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Episcleritis Medication

  • Author: Hampton Roy, Sr, MD; Chief Editor: John D Sheppard, Jr, MD, MMSc  more...
 
Updated: Mar 03, 2016
 

Medication Summary

The goals of pharmacotherapy are to decrease pain, improve quality of life, to reduce morbidity, and to prevent complications.[12]

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Corticosteroids

Class Summary

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

Dexamethasone ophthalmic (Ozurdex, Maxidex)

 

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.

Prednisolone acetate 1% (Pred Forte, Omnipred, Pred Mild)

 

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.

Loteprednol ophthalmic (Alrex, Lotemax)

 

Sterile ophthalmic suspension with an ester steroid. This molecular change from the basic steroid ring structure substitutes an ester rather than a ketone at the 20 position, thus imparting a favorable IOP and cataractogenesis profile. This versatile agent has numerous FDA-approved indications, including postcataract inflammation, anterior uveitis, seasonal allergic conjunctivitis, and giant papillary conjunctivitis.

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Nonsteroidal Anti-inflammatory Agents

Class Summary

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

 

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.

Indomethacin (Indocin, Tivorbex)

 

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.

Ibuprofen (Advil, Motrin, Addaprin, Dyspel, Provil)

 

Ibuprofen is usually the DOC for treating mild to moderate pain if no contraindications exist. It is one of the few NSAIDs indicated for fever reduction.

Ketoprofen

 

Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small patients, elderly patients, and patients with renal or liver disease. Doses higher than 75 mg do not increase the therapeutic effects. Administer high doses with caution and closely observe the patient’s response.

Naproxen (Aleve, Anaprox, Anaprox DS, Naprelan, Naprosyn)

 

Naproxen is used for the relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing COX activity, which results in decreased prostaglandin synthesis.

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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, Pan-American Association of Ophthalmology

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.

R Christopher Walton, MD Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, University of Tennessee College of Medicine

R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, Retina Society, American College of Healthcare Executives, American Uveitis Society

Disclosure: Nothing to disclose.

Chief Editor

John D Sheppard, Jr, MD, MMSc Professor of Ophthalmology, Microbiology and Molecular Biology, Clinical Director, Thomas R Lee Center for Ocular Pharmacology, Ophthalmology Residency Research Program Director, Eastern Virginia Medical School; President, Virginia Eye Consultants

John D Sheppard, Jr, MD, MMSc is a member of the following medical societies: American Academy of Ophthalmology, American Society for Microbiology, American Society of Cataract and Refractive Surgery, Association for Research in Vision and Ophthalmology, American Uveitis Society

Disclosure: Nothing to disclose.

Additional Contributors

Andrew A Dahl, MD, FACS Assistant Professor of Surgery (Ophthalmology), New York College of Medicine (NYCOM); Director of Residency Ophthalmology Training, The Institute for Family Health and Mid-Hudson Family Practice Residency Program; Staff Ophthalmologist, Telluride Medical Center

Andrew A Dahl, MD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Intraocular Lens Society, American Medical Association, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Medical Society of the State of New York, New York State Ophthalmological Society, Outpatient Ophthalmic Surgery Society

Disclosure: Nothing to disclose.

References
  1. Foster CS, Maza MS. The Sclera. Springer-Verlag; 1994. 96-102.

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

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

  4. Watson PG. Episcleritis. Current Ocular Therapy. 5th ed. 809.

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

  6. Yadav S, Rawal G. Tubercular Nodular Episcleritis: A Case Report. J Clin Diagn Res. 2015 Aug. 9 (8):ND01-2. [Medline].

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

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

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

  10. Axmann S, Ebneter A, Zinkernagel MS. Imaging of the Sclera in Patients with Scleritis and Episcleritis using Anterior Segment Optical Coherence Tomography. Ocul Immunol Inflamm. 2015 Aug 10. 1-6. [Medline].

  11. 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].

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

 
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