AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Scleritis is a chronic, painful, and potentially blinding inflammatory disease that is characterized by edema and cellular infiltration of the scleral and episcleral tissues. Scleritis is commonly associated with systemic autoimmune disorders, including rheumatoid arthritis, systemic lupus erythematosus, relapsing polychondritis, spondyloarthropathies, Wegener granulomatosis, polyarteritis nodosa, and giant cell arteritis. Scleritis may be the initial or only presenting clinical manifestation of these potentially lethal disorders. The correct and rapid diagnosis and the appropriate systemic therapy can halt the relentless progression of both ocular and systemic processes, thus preventing destruction of the globe and prolonging survival.

Scleritis may be classified into anterior and posterior. Anterior scleritis can be diffuse, nodular, necrotizing with inflammation (necrotizing), and necrotizing without inflammation (scleromalacia perforans). The most common clinical forms are diffuse scleritis and nodular scleritis. Necrotizing scleritis with or without inflammation is much less frequent, more ominous, and frequently associated with systemic autoimmune disorders. Posterior scleritis is characterized by flattening of the posterior aspect of the globe, thickening of the posterior coats of the eye (choroid and sclera), and retrobulbar edema.

Pathophysiology

An autoimmune dysregulation in a genetically predisposed host is presumed to cause scleritis. Inciting factors may include infectious organisms, endogenous substances, or trauma. The inflammatory process may be caused by immune complex–related vascular damage (type III hypersensitivity) and subsequent chronic granulomatous response (type IV hypersensitivity).

The following interact as part of the activated immune network, which can lead to scleral destruction: immune complex vessel deposition in episcleral- and scleral-perforating capillary and postcapillary venules (inflammatory microangiopathy) and cell-mediated immune responses. The autoimmune nature of scleritis also is supported by the frequent association with systemic autoimmune disorders and by the favorable response to immunosuppressive therapy.

Frequency

United States

The exact incidence is uncertain, although scleritis is not common. The reported prevalence is skewed by the somewhat selected referrals of the reporting institutions. Approximately 2.6% of patients who were referred to the Immunology Service at the Massachusetts Eye and Ear Infirmary Hospital of Boston during an 11-year period had scleritis.

International

Approximately 0.08% of patients who were referred to the Department of Ophthalmology of Southern General Hospital and Victoria Infirmary of Glasgow during an 8-year period had scleritis.

Mortality/Morbidity

Patients with scleritis are at risk for ocular complications and systemic disease association.

• Ocular complications of scleritis, which cause vision loss and eye destruction, appear as a result of the extending scleral inflammation. Peripheral ulcerative keratitis (13-14%), uveitis (about 42%), glaucoma (12-13%), cataract (6-17%), and fundus abnormalities (about 6.4%). These complications are most common in necrotizing scleritis, the most destructive type of scleritis.
• Disease association may be found in about 57% of patients with scleritis. Up to 48% of patients with scleritis present with a known connective tissue or vasculitic disease. Some of these diseases are potentially lethal unless treated with prompt and aggressive therapy. Other patients may present with concomitant trauma, infection, or postsurgical inflammation. Systemic disease association is most common in cases of necrotizing scleritis. Scleritis may be the first manifestation of a potentially lethal systemic disease.

Sex

Women are more likely to have scleritis than men (1.6:1).

Age

Scleritis is most common in the fourth to sixth decades of life. The peak incidence is in the fifth decade.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

When interviewing the patient, investigate the following: the major complaint; a history of the present illness; the past history, including infection, injury, or surgery; and the review of systems.

