudson Family Practice Institute, The Institute for Family Health; Assistant Professor of Surgery (Ophthalmology), New York College of Medicine
Andrew A Dahl, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American College of Surgeons, American Medical Association, American Society of Cataract and Refractive Surgery, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

R Christopher Walton, MD, Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, Assistant Dean for Graduate Medical Education, University of Tennessee College of Medicine; Consulting Staff, Regional Medical Center, Memphis Veterans Affairs Medical Center, St Jude Children's Research Hospital
R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society
Disclosure: Nothing to disclose.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

James P Gills, MD, Founder, St Luke's Cataract and Laser Institute; Professor, Department of Ophthalmology, University of South Florida College of Medicine
James P Gills, MD is a member of the following medical societies: American Academy of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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