• Symptoms can include pain, tearing or photophobia, tenderness, and decreased visual acuity. The primary sign is redness.
• • Pain is the most common symptom for which patients seek medical assistance, and it is the best indicator of active inflammation. Pain results from both direct stimulation and stretching of the nerve endings by the inflammation.
  • The following pain descriptions are characteristic of scleritis:
  • • Severe, penetrating pain that radiates to the forehead, brow, jaw, or sinuses
    • Awakens the patient during the night
    • Exacerbated by touch; extremely tender
    • Only temporarily relieved by analgesics
  • Tearing or photophobia without mucopurulent discharge, which is usually mild or moderate, may occur in about 25% of patients with scleritis.
  • Upon palpation, the patient may describe tenderness that is diffuse with possible radiation to other parts of the head.
  • Decreased visual acuity may be caused by extension of scleritis to the adjacent structures, leading to keratitis, uveitis, glaucoma, cataract, and fundus abnormalities.
  • Redness gradually increases over several days. It has a bluish red tinge, which is seen best when the examination is performed in natural light. It may be localized in one sector or involve the whole sclera; most frequently, it is in the interpalpebral area. This discoloration does not blanche after topical applications of routine sympathomimetic dilating agents (Neo-Synephrine 2.5%).
• Past medical and ocular histories may elucidate systemic diseases, trauma, drugs, or surgical procedures that might cause scleritis:
• • Connective tissue or vasculitic diseases
  • Infectious diseases
  • Miscellaneous diseases (eg, atopy, rosacea, gout, chemical injuries)
  • Blunt or penetrating ocular trauma
  • Drugs, such as pamidronate (Aredia), alendronate (Fosamax), risedronate (Actonel), zoledronic acid (Zometa), and ibandronate (Boniva)
  • Past ocular surgical procedures, especially within a year prior to the onset of scleritis, might be significant.
• Past medical history is also important for discovering certain conditions (eg, gastric ulceration, diabetes, liver disease, renal disease, hypertension) that eventually might modify future therapy.
• Past and present therapies and responses to these interventions should be investigated.
• Because scleritis can be associated with systemic disorders, make a routine inquiry that covers various bodily systems, as follows:
• • Dermatologic (eg, skin, hair, nails)
  • Respiratory
  • Cardiac
  • Genitourinary
  • Rheumatologic
  • Gastrointestinal
  • Neurologic
  • Ear, nose, sinus, and throat

Physical

The head and extremities (eg, nose, mouth, external ear, skin, joints) examinations may reveal significant signs, which might be compatible with a particular underlying disease. An eye examination might detect and characterize scleral disease. Include scleral and general eye examinations.

• Scleral examination
• • Daylight
    • The sclera may appear diffuse, deep bluish red, or violaceous. After several attacks of scleral inflammation, areas of scleral thinning and translucency may appear, allowing the dark uvea to show.
    • A black, grey, or brown area that is surrounded by active scleral inflammation indicates a necrotizing process. If tissue necrosis progresses, the scleral area may become avascular, producing a white sequestrum in the center that is surrounded by a well-defined black or dark brown circle. The slough may be removed gradually by granulation tissue, leaving the underlying uvea bare or covered by a thin layer of conjunctiva.
  • Slit lamp light
    • In scleritis, maximum congestion is in the deep episcleral network with some congestion in the superficial episcleral network. The posterior and anterior edges of the slit lamp beam are displaced forward because of underlying scleral and episcleral edema.
    • In scleritis, topical application of 2.5% or 10% phenylephrine only blanches the superficial episcleral network without significant effect on the deep episcleral network.
  • Red-free light is helpful to the following study areas:
    • Areas that have maximum vascular congestion
    • Areas that display new vascular channels
    • Areas that are totally avascular
• General eye examination: Evaluate adjacent structures in scleritis at every follow-up visit, since involvement is an important reason for vision loss.
• • Extraocular muscles
  • Cornea
  • Uvea
  • Lens
  • Intraocular pressure
  • Dilated fundus

Causes

Scleritis may occur isolated (43%) or in association with several types of disorders (57%).

• Autoimmune (48%)
• • Connective tissue diseases and other inflammatory conditions include the following:
  • • Rheumatoid arthritis
    • Systemic lupus erythematosus
    • Ankylosing spondylitis
    • Reactive arthritis
    • Psoriatic arthritis
    • Gouty arthritis
    • Inflammatory bowel diseases
    • Relapsing polychondritis
    • Polymyositis
    • Sjögren syndrome
    • Mixed connective tissue disease
    • Progressive systemic sclerosis
  • Vasculitic diseases include the following:
  • • Polyarteritis nodosa
    • Allergic angiitis of Churg-Strauss syndrome
    • Wegener granulomatosis
    • Behçet disease
    • Giant cell arteritis
    • Cogan syndrome
• Infectious (7%) - Bacterial, fungal, viral, or parasitic
• Miscellaneous (2%) - Atopy; rosacea; or secondary to foreign bodies, chemical injuries, or drugs (eg, pamidronate, alendronate, risedronate, zoledronic acid, ibandronate)

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Based on the past history, review of systems, and physical examination, select appropriate diagnostic tests to confirm or reject the following suspected associated diseases:
• • Rheumatoid factor - Rheumatoid arthritis
  • Antinuclear antibodies - Systemic lupus erythematosus, rheumatoid arthritis, polymyositis, progressive systemic sclerosis, or mixed connective tissue
  • Antineutrophil cytoplasmic antibodies (ANCA) - Wegener granulomatosis, polyarteritis nodosa, or microscopic polyangiitis
  • Human leukocyte antigen (HLA) typing - Ankylosing spondylitis, reactive arthritis, psoriatic arthritis, or arthritis associated with inflammatory bowel disease
  • Eosinophil count/immunoglobulin E (IgE) - Allergic angiitis of Churg-Strauss syndrome or atopy
  • Uric acid - Gout
  • Erythrocyte sedimentation rate (ESR) - Giant cell arteritis
  • Hepatitis B surface antigen (HBsAg) - Polyarteritis nodosa
  • Serologies - Infectious diseases, including syphilis
  • Tuberculosis (TB) and anergy skin testing - Rare occurrence of TB or sarcoidosis

Imaging Studies

• Chest x-ray - TB, Wegener granulomatosis, allergic angiitis of Churg-Strauss syndrome, or atopy
• Sinus films - Wegener granulomatosis
• Sacroiliac x-ray - Ankylosing spondylitis, reactive arthritis, psoriatic arthritis, or arthritis associated with inflammatory bowel disease
• Limb joint x-ray - Rheumatoid arthritis, psoriatic arthritis, arthritis associated with inflammatory bowel disease, or gout
• Ultrasonography (A- and B-scan) - Posterior scleritis; most helpful test to aid in diagnosing posterior scleritis, which is characterized by flattening of the posterior aspect of the globe, thickening of the posterior coats of the eye (choroid and sclera), and retrobulbar edema
• CT scan - Posterior scleritis; a useful diagnostic tool to aid in detecting the following, which are important to differentiate posterior scleritis from orbital inflammatory diseases and orbital neoplasm: extraocular muscle or lacrimal gland enlargement, sinus tissue involvement, and posterior scleral thickening
• MRI - Posterior scleritis
• • MRI is used to differentiate localized inflammatory pseudotumor from posterior scleritis in proptosis or choroidal tumors from posterior scleritis in subretinal mass.
  • Some orbital tumors, which cause choroidal folds and retinal striae, are also signs of posterior scleritis that are detected successfully by MRI.

Other Tests

• Skin testing
• • Intracutaneous tuberculin purified protein derivative (PPD) - TB
  • Prick test - Atopy
• Smears, cultures, and polymerase chain reaction (PCR) from conjunctival, corneal, episcleral, or scleral scraping - Infectious scleritis
• • Scleral or corneoscleral biopsy is recommended if smears and culture results are negative at 48 hours, infectious scleritis is still the primary clinical suspicion, and the patient is worsening.
    • One third of tissue from a biopsy is sent to the microbiology department, where it is homogenized for smears, cultures, and PCR.
    • The middle third of tissue is transported to the pathology department for histopathology with special stains (eg, periodic acid-Schiff [PAS], Gomori methenamine-silver, acid-fast, calcofluor white).
    • The last third of tissue is sent to the immunology department for immunofluorescence studies with monoclonal antibodies (eg, anti–herpes simplex virus type 1, anti–varicella-zoster virus antibodies).
• PCR of body fluids - Infectious scleritis

Procedures

• Low-dose anterior segment fluorescein angiography (FA) combined with anterior segment indocyanine green (ICG) angiography is recommended. ICG distinguishes totally occluded vessels from the temporary obstruction caused by high endothelial venules or vascular spasm seen as nonperfusion with FA. FA identifies new corneal vessels and leakage, whereas ICG does not. ICG locates the site of maximum inflammation and is more valuable in assessing the effects of treatment and when to withdraw that treatment.
• • Diffuse scleritis
    • FA - Rapid filling, short transit time, extensive leakage, normal vascular pattern, and deep sclera leakage in early disease
    • ICG - Rapid filling, short transit time, no leakage except for local vascular damage, and occasionally late deep leakage
  • Nodular scleritis
    • FA - Rapid transit time, abnormal leakage pattern, and staining nodules
    • ICG - Rapid filling, short transit time, and stained nodules
  • Necrotizing scleritis
    • FA - Hypoperfusion and venular occlusion, increased transit time, new vessel formation, and deep staining
    • ICG - Hypoperfusion and venular occlusion, increased transit time, and late leakage from new or damaged vessels
  • Scleromalacia perforans
    • FA - Virtually no perfusion
    • ICG - Leakage in area of necrotic tissue
  • Posterior scleritis
    • FA - Retinal pigment epithelial detachments, serous retinal detachment, cystoid edema, choroidal folds, and hyperfluorescent and hypofluorescent areas
    • ICG - Diffuse zonal choroidal hyperfluorescence intermediate or late phase, pinpoint leakage, delayed choroidal perfusion, and hyperfluorescence in areas of maximal activity

Histologic Findings

Diffuse scleritis or nodular scleritis

A nongranulomatous inflammatory reaction occurs that is characterized by infiltration of mononuclear cells, such as macrophages, lymphocytes, and plasma cells. In the most severe cases, mononuclear cells may organize into granulomatous lesions. Mast cells, neutrophils, and eosinophils may also be present.

Necrotizing scleritis

A granulomatous inflammatory reaction occurs that is characterized by a central area of fibrinoid necrosis, surrounded by epithelioid cells, multinucleated giant cells, lymphocytes, and plasma cells. Neutrophils, mast cells, and eosinophils are dispersed throughout the inflamed tissue and around vessels. Inflammatory microangiopathy, which is characterized by neutrophilic infiltration in and around the episclera and sclera that perforates the vessel walls with or without fibrinoid necrosis, is frequently seen.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Treatment almost always requires systemic therapy. Patients with an associated disease, such as rosacea, gout, atopy, or infection, need specific treatment.

• Treatment of noninfectious scleritis: Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or immunomodulatory drugs are indicated. Topical therapy is routinely insufficient. This treatment must be individualized for the severity of the scleritis, response to treatment, adverse effects, and presence of the associated disease.
• • Diffuse scleritis or nodular scleritis
  • • The initial therapy consists of an NSAID; in case of therapeutic failure, 2 different NSAIDs should be tried in succession with the first drug. In high-risk patients, consider appropriate gastrointestinal protection with misoprostol or omeprazole.
    • If NSAIDs are not effective or have untoward complications, oral corticosteroids can be substituted. Remission may be maintained with continued NSAIDs.
    • Periorbital and subconjunctival steroid injections have been reported to be efficacious as adjunctive therapy. Caution should be observed.
    • In case of therapeutic failure of corticosteroids, immunosuppressive drugs should be added or substituted. Methotrexate can be the first choice, but azathioprine, cyclophosphamide, or cyclosporine may be helpful. Cyclophosphamide should be the first choice in treating patients with associated potentially lethal vasculitic diseases, such as Wegener granulomatosis or polyarteritis nodosa.
    • In case of therapeutic failure, other immunomodulatory drugs, such as the tumor necrosis factor alpha (TNF-alpha) inhibitor infliximab, may be effective, although further investigation is warranted.
  • Necrotizing scleritis
  • • The initial therapy consists of immunosuppressive drugs that are supplemented with corticosteroids during the first month; the latter is tapered slowly, if possible. Cyclophosphamide is the most effective drug.
    • In case of therapeutic failure, another immunomodulatory drug, such as infliximab, may be effective. Other alternatives are daclizumab and rituximab, although their efficacy awaits further study.
    • Periocular steroid injections should be applied with great caution in cases of necrotizing scleritis or peripheral ulcerative keratitis. Some authors believe that depot steroids actually may exacerbate necrotizing disease.
    • Pulse intravenous cyclophosphamide with or without pulse intravenous corticosteroids may be required for urgent cases and may be followed by maintenance therapy.
• Treatment of infectious scleritis: Systemic treatment with or without topical antimicrobial therapy always is required. Differentiating infectious scleritis from noninfectious scleritis is important because corticosteroid therapy and immunosuppressive therapy (often used in noninfectious autoimmune scleritis) are contraindicated in active infections.

Surgical Care

• Tectonic surgical procedures rarely may be required to preserve the integrity of the globe.
• • Scleral grafts are fresh sclera or glycerin-preserved sclera that is available through eye banks. Grafts may be performed in cases of pending perforation during the time before the effects of systemic immunosuppressive agents manifest.
  • Corneal tissue may be used for associated corneal disease.

Consultations

• Rheumatology or internal medicine consultation for associated disease
• Hematology, oncology, or internal medicine consultation for immunosuppressive therapy

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Drug Category: Corticosteroids

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

Drug Category: Immunosuppressive drugs

Inhibit immune system activities.

Drug Category: Monoclonal antibodies

Selective immunomodulators that affect specific aspects of the inflammatory pathways.

Drug Category: Blood products

Are used to improve clinical and immunologic aspects of the disease. They may decrease autoantibody production and increase solubilization and removal of immune complexes.

Drug Category: Nonsteroidal anti-inflammatory drugs

Have analgesic, anti-inflammatory, and antipyretic activities. 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. Systemic therapy with NSAIDs, corticosteroids, and immunosuppressive agents may be effective in patients with noninfectious scleritis.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• In cases of pending scleral perforation, peripheral ulcerative keratitis perforation, or positive Seidel test, admit for scleral patch grafting.

Further Outpatient Care

• Patients should have a scleral examination and general eye examination at every follow-up visit.
• Carefully monitor medication type, dose, and adverse effects. In case of therapeutic failure, change the medication type.
• Consultation with other specialists for associated systemic disease and/or immunosuppressive therapy follow-up care is recommended.

In/Out Patient Meds

• Systemic medications include NSAIDs, corticosteroids, or immunomodulatory agents, depending on the type of scleritis and/or associated disease.

Complications

• Keratopathy - Peripheral corneal thinning, acute stromal keratitis, sclerosing keratitis, or peripheral ulcerative keratitis
• Uveitis - Anterior or posterior
• Glaucoma
• Cataract
• Fundus abnormalities - Choroidal folds, subretinal mass, disk edema, macular edema, annular ciliochoroidal detachment, or serous retinal detachment

Prognosis

• Ocular prognosis of scleritis with systemic autoimmune diseases varies, depending on the specific autoimmune disease.
• • Scleritis in spondyloarthropathies or in systemic lupus erythematosus, usually a relatively benign and self-limiting condition, is diffuse scleritis or nodular scleritis without ocular complications.
  • Scleritis in Wegener granulomatosis is a severe disease that can lead to permanent blindness; it is usually necrotizing scleritis with ocular complications.
  • Scleritis in rheumatoid arthritis or relapsing polychondritis is a disease of intermediate severity; it may be diffuse, nodular, or necrotizing scleritis with or without ocular complications.
  • Scleritis without systemic disease association is often more benign than scleritis accompanied by infection or autoimmune disease. These cases of idiopathic scleritis may be mild, shorter in duration, and more likely to respond to topical steroid drops alone.

Patient Education

• For excellent patient education resources, visit eMedicine's Eye and Vision Center. Also, see eMedicine's patient education article Eye Pain.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to inform patient and family of the adverse effects of NSAIDs, corticosteroids, or immunomodulatory agents
• Failure to treat with immunosuppressive agents in cases of scleritis associated with Wegener granulomatosis or polyarteritis nodosa
• Failure to establish or attempt to identify an underlying infectious or autoimmune etiology in severe, recurrent, or recalcitrant cases of scleritis

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Ahmadi-Simab K, Lamprecht P, Nölle B, Ai M, Gross WL. Successful treatment of refractory anterior scleritis in primary Sjögren´s syndrome with rituximab. Annals of Rheumatic Diseases. 2005;64:1087-1088. [Medline].
• Cazabon S, Over K, Butcher J. The successful use of infliximab in resistant relapsing polychondritis and associated scleritis. Eye. Feb 2005;19(2):222-4. [Medline].
• Cheung CMG, Murray PI, Savage COS. Successful treatment of Wegener´s granulomatosis associated scleritis with rituximab. Br J Ophthalmol. 2005;89:1542-1543. [Medline].
• Fong LP, Sainz de la Maza M, Rice BA, Kupferman AE, Foster CS. Immunopathology of scleritis. Ophthalmology. Apr 1991;98(4):472-9. [Medline].
• Hakin KN, Ham J, Lightman SL. Use of orbital floor steroids in the management of patients with uniocular non-necrotising scleritis. Br J Ophthalmol. Jun 1991;75(6):337-9. [Medline].
• Murphy CC, Ayliffe WH, Booth A, Makanjuola D, Andrews PA, Jayne D. Tumor necrosis factor alfa blockade with infliximab for refractory uveitis and scleritis. Ophthalmology. 2004;111(2):352-356. [Medline].
• Murphy CC, Ayliffe WH, Booth A, Makanjuola D, Andrews PA, Jayne D. Tumor necrosis factor alpha blockade with infliximab for refractory uveitis and scleritis. Ophthalmology. Feb 2004;111(2):352-6. [Medline].
• Nieuwenhuizen J, Watson PG, Emmanouilidis-van der Spek K, Keunen JE, Jager MJ. The value of combining anterior segment fluorescein angiography with indocyanine green angiography in scleral inflammation. Ophthalmology. Aug 2003;110(8):1653-66. [Medline].
• Papaliodis GN, Chu D, Foster CS. Treatment of ocular inflammatory disorders with daclizumab. Ophthalmology. Apr 2003;110(4):786-9. [Medline].
• Sainz de la Maza M, Foster CS, Jabbur NS. Scleritis associated with rheumatoid arthritis and with other systemic immune-mediated diseases. Ophthalmology. Jul 1994;101(7):1281-6; discussion 1287-8. [Medline].
• Sainz de la Maza M, Foster CS, Jabbur NS. Scleritis associated with systemic vasculitic diseases. Ophthalmology. Apr 1995;102(4):687-92. [Medline].
• Sainz de la Maza M, Jabbur NS, Foster CS. An analysis of therapeutic decision for scleritis. Ophthalmology. Sep 1993;100(9):1372-6. [Medline].
• Sainz de la Maza M, Jabbur NS, Foster CS. Severity of scleritis and episcleritis. Ophthalmology. 1994;101(2):389-396. [Medline].
• Sainz de la Maza M, Tauber J, Foster CS. Scleral grafting for necrotizing scleritis. Ophthalmology. Mar 1989;96(3):306-10. [Medline].
• Sobrin L, Kim EC, Christen W, Papadaki T, Letko E, Foster CS. Infliximab therapy for the treatment of refractory ocular inflammatory disease. Arch Ophthalmol. Jul 2007;125(7):895-900. [Medline].
• Tuft SJ, Watson PG. Progression of scleral disease. Ophthalmology. 1991;98(4):467-471. [Medline].
• Wakefield D, McCluskey P. Cyclosporin therapy for severe scleritis. Br J Ophthalmol. 1989;73(9):743-746. [Medline].
• Watson PG, Hayreh SS. Scleritis and episcleritis. Br J Ophthalmol. Mar 1976;60(3):163-91. [Medline].

Article Last Updated: Nov 8, 2007